Effects of Ca2+ antagonism on energy metabolism: Ca2+ and heart function after ischemia.
Isolated rat hearts reperfused after 25 min of ischemia have 23% of control mechanical function, 65% of control nucleotides, 52% of control ATP, and 75% of control creatine phosphate, whereas cellular calcium is increased 2.3-fold. Initiating reperfusion with verapamil or low Ca2+-containing buffer did not alter these tissue parameters or improve function over hearts reperfused with control buffer only. Also, when verapamil was present before and during ischemia, improvement in cardiac function resulted, and the adenine nucleotides, tissue ATP, and creatine phosphate concentrations were increased while cellular Ca2+ was reduced compared with the other reperfused ischemic hearts. Verapamil apparently improves recovery of function by decreasing energy demand during ischemia rather than by blocking Ca2+ influx during reprefusion. The respiration of isolated mitochondria and homogenates from reperfused ischemic hearts and homogenates of ischemic hearts was decreased by 20-30%, possibly due to sarcolemmal damage, although the respiration of isolated cells from ischemic hearts was normal. Cells isolated from ischemic hearts may represent a selected population lacking sarcolemmal damage.
D000227:Adenine Nucleotides / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D003327:Coronary Disease / Q000378:metabolism*; D006321:Heart / Q000502:physiology; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism*; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D010477:Perfusion; D051381:Rats; D014700:Verapamil / Q000494:pharmacology
D000227:Adenine Nucleotides; D000255:Adenosine Triphosphate; D014700:Verapamil; D002118:Calcium