Myocardial calcium overload during reperfusion may contribute to myocardial stunning. The protective effect of nicardipine against post-ischemic myocardial dysfunction was investigated.

Twenty-two halothane-anesthetized dogs were subjected to 15 minutes of left anterior descending coronary artery (LAD) occlusion and subsequent 3 hour reperfusion. One group of dogs (n=11) received nicardipine (1 microgram/kg/min) and another group (n=11) received saline (0.5 ml/kg/h) through intracoronary catheter for 1 hour beginning 15 minutes before LAD occlusion. Systolic shortening (%SS) and preload recruitable stroke work slope (Mw), as an index of regional myocardial contractility, and IMP-tau (time constant of myocardial relaxation based on intramyocardial pressure (IMP)) and post-systolic shortening (%PSS), as an index of regional diastolic function, were evaluated. LAD blood flow was measured by Doppler flowmeters as well.

Regional systolic as well as diastolic functions during acute myocardial ischemia were similar between the two groups. However, Mw recovered to the baseline value with the onset of reperfusion in the nicardipine group but was significantly decreased throughout the reperfusion period in the controls. After 3 hours of reperfusion, the nicardipine group had recovered 67% of %SS, compared with 20% of the control group. IMP-tau was restored to the baseline value by 60 min of reperfusion in the control group but was significantly prolonged in the nicardipine group throughout the reperfusion period.

Intracoronary nicardipine enhances the recovery of regional contractile function but prolongs myocardial relaxation in the canine model of myocardial stunning.