October 17-21, 2009New Orleans, LA

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JOURNAL SYMPOSIUM/Best Abstracts of the Meeting/Anesthesiology/FAER

Room 252-254 Monday. 8-10BA01 Best Abstracts of the Meeting: Anesthesiology Editors'

PicksA: 1594-1605

Room 395-396 Tuesday. 8-11 JS01 Journal SymposiumA: 1618-1626

Room 386-387 Tuesday. 1-4 FS01 Anesthesiology/FAER SessionA: 1606-1617

POSTER DISCUSSION/ORAL SESSION

Saturday10/17 8:00 - 9:30 10:00 - 11:30 1:00 - 2:30 3:00 - 4:30

Room 354Clinical Circulation

OR03-01 A: 1-6

Pediatric Anesthesia OR16-02

A: 169-174

Ambulatory andGeriatricOR01-01

A: 191-196

Clinical CirculationOR03-03

A: 285-290

Room 355ExperimentalCirculation OR08-01 A: 7-12

Regional Anes/Acute PainOR10-03

A: 163-168

Chronic-Cancer PainOR11-01

A: 197-202

Patient SafetyOR14-04

A: 291-296

Room 356Clinical Neurosciences

PD04-02 A: 13-20

Equip-MonitoringPD07-03

A: 183-190

Clinical CirculationPD03-05

A: 203-210

Regional AnesthesiaPD10-01

A: 305-312

Room 357Patient Safety

PD14-01 A: 21-28

Critical CarePD05-04

A: 175-182

ObstetricPD13-01

A: 211-218

Equip-MonitoringPD07-04

A: 297-304

Sunday10/18 8:00 - 9:30 10:00 - 11:30 1:00 - 2:30 3:00 - 4:30

Room 354Anes. Action/Bio

OR02-01A: 313-318

Drug Disposition OR06-01

A: 460-465

Clinical CirculationOR03-02

A: 486-491

Critical CareOR05-01

A: 646-651

Room 355Equipment/Mont

OR07-01A: 319-324

ExperimentalNeurosciences

OR09-04A: 466-471

AmbulatoryPD01-03

A: 492-499

Anesthetic Action PD02-04

A: 652-659

Room 356Experimental Neuro

PD09-01 A: 325-334

Patient SafetyPD14-02

A: 480-485

Clinical CirculationPD03-04

A: 500-507

History/EducationPD15-01

A: 668-675

Room 357RespirationPD17-02

A: 335-342

Equip-MonitoringPD07-05

A: 472-479

Drug DispositionPD06-03

A: 508-515

ClinicalNeurosciences

PD04-04 A: 660-667

Monday10/19 9:00 - 10:30 1:00 - 2:30 3:00 - 4:30

Room 354Regional Anes/Acute

PainOR10-02

A: 676-681

Experimental CirculationOR08-02

A: 847-852

Clinical NeuroscienceOR04-01

A: 1012-1017

Room 355Pediatric Anesthesia

OR16-03 A: 682-687

NeuromuscularOR12-01

A: 853-858

Equipment/MontOR07-02

A: 1018-1023

Room 356Experimental Neuro

PD09-03 A: 688-696

Patient SafetyPD14-03

A: 867-873

Amb/GeriatricPD01-02

A: 1024-1031

Room 357Regional Anesthesia

PD10-04 A: 697-704

ObstetricPD13-02

A: 859-866

Critical CarePD05-05

A: 1032-1039

Tuesday10/20 8:00 - 9:30 1:00 - 2:30 3:00 - 4:30

Room 354Pediatric Anesthesia

OR16-04A: 1046-1051

Anes.ActionPD02-03

A: 1224-1231

RespirationOR17-01

A: 1376-1381

Room 355Chronic-Cancer Pain

OR11-02 A: 1040-1045

Regional Anes/Acute PainOR10-05

A: 1218-1223

Patient SafetyPD14-05

A: 1390-1396

Room 356Drug Disposition

PD06-02 A: 1052-1059

Regional AnesthesiaPD10-06

A: 1232-1240

Experimental NeuroPD09-02

A: 1382-1389

Room 357Patient Safety

PD14-07 A: 1060-1066

History/EducationPD15-02

A: 1241-1248

Wednesday 8:00 - 9:30 10:00-11:30

10/21 8:00 - 9:30 10:00-11:30

Room 354Critical CareOR05-02

A: 1403-1408

Pediatric AnesthesiaOR16-01

A: 1564-1569

Room 355Anes. Action/Bio

OR02-02 A: 1397-1402

Clinical CirculationPD03-06

A: 1570-1577

Room 356Regional Anesthesia

PD10-07 A: 1417-1424

Patient SafetyPD14-06

A: 1586-1593

Room 357Clinical Neurosciences

PD04-03 A: 1409-1416

Critical CarePD05-03

A: 1578-1585

POSTER SESSIONS - ALL Sessions in Hall F (Max of 30 papers per session)

Saturday9-11 A.M.

Hall F

P01-A PediatricsPO16-01

A: 144-162

P02-B Chronic/Cancer

Pain PO11-01

A: 126-143

P03-C RegionalPO10-01

A: 111-125

P04-D Experimental

NeurosciencesPO09-01 A: 97-110

P05-E Clinical

CirculationPO08-01 A: 81-96

P06-F Equip-

MonitoringPO07-01 A: 61-80

P07-GClinical

CirculationPO03-01A: 46-60

P08-HAmb/Geriatric

PO01-01A: 29-45

Saturday2-4 P.M.Hall F

P09-I Critical Care

PO05-01 A: 230-245

P10-J Respiration PO17-01

A: 266-284

P11-K Clinical Neuro

PO04-01 A: 219-229

P12-L Patient Safety

PO14-01 A: 246-265

Sunday9-11 A.M.

Hall F

P13-A History-

EducationPO15-03

A: 440-459

P14-B Experimental

Neurosciences PO09-07

A: 404-415

P15-C Neuromuscular

PO12-01 A: 429-439

P16-D RegionalPO10-06

A: 416-428

P17-E Drug

DispositionPO06-01

A: 374-388

P18-F Equip-

MonitoringPO07-06 A: 389-

403

P19-GClinical

CirculationPO03-02 A: 343-

357

P20-HCritical CarePO05-02

A: 358-373

Sunday2-4 P.M.Hall F

P21-I PediatricsPO16-02

A: 628-645

P22-J Chronic/Cancer

PainPO11-02

A: 586-602

P23-K Regional PO10-02

A: 573-585

P24-L Experimental

NeurosciencesPO09-02

A: 559-572

P25-M Clinical

CirculationPO08-02

A: 544-558

P26-N Equip-

MonitoringPO07-02 A: 529-

543

P27-OClinicalNeuro

PO04-03 A: 516-

528

P28-PPatientSafety

PO14-04 A: 603-627

Monday9-11 A.M.

Hall F

P29-A Experimental

NeurosciencesPO09-03

A: 774-789

P30-B PediatricsPO16-03

A: 828-846

P31-C RegionalPO10-03

A: 790-807

P32-D Clinical

CirculationPO08-03

A: 754-773

P33-E ObstetricPO13-01

A: 808-827

P34-F Equip-

MonitoringPO07-03 A: 737-

753

P35-G Clinical

CirculationPO03-06 A: 722-

736

P36-HAmb/Geriatric

PO01-02 A: 705-721

Monday2-4 P.M.Hall F

P37-I Patient Safety

PO14-03 A: 987-1011

P38-J Chronic/Cancer

PainPO11-03

A: 970-986

P39-K RegionalPO10-07

A: 953-969

P40-L Experimental

NeurosciencesPO09-06

A: 938-952

P41-M Equip-

MonitoringPO07-07

A: 922-937

P42-N Clinical

CirculationPO03-03 A: 874-

888

P43-O CriticalCare

PO05-03 A: 906-

921

P44-PClinicalNeuro

PO04-04A: 889-905

Tuesday9-11 A.M.

Hall F

P45-A Patient Safety

PO14-06 A: 1163-1181

P46-B PediatricsPO16-04

A: 1182-1198

P47-C Experimental

NeurosciencesPO09-04

A: 1129-1144

P48-D Clinical

CirculationPO03-04

A: 1099-1113

P49-E Amb/Geriatric

PO01-03 A: 1067-

1083

P50-F RespirationPO17-02 A: 1199-

1217

P51-GClinicalNeuro

PO04-02 A: 1114-

1128

P52-HAnes. Action

PO02-01 A: 1084-

1098

Tuesday2-4 P.M.Hall F

P53-I Chronic/Cancer

Pain PO11-04

A: 1145-1162

P54-J Clinical

CirculationPO08-04

A: 1295-1322

P55-K RegionalPO10-04

A: 1323-1334

P56-L ObstetricPO13-02

A: 1335-1354

P57-M Equip-

MonitoringPO07-04 A: 1280-

1294

P58-N CriticalCare

PO05-04 A: 1264-

1279

P59-OAnes.Action

PO02-02 A: 1249-

1263

P60-PHistory-

EducationPO15-01 A: 1355-

1375

Wednesday9-11 A.M.

Hall F

P61-A Patient Safety

PO14-05 A: 1499-1522

P62-B PediatricsPO16-05

A: 1544-1563

P63-C RegionalPO10-05

A: 1487-1498

P64-D Experimental

NeurosciencesPO09-05

A: 1472-1486

P65-E History-

EducationPO15-02 A: 1523-

1543

P66-F Equip-

MonitoringPO07-05 A: 1456-

1471

P67-GClinical

CirculationPO03-05 A: 1425-

1439

P68-HCritical CarePO05-05 A: 1440-

1455

Copyright © 2009, American Society of Anesthesiologists. All rights reserved.

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A129 October 17, 2009 9:00 AM - 11:00 AMRoom Area B

Role of the CNBD in Glycosylation and Plasma Membrane Targeting of theHCN Channels ** Ryuji Kaku, M.D., Ph.D., Tomoko Kawakami, M.D., Ph.D., Maya Mikami, M.D., Ph.D., Jay Yang, M.D.,Ph.D.Anesthesiology, Columbia University P&S, New York, New York

Introduction : Many painful clinical and experimental neuropathies are characterized by the generation ofspontaneous action potentials in nerves 1 . While the precise mechanism responsible for the spontaneousaction potentials is likely multifactorial, the HCN ion channels appear to play a role and upregulation andaccumulation of HCN has been observed in nerves in experimental models of neuropathic pain 2 . HCN,like many ion channels, is a glycoprotein and glycosylation plays a role in proper targeting of this protein tothe plasma membrane 3, 4 . Since the amount of HCN ion channels in the plasma membrane regulatesexcitability and generation of spontaneous action potentials, we investigated the role of glycosylation in theplasma membrane targeting of HCN1 and HCN2, the predominant isoforms found in dorsal root ganglionand the spinal cord.

Methods : Wild type mouse HCN1 and HCN2 cDNAs were subcloned into pCI/neo and expressed inHEK293 cells after transfection. The glycosylation deficient mutants HCN1-N327Q and HCN2-N380Q werecreated by overlap PCR and the truncation mutants by simple PCR and 3 piece ligation. The proteinspresent in the plasma membrane were assessed by surface biotinylation and protein-protein interactionsby co-immunoprecipitation followed by Western blot analyses. Pharmacological increase in cAMP wasaccomplished by a treatment with forskolin (2.5 to 10 µM) and a decrease in cAMP with SQ22536 (250 to1000 µM).

Results : Both wild type mHCN1 and HCN2 are N-glycosylated glycoproteins as demonstrated by amobility shift after treatment with PNGase F that selectively cleaves N-glycosylation. Biotinylationexperiments demonstrated that the wt-HCN1, wt-HCN2, and HCN1-N327Q when expressed by itself allproperly target to the plasma membrane. In contrast, HCN2-N380Q failed to insert into the plasmamembrane. Co-expression of wt- and glycosylation mutants demonstrated that wt- or HCN1-N327Q failedto rescue HCN2-N380Q mutant not allowing surface expression of the heterodimers. Expression of HCN1C-terminal truncation mutants unexpectedly revealed the critical role of the cyclic nucleotide bindingdomain (CNBD) in HCN1 glycosylation. Truncation mutants devoid of the CNBD domain were notglycosylated. Since CNBD couples cAMP to channel modulation, we tested the hypothesis that cAMP mayalso modulate glycosylation. Treatment with forskolin reduced whilst SQ22536 increased the glycosylationof HCN1 and HCN2. Experiments are in progress to determine whether similar cAMP mediated modulationof HCN glycosylation and plasma membrane targeting occur in the spinal cord.

Conclusions : HCN1 targeted to the plasma membrane regardless of the glycosylation status in contrastto the previously reported obligatory role of glycosylation in plasma membrane targeting of other HCNisoforms. Furthermore, wt-HCN1 failed to rescue HCN2-N380Q mutants indicating a novel dominant-negative role of non-glycosylated HCN2 in inhibiting plasma membrane targeting of heterodimers. cAMP,possibly through conformational change induced by binding to CNBD, regulated HCN1 and HCN2glycosylation.

References :

1. Devor M, Seltzer Z (1999) Textbook of pain pp 129-63.

2. Brown SM, Dubin AE, Chaplan SR (2004) Pain Pract 4: 182-93.

3. Much B, Wahl-Schott C, Zong Z, et al (2003) J Biol Chem 278: 43781-6.

4. Zha Q, Brewster AL, Richichi C, et al (2008) J Neurochem 105: 68-77.

From Proceedings of the 2009 Annual Meeting of the American Society Anesthesiologists.

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A114 October 17, 2009 9:00 AM - 11:00 AMRoom Area C

Anti-Nociceptive Effect of Decoy ODN Inhibiting BDNF in Rat InflammatoryPain Model ** Norihiko Obata, M.D., Yoshikazu Matsuoka, M.D., Ph.D., Yoshitaro Itano, Ph.D., MasatakaYokoyama, M.D., Ph.D., Kiyoshi Morita, M.D., Ph.D.Anesthesiology and Resuscitology, Okayama University Hospital, Okayama, Japan

Introduction:

Brain-derived neurotrophic factor (BDNF) is upregulated in dorsal root ganglion (DRG) in response toperipheral tissue or nerve injury. BDNF is thought to be transported to spinal dorsal horn and potentiatepain transduction from primary sensory neurons. BDNF gene consists from nine exons (Exons 1 through9), which are transcribed into splice-variants mRNA separately (1). We previously reported that BDNFExon 1 might play an important role in inflammatory pain transduction (2). Therefore, we investigated theeffect of decoy oligodeoxynucleotide (ODN) inhibiting BDNF Exon 1 on rat inflammatory pain.

Materials and Methods:

Animal model

Male Sprague–Dawley rats were used. Inflammation was induced by intraplantar injection of 0.1 mLcomplete Freund's adjuvant (CFA) into the left hind paw. Seven days before CFA injection, intrathecalcatheter was inserted between L6 and S1 to have the top of the catheter locating near L5 DRG underanesthesia. DNA decoy or control was injected intrathecally once a day for three days just before CFAinjection. Behavioral tests were performed for three days before and five days after CFA injection (n = 5).Mechanical hyperalgesia were assessed as 50% paw withdrawal threshold (PWT) by Chaplan's up-downmethod using von Frey filaments.

Synthesis of decoy ODN

Three kinds of decoy fragments were cloned into plasmid vectors. We amplified the double-stranded DNAcontaining decoy fragments by PCR using these vectors as templates. These PCR products were purifiedand mixed in equal amounts. This mixed solution was used as the decoy. Plasmid vector without any ofdecoy fragments was used as a control ODN.

Statistical analysis

Data are shown as mean ± S.E.M. Differences were evaluated by Welch's t test. P < 0.05 was consideredstatistically significant.

Results:

Intrathecal injection of the decoy and the control before CFA injection did not change 50% PWT. In bothgroups, CFA injection into left hind paw decreased ipsilateral 50% PWT for five days after CFA injection.Ipsilateral 50% PWT in the decoy group on the day 1, 2, 3, and 5 were significantly higher than those inthe control group.[figure1]Contralateral 50% PWT did not change at any time points in both groups.

No motor deficiency was observed during experimental period.

Conclusions:

Intrathecal injection of decoy ODN to BDNF Exon 1 suppressed CFA-induced inflammatory pain. Thisstudy suggests that suppression of BDNF Exon 1 may be a novel strategy to treat inflammatory pain.

Reference:

1. Aid, T et al. Mouse and rat BDNF gene structure and expression revisited., J Neurosci Res, 85, 3, 2007

2. Matsuoka, Y et al. Expression profiles of BDNF splice variants in cultured DRG neurons stimulated withNGF., Biochem Biophys Res Commun, 362, 3, 2007.

From Proceedings of the 2009 Annual Meeting of the American Society Anesthesiologists.

Figure 1

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A270 October 17, 2009 2:00 PM - 4:00 PMRoom Area J

Rho-Kinase Inhibitors Augment Anesthetics-Induced Relaxation in RatAirway Smooth Muscle ** Motohiko Hanazaki, M.D., Masataka Yokoyama, M.D., Kiyoshi Morita, M.D., Atsushi Kohjitani, D.D.S.,Yoshihiko Chiba, Ph.D.Department of Anesthesiology and Resuscitology, Okayama University Medical School, Okayama, Japan

Introduction

Most anesthetic agents relax airway smooth muscle (ASM). ASM contraction is caused by both increasingintracellular Ca 2+ ([Ca 2+ ]i) and increasing the force at the same [Ca 2+ ]i (increase in Ca 2+ sensitivity).The small G-protein RhoA and Rho-kinase (ROCK) play important roles in regulating Ca 2+ sensitivity. Inthis study, we investigated the effects of selective ROCK inhibitors on ASM contraction and the influenceof ROCK inhibitors on anesthetic-induced relaxation in ASM to test the hypothesis; although bothanesthetics and ROCK inhibitors relax ASM independently, anesthetic-induced relaxation would beenhanced by addition of a low concentration ROCK inhibitor.

Methods

Ring strips from intrapulmonary bronchus of male Wistar rats (6 weeks, 180-220 g) were placed in 400-µlorgan baths containing Krebs–Henseleit solution (bubbled with 95% O 2 -5% CO 2 , 37°C, resting tension50mg). After obtaining stable contraction with 30 µM acetylcholine (ACh), isometric forces were measuredwith the following protocols:

(1) Y-27632 (0.01 – 300 µM), fasudil (0.01 – 100 µM), or H-1152 (0.01 - 100 µM) were cumulativelyapplied.

(2) propofol (1 µM – 1 mM), with or without Y-27632, fasudil or H-1152 (0.03, 0.1 µM), was cumulativelyapplied.

(3) isoflurane (0.5 – 4.0%), with or without Y-27632 (1 µM), was cumulatively applied. Statisticalsignificance of difference between groups was determined by Two-way analysis of variance (ANOVA),followed by Bonferroni's test (p<0.05 was considered significant).

Results

(1) All ROCK inhibitors, especially H-1152, produced concentration-dependent relaxation. (n=5 each)

(2) 0.03 µM Y-27632 and fasudil did not affect the relaxation by propofol, while 0.1 µM both agentssignificantly shifted concentration-response curves to the left (p=0.040 (Y-27632), p=0.023 (Fasudil)) (n=5each).

H-1152 (0.03 and 0.1 µM) significantly shifted the concentration-response curve to the left (p<0.001). (n=5each)

(3) Y-27632 significantly shifted the concentration-response curve for isoflurane to the left. (P<0.001)(n=5)

Discussion

ROCK inhibitors, especially H-1152 showed the inhibitory effects on ASM. Previous report showed that Y-27632 inhibit Ca 2+ sensitivity in skinned rat ASM with the experimental system same as this study,strongly suggesting that ROCK inhibitors commonly inhibit Ca 2+ sensitivity by inhibiting RhoA.

ROCK inhibitors at a very low concentration augmented anesthetics-induced relaxation of ASM. SinceROCK inhibitors per se exhibit a relaxation in ASM, we used two relative low concentrations (0.03 and 0.1µM) of ROCK inhibitors. Combination of ROCK inhibitor and propofol showed the great relaxation, whichexceed the simple sum of relaxation by both ROCK inhibitor and propofol. The combination of Y-27632and isoflurane showed the same result.

Therefore, we think that this is not just the additive effects of ROCK inhibitors and anesthetics, and a

certain kind of synergistic effect was caused in this experimental condition.

Conclusions

1) ROCK inhibitors augment anesthetics-induced relaxation of rat airway smooth muscle.

2) Combined use of ROCK inhibitor and anesthetics causes further relaxion.

References

1) Anesthesiology 2000; 92:133-139

2) Anesthesiology 2001; 94:129-136

3) Eur J Pharmacol 2001; 427:77-82.

From Proceedings of the 2009 Annual Meeting of the American Society Anesthesiologists.

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A1020 October 19, 2009 3:00 PM - 4:30 PMRoom Room 355

Glucose Variability and Oxidative Stress during Cardio-Pulmonary Bypass ** Moritoki Egi, M.D., Kazuyoshi Shimizu, M.D., Yuichiro Toda, M.D., Ph.D., Tatsuo Iwasaki, M.D., Ph.D.,Kiyoshi Morita, M.D., Ph.D.Deapartment of Anesthesiology and Resuscitology, Okayama University Hospital, Okayama City, Japan

Background; Swings in glucose levels (GV; glycemic variability) might have biological toxicity. Oxidativestress was higher in the presence of fluctuations from hyperglycemia to normoglycemia when comparedwith sustained hyperglycemia. Such increased oxidative stress can result in endothelial dysfunction andcontribute to organ damages. Although a maximum and mean glucose level during cardiopulmonarybypass (CPB) is reported as an independent risk factor for death and morbidity, there is no study toassess the impact of glycemic variability on oxidative stress and morbidity in this cohort.

Objective; To test the association of GV, calculated with standard deviation of glycemia during CPB, withpostoperative oxidative stress and kidney injury. To compare these associations with those of meanglycemia (Ave), max and minimum glucose levels (Max and Min) during CPB.

Patients; 15 cardiac surgery patients requiring CPB.

Measurements and methods; Continuous glucose monitoring (CGM) was performed using Model STG-22(Nikkiso, Tokyo, Japan), which enable to measure blood glucose every 12 seconds. The absolute changein serum creatinine from baseline to the peak within the first 48 hours after operation (M-Cre) were usedas surrogates of post-operative kidney injury. Activation of oxidative stress estimated from measurementsof serum reactive oxygen species (ROS) and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) at the end ofoperation. The correlations of two values were assessed using Pearson's correlation coefficient.

Results; CGM was successfully performed in all 15 patients during CPB. GV and Ave were significantlyassociated with M-Cre (GV;R=0.60, P=0.017 and Ave;R=0.56, P=0.029). Serum ROS levels weresignificantly associated with GV and Max, but not with Ave and Min. Urinary 8-OHdG levels weresignificantly associated with GV, Ave and Max, but not with Min. The strongest association with serumROS levels, Urinary 8-OHdG levels and M-Cre was seen in GV among 4 glucose indices duringCPB.[table1] Conclusion; Glucose variability during CPB calculated using continuous glucosemeasurements had significant correlation with activation of oxidative stress and post operative kidneyinjury. These correlations were stronger than other commonly used glucose indices. Decreasing variabilityrather lowering glycemia might be an important dimension of glucose management and an important goalof glucose management during CPB.

From Proceedings of the 2009 Annual Meeting of the American Society Anesthesiologists.

The correlation of glucose indices with activation of oxidative stress and postoperative kidney injury

Standarddeviation ofbloodglucoselevels (GV)

Meanbloodglucoselevels(Ave)

Maximumbloodglucoselevels(Max)

Minimumbloodglucoselevels(Min)

The absolute change in serumcreatinine from baseline to thepeak within the first 48 hoursafter (M-Cre)

R=0.60(P=0.017)*

R=0.56(P=0.029)*

R=0.34(P=0.22)

R=0.40(P=0.14)

Post operative reactive oxygenspecies (ROS)

R=0.65(P=0.008)*

R=0.44(P=0.10)

R=0.54(P=0.037)*

R=0.006(P=0.98)

Post operative urinary 8-hydroxy-2'-deoxyguanosine(8-OHdG)

R=0.58(P=0.024)*

R=0.54(P=0.040)*

R=0.54(P=0.038)*

R=0.028(P=0.92)

R:Pearson's correlation coefficient, *:significant correlation

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A709 October 19, 2009 9:00 AM - 11:00 AMRoom Area H

Effects of Remifentanil vs Fentanyl on Hemodynamic Changes duringInduction in the Elderly ** Takeshi Samuta, M.D., Ken Takada, M.D., Kenji Sato, M.D., Kiyoshi Morita, M.D.Anesthesia, Takasago Municipal Hospital, Takasago City, Hyougo, Japan

Background: Remifentanil(REMI) provides a highly predictable onset and offset of actions. A single bolusinjection of REMI may be advantageous for attenuating cardiovascular response to a brief, but intensenoxious stimuli such as laryngoscopy and tracheal intubation. Fentanyl(FENT) is used to the first-lineopioid selected for induction of anesthesia in Japan before REMI was launched in 2007. The aim of thepresent study was to assess the effects of equivalent bolus dose of REMI and FENT, which provide similareffect site-concentration (Ce) at the time of intubation, on hemodynamic stability and intubation conditionsin the elderly. Methods: After hospital ethical committee approved the study, 30 patients of ASA - PS I-II(age 70-79) were allocated into group R (a single bolus injection of 0.6µg/kg of remifentanil) and groupF(a single bolus injection of 2µg/kg of fentanyl). All patients received 1.5-2.0 mg/kg of propofol followed by10mg/kg/hr of continuous infusion. In Group R, bolus injection was applied over 30s after loss ofconsciousness (LOC) was obtained and airway was secured. Rocuronium 0.8mg/kg was given to facilitatetracheal intubation followed by laryngoscopy in 1minutes later. In group F, bolus injection of FENT wasapplied 1min before Propofol. After LOC, same dose of rocuronium was given and laryngoscopy wasperformed 1min later. Blood pressure (BP) and heart rate (HR) was recorded 1min intervals from beforeinduction of anesthesia until 5min after intubation. Intubating condition was assessed and scored usingpre-determined scoring criteria by blinded anesthesiologist. We defined hypotension as SBP<80mmHg,hypertension as SBP>180mmHg and bradycardia as <40bpm. We simulated Ce at intubation using theMinto model in TIVAtrainer. Mann-Whitney test was used for comparing Intubating condition scorebetween groups. Parametric data were analysed using repeated ANOVA. P<0.05 was consideredstatistically significant. Results: Systolic BP significantly decreased in both groups from baseline (138±5mmHg,146±4) (Mean ± SE) to at intubation (101±3, 97± 4) in group F and Group R respectively. Afterintubation it significantly increased into 144±6 in group F but no significant increase was seen on group R(100± 6). HR also significantly decreased in both groups from baseline (78±5 bpm, 78±4) to at intubation(60±2, 56±4) in group F and Group R respectively. But after intubation it significantly increased into 88±4 ingroup F but no significant increase was seen on group R (60± 4). Ce at intubation was 2.2±0.3 ng/ml(mean ± SE) in group F and 2.1±0.2 in group R. There was no significant difference between groups.Incidence of hypotension was 4 of 15 (27%) in group R,and 1of 15 (7%) in group F but 4 patients (27%) ingroup F caused hypertension. Bradycardia.did not occur in neither group. All patients in group R weresatisfying condition for intubation but 3 of 15 (20%) in group F was judged as unacceptable. Conclusions:0.6µg/kg of REMI was sufficient enough for blunting cardiovascular response to intubation and relatedacceptable low incidence of hypotension during induction of anesthesia combined with propofol.Meanwhile 2µg/kg of FENT failed to attenuate the stress response to intubation. A single induction bolusof REMI is a safe and effective administering means for the elderly.

From Proceedings of the 2009 Annual Meeting of the American Society Anesthesiologists.

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A1186 October 20, 2009 9:00 AM - 11:00 AMRoom Area B

Serum Tranexamic Acid Level and Blood Loss in Pediatric Cardiac SurgeryPatients ** Yuichiro Toda, M.D., Ph.D., Kazuyoshi Shimizu, M.D., Tatsuo Iwasaki, M.D., Ph.D., MamoruTakeuchi, M.D., Ph.D., Kiyoshi Morita, M.D., Ph.D.Department of Anesthesiology and Intensive Care, Okayama University Hospital, Okayama-shi, Okayama,Japan

[Background] There are several studies to assess the effect of the intravenous tranexamic acid (TXA)administration on the blood loss in pediatric cardiac surgery patients. We have also shown 21% relativereduction of postoperative blood loss using TXA infusion in our randomized controlled trial conducted in160 pediatric cardiac surgery patients (reported in 2008 ASA annual meeting). However, the reportedeffect of TXA are conflicted, and variation in dose of TXA is considered as one mechanism on thisconfusion.

[Objective] To investigate TXA level in our study cohort and to determine the association between TXAlevel and blood loss.

[Methods] Eighty pediatric patients (18 years old or younger) who underwent cardiac surgery with the useof cardiopulmonary bypass (CPB) during Jan 2006 to Aug 2007 were included. Neonates born within 1month were excluded from the study. Written informed consents were obtained from the parents. Fiftymg/kg of TXA was administered as an initial bolus before skin incision followed by continuous infusion of15 mg/kg of TXA until surgery was completed. Another 50 mg/kg of TXA was added to CPB circuits. Bloodsamples were obtained for measurement of TXA concentration at pre-bolus, after bolus, 15 min afterinitiation of CPB, and the end of CPB. Measurement of TXA level was made by high performance liquidchromatography. The amount of blood loss was defined as mediastinal and pericardial drainage over 24hrs postoperative periods.

[Results] Forty cyanotic and 40 acyanotic patients were identified in the 80 participants. Their age wasmedian of 23 months [interquatile range (IQR); 8.0-44.5], the body weight was median of 9.4 kg (IQR; 6.1-13.2), and male patients were 51.2% (41/80). TXA concentration markedly increased immediately afterbolus and gradually decreased during CPB.[figure1]The difference in TXA concentration were not seenbetween cyanotic and acyanotic children. If participants were divided by cut of TXA level of 200 µg/ml atinitiation of CPB, the amount of blood loss over 24 hrs was significantly smaller in children with higher TXAlevels (n=35) than those with lower levels (n=45). (TXA level>200 vs level<200 µg/ml, 15.0ml/kg[95%CI;10.9-19.2] vs 21.5 ml/kg[95%CI;17.9-25.2], p=0.02) When patients were divided by cut offblood loss of 15 ml/kg during 24 hrs, TXA concentration at post bypss was significantly higher in smallerblood loss group than those in children whose loss was over 15 ml/kg. (blood loss<15ml/kg[n=45] vsloss>15ml/kg[n=35], 150.9 µg/ml[95%CI; 129.0-172.9] vs 109.4 µg/ml[95%CI; 84.1-134.7], p=0.02)

[Conclusion] TXA concentration was successfully determined in children undergoing cardiac surgery withCPB. TXA level may be one of factors to determine the amount of blood loss.

From Proceedings of the 2009 Annual Meeting of the American Society Anesthesiologists.

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A1189 October 20, 2009 9:00 AM - 11:00 AMRoom Area B

Impact of Hypoglycemia to the Outcome of the Pediatric Patients withCongenital Heart Surgery ** Tatsuo Iwasaki, M.D., Moritoki Egi, M.D., Yuichiro Toda, M.D., Kazuyoshi Shimizu, M.D., KiyoshiMorita, M.D., Ph.D.Anesthesiology & Resuscitology, Okayama University Graduate School of Medicine, Okayama City,Okayama Prefecture, Japan

[Background]

Intensive insulin therapy (IIT) (target glucose concentration of 80-110 mg/dL) has been reported to reducemortality (relative mortality reduction=43%, p=0.04) in selected surgical patients with 6.7 times increase inhypoglycemia. Accordingly, lowering blood glucose levels has been recommended in internationalconsensus guidelines as a means of improving patient outcomes. However, NICE-SUGAR trial, recentlyreported largest randomized controlled trial, has shown that IIT increased 90 days mortality significantly(relative mortality increase=10%, P=0.02) with 14.7 times increase in hypoglycemia. These results mightsuggest that IIT might have some degree of benefit, if any, which may be negated by increased incidenceof hypoglycemia. This caution was also supported by several investigations to show the association ofhypoglycemia with worse outcome in adult critically ill patients. However, there is limited information on theimpact of hypoglycemia in pediatric critically ill patients.

[Objective]

To investigate the association between lowest blood glucose level during first 24 hours and clinicaloutcomes in pediatric post-cardiac surgery patients.

[Material and Method]

A retrospective chart review was conducted for 618 children under 18 years old who underwent open heartsurgery between 2007 and 2008. The association of the lowest blood glucose level with mortality, length ofstay in ICU and duration of mechanical ventilation was assessed by student t-test and Pearson'scorrelation analysis.

[Results]

There are 15 non-survivors (2.4%) in study cohort. The lowest blood glucose level in non-survivor groupwas 105±46 mg/dl, which is not significantly difference with 114±33 mg/dl of survivor group (P= 0.29). Thehypoglycemia (<60mg/dl) occurred in 12 patients, in which mortality is 16.6%. The patients withhypoglycemia was significantly more likely to die, compared with those without hypoglycemia (Oddsratio=7.3, P=0.002). The lowest blood glucose level had significant inverse correlation with duration ofmechanical ventilation (r = -0.15; p < 0.01), and length of ICU stay (r = -0.12; p < 0.01).

[Conclusion]

The patients with hypoglycemia had significantly higher mortality compared with those withouthypoglycemia. The lowest blood glucose level during first 24 hours was associated with longer duration ofmechanical ventilation and longer ICU stay in patients after pediatric cardiac surgery. The furtherinvestigation about the adverse effect of hypoglycemia is required.

[References]

1) Lancet. 2009; 373: 547-56

2) N Engl J Med. 2009; 360: 1283-97.

From Proceedings of the 2009 Annual Meeting of the American Society Anesthesiologists.

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A1585 October 21, 2009 10:00 AM - 11:30 AMRoom Room 357

Development of a Pharyngeal Cooling System That Enables BrainTemperature To Be Immediately Reduced * Yoshimasa Takeda, M.D., Ph.D., Kensuke Shiraishi, M.D., Naoki Morimoto, M.D., Ph.D., HiromichiNaito, M.D., Kiyoshi Morita, M.D., Ph.D.Anesthesiology & Resuscitology, Okayama University Medical School, Okayama, Japan

Introduction: Mild hypothermia is known to ameliorate neurological outcome after resuscitation in humans.If hypothermia can be initiated immediately after the onset of resuscitation, neurological outcome would beimproved. Since bilateral common carotid arteries exist at 1 cm from the pharynx, cooling the pharyngealregion decreases brain temperature by cooling arterial blood without lowering systemic temperature. Wedeveloped a pharyngeal cooling system that enables brain temperature to be immediately reduced withoutcausing cold injury in the pharynx. In the present study, we investigated effects of pharyngeal cooling onbrain temperature, tympanic temperature, rectal temperature and mucous membrane in the pharynx inmonkeys and in humans.

Method 1: Japanese monkeys (7.5±2.4 kg) were divided into a control group (n=6) and a pharyngealcooling group (n=3) and were anesthetised with 1% isoflurane. Cardiac arrest (12 min) was initiated withelectrical stimulation. In the pharyngeal cooling group, a pharyngeal cuff was inserted into the pharynx andwas perfused with saline (5°C) at the rate of 500 ml/min from the onset of resuscitation for 30 min. Oneday (n=1) and 7 days (n=2) after the initiation of pharyngeal cooling, animals were perfuse-fixed forhistological evaluation of the mucous membrane of the pharynx.

Method 2: Three resuscitated patients (77±10 years) who were scheduled to undergo mild hypothermiawere subjected to pharyngeal cooling for 30 min. Changes in tympanic temperature, bladder temperature,systemic blood pressure and heart rate were monitored. Macroscopic observation of the mucousmembrane of the pharynx was performed for 3 days.

Results 1: During cardiac arrest, epidural and sub-cortical temperatures decreased to 33.3±0.7°C and35.8±0.5°C, respectively, in both groups. In the control group, however, epidural and sub-corticaltemperatures increased with the initiation of resuscitation and reached 35.1±0.5°C and 36.5±0.2°C,respectively, 30 min later. In the pharyngeal cooling group, epidural and sub-cortical temperaturesdecreased and reached 31.1±1.5°C and 32.4±1.3°C, respectively, 30 min later. Rectal temperature wasunchanged in both groups. Microscopic observation (HE staining) showed that mucous membranes of thepharynx were intact. No inflammatory cell infiltration was observed

Results 2: Tympanic temperature (36.3±1.2°C) was decreased to 35.7±1.0°C 30minutes after initiation ofpharyngeal cooling. Bladder temperature (36.3±0.9°C), mean arterial blood pressure (90±16 mmHg) andheart rate (90±24 /min) were unchanged at 30 minutes after initiation of pharyngeal cooling (bladdertemperature, 36.3±1.0°C; mean arterial blood pressure, 96±18 mmHg; and heart rate, 93±21 /min). Edemaformation or inflammatory findings, suggesting development of cold injury, were not observed in thepharyngeal mucous membrane for 3 days.

Conclusions: Brain temperatures were decreased by the initiation of pharyngeal cooling without any effecton rectal temperature, blood pressure and heart rate in monkeys and in humans. Since the mucousmembrane in the pharynx was intact after 30 minutes of cooling, pharyngeal cooling could be a usefultechnique for protecting the brain from ischemic injury in a clinic.

From Proceedings of the 2009 Annual Meeting of the American Society Anesthesiologists.

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A1433 October 21, 2009 9:00 AM - 11:00 AMRoom Area G

Intra-Abdominal Pressure after Living Donor Liver Transplantation ** Takashi Matsusaki, M.D., Hiroshi Morimatsu, M.D., Junya Matsumi, M.D., Tetsufumi Sato, M.D.,Kiyoshi Morita, M.D.Department of Anesthesiology and Resuscitology, Okayama University Hospital, Okayama, Japan

Objective: There is growing evidence that increased intra-abdominal pressure (IAP) adversely affectsalmost all organ systems and is a cause of significant morbidity and mortality. The objectives of this studywere to measure the IAP after living donor liver transplantation and to evaluate the correlation of intraabdominal pressure with systemic and hepatic hemodynamics and postoperative clinical outcomes.

Materials and Methods: This is a prospective observational study. Living donor liver transplantantionrecipients were included into the study. The IAP was measured via a urinary catheter daily. This catheterwas equipped with a closed circuit for IAP measurement and only 20 ml of saline were needed. Using thisdevice, the IAP can be measured easily and in sterile fashion. Postoperative liver function test, liver artery(HA) and portal vein flow (PV) by abdominal pulsed-Doppler echography were collected daily during thepostoperative one week. The HA systolic and diastolic flow velocities were recorded and resistive indexwas calculated. The PV flow velocity has been described as being hepatopetal with pulsatility variations. Avalue of P<0.05 was considered statistically significant. The differences between groups were assessedusing independent-sample t test for normally distributed data.

Results: Nine patients were included into the study. The IAP gradually decreased during the postoperativecourse. We had two re-laparotomy cases due to bleeding postoperatively. The IAP of these two cases wasrelatively higher compared with the other cases. We found the positive relationship between the IAP andCVP (p value=0.002). No significant association was seen between the IAP and other parameters such asheart rate and mean artery pressure. The flow velocities in the PV and HA were variable during thepostoperative course. Unfortunately, we could not find any significant relationship between the IAP andliver flow velocities. We also could not find the relationship between the IAP and postoperative liverfunction tests (AST, ALT, T-Bil).

Conclusions. This study shows a close positive correlation between CVP and IAP. Moreover, patients whohave re-laparotomy due to bleeding are having higher IAP. These findings suggest that the IAP monitoringmight be useful in the early postoperative periods, especially in liver transplantation.

From Proceedings of the 2009 Annual Meeting of the American Society Anesthesiologists.

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A1426 October 21, 2009 9:00 AM - 11:00 AMRoom Area G

Increased Heme Oxygenase-1 Gene Expression after Reperfusion of theLiver during Transplantation ** Junya Matsumi, M.D., Hiroshi Morimatsu, M.D., Ph.D., Toru Takahashi, M.D., Ph.D., Hiroko Shimizu,M.D., Ph.D., Kiyoshi Morita, M.D., Ph.D.Department of Anesthesiology and Resusciology, Okayama University Hospital, Okayama, Japan

Introduction

Reperfusion of the grafted liver causes the production of oxygen-free radicals which leads to certaindegree of graft dysfunction. Heme oxygenase-1 (HO-1), the rate-limiting enzyme in heme catabolism, isinduced not only by its substrate heme but also by oxidative stress. HO-1 is thought to confer protectionagainst oxidative tissue injuries in part by removing free heme, a potent pro-oxidant. HO-1 expression hasbeen reported to increase in the graft liver after reperfusion during liver during living donor livertransplantation (LDLT). In this observational study, we determined gene expression of HO-1, as well asnon-specific d-aminolevulinate synthase (ALAS1), the rate limiting enzyme in heme biosynthesis, in thegrafted liver during LDLT and examined its relationship to post transplantation liver damage.

Materials and Methods

This prospective, observational study was conducted in Okayama University Hospital between 2006 and2008. 30 patients undergoing LDLT were recruited to this study. Liver biopsy was taken from donor liverjust before graft resection. The same amount of liver biopsy was taken from the grafted liver just beforeskin closure of recipients to assess the effects of ischemia reperfusion. From these biopsies, mRNAexpressions of HO-1 and ALAS 1 were measured using reverse transcription polymerase chain reaction(RT-PCR). Post transplantation liver damage was assessed with serum alanine aminotransferase (ALT).

Results

We studied 30 patients undergoing LDLT and 16 were male and 14 were female. 12 patients suffered fromviral liver cihrrosis, 5 patients were billirary atresia. Hepatic HO-1 mRNA was markedly up-regulated afterreperfusion of the graft liver compared with those of pre-reperfusion. The average level of HO-1 mRNAshowed almost 3-fold increase in post-reperfusion value compared with the pre-reperfusion. In contrast toHO-1 gene expression, ALAS1 gene expression was decreased after reperfusion compared with those ofpre-reperfusion.[figure1]Of note, the increased HO-1 expression in the grafted liver was significantlycorrelated with serum ALT concentrations after transplantation.[figure2]Conclusions

Following reperfusion of the graft liver, there is a marked up-regulation of HO-1 gene expression which issignificantly correlated with serum ALT level after transplantation. In contrast, ALAS1 expression, which isknown to be exquisitely sensitive to free heme concentration in hepatocytes, is down-regulated afterreperfusion of the graft liver. These findings suggest that an increase in intracellular free hemeconcentration may contribute to increased HO-1 gene expression, which could reflect the degree of earlygraft dysfunction due to free-heme mediated oxidative stress.

From Proceedings of the 2009 Annual Meeting of the American Society Anesthesiologists.

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