The role of calcium in the ischemic myocardium.
Ischemia of the myocardium results in a loss of ultrastructure and function. Tension generation is diminished or abolished, electrolyte imbalance occurs, and the ATP-generating capacity of the mitochondria is reduced. An intracellular accumulation of Ca2+ appears to precipitate many of these changes, the intracellular accumulation of Ca2+ being caused, in turn, by a failure of the ATP-dependent mechanisms responsible for maintaining intracellular homeostasis with respect to Ca2+. This hypothesis has been tested by the use of hypothermia, pretreatment with verapamil and a reduced extracellular Ca2+ to modify the events precipitated by an ischemic episode.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000037:antagonists & inhibitors / Q000378:metabolism*; D003327:Coronary Disease / Q000378:metabolism*; D003600:Cytosol / Q000378:metabolism; D007035:Hypothermia; D008297:Male; D008928:Mitochondria / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D011817:Rabbits; D014700:Verapamil / Q000494:pharmacology
D000255:Adenosine Triphosphate; D014700:Verapamil; D002118:Calcium