The effect of short term normothermic global ischemia and acidosis on cardiac myofibrillar Ca2+-Mg2+ ATPase activity.
There is now good evidence to indicate the onset of myocardial ischemia is accompanied by a decline in intracellular pH which parallels the decrease in tension development. The component of the excitation--contraction coupling system which is responsible for the loss in tension development has not been determined although the contractile proteins are a likely candidate since the calcium sensitivity of tension development and of myofibrillar ATPase are both inhibited by a decrease in pH. However, these studies have utilized normal tissues and the effects of pH compounded with ischemia have not been determined. It is plausible to suggest that there may occur ischemic damage to the excitation--contraction coupling system which would depress function in a manner distinct from that incurred by acidosis. Toya-Oka and Ross have demonstrated a loss in regulatory proteins during regional ischemia, suggesting an effect of ischemia independent of pH. We recently demonstrated, in sarcoplasmic reticulum isolated from ischemic myocardium, a defect in function which could not be accounted for solely on the decrease in pH. It was, therefore, the purpose of this study to determine the effects of decreasing pH on cardiac myofibrillar ATPase activity isolated from hearts which had been subjected to short-term, global normothermic ischemia. This design permits us to answer the following questions: Is there a decrease in myofibrillar ATPase activity in the canine heart following 30 min of normothermic global ischemia? Does acidosis play a contributory role in any observed depression of myofibrillar ATPase activity during ischemia? and Does the ischemic process, independent of acidosis, produce a further depression of myofibrillar ATPase activity?
Krause
S M
SM
Hess
M L
ML
D000138:Acidosis / Q000150:complications / Q000201:enzymology* / Q000503:physiopathology; D000208:Acute Disease; D000818:Animals; D001831:Body Temperature; D017301:Ca(2+) Mg(2+)-ATPase; D002118:Calcium / Q000494:pharmacology; D000252:Calcium-Transporting ATPases / Q000378:metabolism*; D003327:Coronary Disease / Q000150:complications / Q000201:enzymology* / Q000503:physiopathology; D004285:Dogs; D006863:Hydrogen-Ion Concentration; D009206:Myocardium / Q000201:enzymology*; D009210:Myofibrils / Q000201:enzymology*
D017301:Ca(2+) Mg(2+)-ATPase; D000252:Calcium-Transporting ATPases; D002118:Calcium