Previous investigators have suggested that calcium may play a role in the pathogenesis of myocardial cell damage following ischemia and reperfusion. Twenty-six in-situ blood perfused isovolumic canine preparations were divided into four groups. Group I dogs were maintained normocalcemic during 45 min of reperfusion following 45 min of hypothermic (27 degrees C) ischemic arrest; Group II dogs received CaCl2 (7 mg/kg) after 15 min of reperfusion; Group III dogs received citrate solution (0.8 ml/kg citrate-phosphate-dextrose [CPD]) after 15 min of reperfusion; Group IV dogs received 7 mg/kg of CaCl2 at 5 min after receiving the same citrate dose as Group III after 15 min of reperfusion. In Group II hearts, calcium improved the left ventricular contractility (P < 0.05 vs Group I) without causing additional cellular or subcellular injury. Calcium also appeared to increase myocardial stiffness (alpha(n)) compared to Group I hearts (P < 0.01). In Group III hearts, citrate reduced contractility (P < 0.01 vs Group I) and increased myocardial edema (P < 0.005 vs Group I) without any apparent improvement in cellular or subcellular preservation. In Group IV hearts, calcium reversed the depression of contractility caused by citrate, resulted in no additional morphologic injury, increased myocardial stiffness compared to Group I or Group III (P < 0.005), and minimized myocardial edema (P < 0.005 vs Group I or III). These results suggest that calcium administered after 15 min of reperfusion improves the depression of contractility that follows hypothermic ischemic arrest without causing additional myocardial damage.
|Original language||English (US)|
|Issue number||3 Pt 2|
|State||Published - Sep 1978|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)