By using the isolated rat heart with regional ischemia and a perfusate Ca2+ of 2.4 mM, we have observed a bell-shaped relationship between the incidence of reperfusion-induced ventricular fibrillation (VF) and the duration of preceding ischemia. With 5, 10, 20, 30, and 40 min of ischemia, 8, 83, 58, 25, and 8% of the hearts (n = 12 per group) exhibited irreversible VF. In additional studies (10 min ischemia) perfusate Ca2+ was reduced (to 0.1, 0.4, 0.8, 1.2, 1.6, and 2.0 mM) for 1 min before coronary occlusion (to trap low Ca2+ in the ischemic zone) and for 1 min before and throughout reperfusion. VF fell in a dose-dependent manner from its control incidence of 83% (2.4 mM Ca2+) to 17 (P < 0.01), 25 (P < 0.01), 41, 58, 91, and 83%, respectively. In further studies Ca2+ was reduced to 0.4 mM just before ischemia and also just before and during reperfusion, and the ischemic time was varied (5, 10, 20, 30, or 40 min), VF was reduced from its time-matched control (2.4 mM Ca2+) values of 8, 83, 58, 25, and 8% to 0, 25 (P < 0.01), 8 (P < 0.05), 0, and 0%, respectively. In a final series of experiments, Ca2+ reduction (to 0.4 mM) was carried out only during reperfusion (1 min before and throughout reperfusion). When time-vulnerability curves were constructed some protection was observed after 20 min of ischemia (VF fell from its control incidence of 58 to 8%). We conclude that extracellular Ca2+ concentration can influence vulnerability to reperfusion-induced arrhythmias. This is in part due to a direct effect which is operative during the reperfusion period; however, most benefit is obtained when the Ca2+ is reduced during the preceding ischemic period.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Publication status||Published - 1987|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)