Abstract
Objective To evaluate the effect of hydromorphone postconditioning on the electrophysiological stability during ischemia-reperfusion (I/R) in isolated rat hearts. Methods Healthy adult male Sprague-Dawley rats, aged 2-3 months, weighing 280-360 g, were heparinized and anesthetized with pentobarbital sodium.Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95% O2-5% CO2 at 37 ℃.Twenty-four Langendorff-perfused hearts were divided into 3 groups (n=8 each) using a random number table: control group (group C), I/R group and hydromorphone postconditioning group (group HM). The isolated hearts were subjected to 60 min ischemia followed by 60 min reperfusion to establish the model of isolated heart I/R injury.The isolated hearts were perfused with K-H solution containing 4.1 ng/ml hydromorphone for 10 min starting from onset of reperfusion in group HM.Heart rate, electrocardiogram, coronary flow, and monophasic action potential amplitude, in the left ventricular endocardium, mid-myocardium and epicardium the maximal increase rate (Vmax) at the 0 phase, and monophasic action potential duration at 50% and 90% repolarization (MAPD50 and MAPD90, respectively) were recorded at 20 min of stabilization (T0) and 10, 25, 40 and 60 min of reperfusion (T1-4). The transmural dispersion of repolarization (TDR) was calculated, and the time for restoration of spontaneous heart beat was recorded. Results There was no significant difference in the heart rate, coronary flow or monophasic action potential amplitude between the three groups (P>0.05). Compared with group C, Vmax in the epicardium was significantly decreased, MAPD50 and MAPD90 in the three transmural layers were prolonged, and TDR was prolonged in group I/R (P 0.05). Conclusion Hydromorphone postconditioning is helpful in maintaining the electrophysiological stability during I/R in isolated rat hearts. Key words: Hydromorphone; Myocardial reperfusion injury; Cardiac electrophysiology; Ischemic postconditioning
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