236

Abstract

Introduction: Hemorrhagic shock causes global ischemia-reperfusion injury and contributes morbidity and mortality. Hypothesis: The inhibition of mitochondrial permeability transition pore (mPTP) opening during ischemia-reperfusion can ameliorate injuries in the specific organs. We investigated the effects of cyclosporine A on hemodynamics and survival in hemorrhagic shock. Methods: Male Sprague-Dawley rats were subjected to pressure-controlled hemorrhagic shock (mean arterial pressure = 38 ± 1mmHg) for 90minutes. After hemorrhagic shock period, rats were randomly allocated to one of three groups (control group, n=7; CsA10 group, n=7; CsA50 group, n=5). Cyclosporine A (10 mg/kg for CsA10 group; 50 mg/kg for CsA50 group) or vehicle (normal saline) were administered via tail vein for 10 minutes and shed blood were transfused for 15 minutes. Survival time and blood pressure were observed until death and compared among groups. Results: Survival times were significantly longer in CsA groups than in control group (Median survival time was 283.5 minutes in control group, 365 minutes in CsA10 group, and 720 minutes in CsA50 group; log-rank test p=0.0121 for control vs. CsA10, p=0.0011 for CsA10 vs. CsA50). MAP during the reperfusion and observation period was significantly higher in CsA groups than in normal saline group. Conclusions: Cyclosporine A increased MAP dose-dependently during resuscitation period and consequently increased survival time.