Abstract
This study investigates the efficacy of pinacidil, an adenosine triphosphate-sensitive potassium (KATP) channel opening agent, added to custadiol solution on myocardial protection during deep hypothermia and prolonged global ischemia on isolated rat hearts. After 20 minutes of stabilization, 24 rats were divided into two groups. In group I (n=12), hearts were arrested with cold (4 degrees C) custadiol solution containing 50 micromol/L of pinacidil and subsequently dipped into the same solution for 120 minutes at 4 degrees C. Group I hearts were perfused with low-flow pinacidil-custadiol (PC) solution during the ischemic period. Group II (n=12) hearts, after the stabilization period, were arrested with cold custadiol solution only, then subsequently dipped and perfused with the same solution for 120 minutes at 4 degrees C. All hearts were reperfused with Krebb's-Henseleit solution at 37 degrees C for 60 minutes. Hemodynamic parameters (peak systolic pressure, end diastolic pressure, maximum rate of increase of left ventricular pressure [+dP/dt], ischemic contracture, and coronary sinus flow) were recorded at the end of the stabilization period and at 10-minute intervals during the reperfusion period. Biochemical data (creatine kinase [CK-MB] washout and troponin I [cTnI] levels) were compared between the two groups. There was no significant difference in any hemodynamic or biochemical parameters between the two groups during the stabilization period. The peak systolic pressure, +dP/dt, ischemic contraction amplitude, and coronary flow values were significantly higher in group I ( P<0.05) compared with group II during reperfusion. End diastolic pressures as well as CK-MB and cTnI levels were lower in the pinacidil-treated group, which is consistent with improved functional recovery during the reperfusion period. The addition of pinacidil to the preservation solution, custadiol, improves myocardial recovery after deep hypothermia and prolongs ischemia.
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