Introduction: Hemorrhagic shock and resuscitation is a status of global ischemia and reperfusion that causes cardiac dysfunction. Studies have demonstrated that hemorrhagic shock causes myocardial diastolic dysfunction. We investigated whether remote ischemic pre-conditioning (RIPC) would reduce cardiac diastolic dysfunction during and following hemorrhagic shock. Methods: Twenty-one male Sprague-Dawley rats were randomized into three groups:1) RIPC; 2) RIPC with the KATP channel blocker (RIPC+blocker); 3) Control. RIPC was induced by four cycles of 5 mins of limb ischemia followed by reperfusion for 5 mins. Hemorrhagic shock was induced by removing 50% of the estimated total blood volume over an interval of 1 hr. Thirty-minutes after bleeding, the animals were reinfused with shed blood during the ensuing 30 mins. Myocardial function was measured by echocardiography at baseline, 1 hr after bleeding, 30 mins after shock, 30 mins after reinfusion and at hourly intervals after reinfusion. Results: At 2 hrs after reinfusion, myocardial performance index [(0.81 ± 0.05) vs. (1.18 ± 0.05), P<0.001] and end diastolic left ventricular posterior wall thickness [(0.240 ± 0.024) vs. (0.304 ± 0.024), P<0.001] were significantly decreased in the RIPC group than those of the control group. However, pre-treatment of the KATP channel blocker completely abolished the protective effects of RIPC. Conclusions: In a rat model of severe hemorrhagic shock, RIPC improved cardiac diastolic dysfunction by activation of the KATP channel.
1Weil Institute of Critical Care Medicine, Rancho Mirage, CA, 2The second hospital of Anhui medical University, Heifei, China, 3Weil Institute of Critical Care Medicine, rancho mirage, CA, 4Weil Institute of Critical Care Medicine, Rancho Mirage, CA