Myocardial Protection by Preconditioning with Sevoflurane Is Further Enhanced by Sevoflurane Administration during Reperfusion: 2002[A-607]

Detlef Obal; Horst Scharbatke; Jost Müllenheim; Benedikt Preckel; Wolfgang Schlack

doi:10.1097/00000542-200209002-00607

Background: Myocardial protection against cellular damage after ischemia-reperfusion is achievable by administration of a volatile anesthetic before ischemia 1 or by administration of a volatile anesthetics during early reperfusion.2 Whether both protective mechanisms are linked with each other or work additively is unknown. Methods: Twenty-nine a-chloralose anesthetized rats were subjected to 25 min of coronary occlusion, followed by 120 min of reperfusion. The sevoflurane preconditioning group (PC, n=7) received 1.0 MAC sevoflurane over two 5 min periods followed by 10 min of washout before ischemia. In a second group, 1.0 MAC sevoflurane was administered for the first 2 min of reperfusion (REP, n=6). In a third group, both protocols were combined (PC+REP, n=8). Eight rats served as untreated controls. We measured maximum left ventricular dP/dt (dP/dt, catheter tip manometer), cardiac output (CO; flow probe around the pulmonary artery), mean aortic pressure (AOP; femoral artery catheter) and infarct size (percentage of area at risk; TTC staining). Statistics: ANOVA, Tukey's test. All data are mean values +/- 95% confidence interval. Results: Infarct size was 56 (43-68) % in controls. Both, PC (27 (15-39) %) and REP (17 (11-23) %) reduced infarct size significantly (both p<0.05 vs. control). The combination of PC and REP reduced infarct size further compared to PC alone (11 (7-16); p<0.05). Baseline dP/dt was 8160 (7095-9225) mmHg s-1 and AOP 115 (106-124) mmHg, similar in all groups. At the end of the experiments, dP/dt was 5006 (4493-5519) mmHg s-1 and AOP 74 (62-86) mmHg. Sevoflurane reduced both dP/dt and AOP during preconditioning (dP/dt to 3843 (2624-5062) mmHg s-1; AOP to 68 (28-109) mmHg for PC and PC+REP) and during reperfusion (dP/dt to 3973 (2773-5174) mmHg s-1; AOP to 52 (42-62) mmHg for PC+REP and REP). After discontinuation of sevoflurane, recovery of both variables was similar in all groups. CO was 36 (32-39) ml min-1 (baseline, similar in all groups) and remained constant during the experiments. Conclusion: Administration of sevoflurane as a preconditioning stimulus or only during early reperfusion can both protect the heart against ischemia-reperfusion injury. The protection by sevoflurane during reperfusion is stronger than after its administration as a preconditioning stimulus. One could speculate that the enhanced protection seen after the combination of sevoflurane preconditioning and sevoflurane during reperfusion is mainly caused by its reperfusion effects.

Myocardial Protection by Preconditioning with Sevoflurane Is Further Enhanced by Sevoflurane Administration during Reperfusion: 2002[A-607]

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