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Enhanced myocardial protection with verapamil prior to postischemic reflow
Insights
Verapamil, a calcium channel blocker, protects heart cells from damage during reperfusion after ischemia. This treatment improves heart function and cellular preservation without negatively impacting heart performance.
Area of Science:
- Cardiology
- Pharmacology
- Cellular Biology
Background:
- Myocardial ischemia can lead to significant heart cell damage upon reperfusion due to calcium overload.
- Reflow injury is a major concern following cardiac ischemia treatments.
Purpose of the Study:
- To investigate the protective effects of verapamil, a slow channel calcium blocker, against myocardial reperfusion injury.
- To determine if verapamil reduces reflow injury without compromising cardiac function.
Main Methods:
- Thirty-two isolated rabbit hearts underwent either normothermic or hypothermic global ischemia.
- Hearts were divided into two groups: one received verapamil prior to reperfusion, the other served as a control.
- Left ventricular function and ultrastructure were assessed after 60 minutes of reperfusion.
Main Results:
- Verapamil treatment significantly improved left ventricular contractivity and compliance post-ischemia compared to controls.
- Hearts treated with verapamil showed superior ultrastructural preservation.
- No adverse effects on coronary flow, myocardial water content, or electromechanical activity onset were observed.
Conclusions:
- Administering verapamil just before reperfusion effectively mitigates myocardial reperfusion injury.
- Verapamil enhances recovery of heart function and preserves cellular integrity.
- The protective mechanism is likely related to the reduction of calcium influx into heart cells.
Abstract:
Reperfusion of the heart after induced myocardial ischemia may be associated with severe myocardial damage, characterized by massive calcium influx and accumulation in the heart cells. The present study was undertaken to investigate whether verapamil, a slow channel calcium blocker, administered prior to reperfusion, might reduce this reflow injury without causing depression of heart function. Thirty-two isolated, perfused rabbit hearts were subjected either to 45 minutes of normothermic or 150 minutes of hypothermic global ischemia. Half of the heart in each group received verapaMil immediately prior to reperfusion, while the remaining hearts received no verapamil. Following ischemia and 60 minutes of reperfusion, left ventricular (LV) contractivity was superior in both groups of verapamil-treated hearts, compared to control hearts (LV developed pressure [DP] in normothermic hearts 63 +/- 6% of preischemic DP for verapamil-treated hearts versus 46 +/- 6% of preischemic DP for control hearts; in the hypothermic group, 65 +/- 8% of preischemic DP for verapamil-treated hearts versus 33 +/- 10% DP for control hearts). Postischemic LV compliance also was significantly improved in the verapamil-treated hearts through the period of reperfusion, compared to control hearts. No differences were noted in coronary flow, myocardial water content, or the onset of electromechanical activity between the verapamil and control hearts, but there was significantly improved ultrastructural preservation in both verapamil groups. These data demonstrate that verapamil, when administered just prior to reperfusion, results in improved recovery of myocardial function and excellent cellular preservation, presumably for reducing calcium influx into myocardial cells.