The effect of ischemic injury on calcium and magnesium distribution in dog myocardial cells was investigated in tissue damaged by occlusion of the circumflex branch of the left coronary artery for 60 minutes or for 40 minutes followed by 20 minutes of reperfusion of the damaged tissue by arterial blood. No significant change in the concentration of these cations was noted in permanently ischemic, irreversibly injured myocardial cells, but tissue calcium was markedly increased in cells killed by an episode of transient ischemia. Tissue water and sodium also were increased and magnesium was decreased significantly in the transient ischemia model. Investigation of the localization of the increased Ca(--) by cellular fractionation and chemical analysis as well as by electron miscroscopy and microincineration showed that much of it was localized in dense bodies within the mitochondria. Within the intramitochondrial dense bodies, the calcium appeared to be a precipitate of an as yet undefined form of calcium phosphate.

Animals↗

PubMed1972

Kinetics of calcium accumulation in acute myocardial ischemic injury.

The effect of ischemic injury on calcium uptake by dog myocardial cells was investigated in tissue damaged by transient or permanent occlusion of the circumflex branch of the left coronary artery. Tracer doses of (45)CaCl(2) were given at selected intervals before or after occlusion, and tissue uptake was measured in damaged and control left ventricular myocardium. No significant uptake of (45)Ca occurred after 60 minutes of ischemia produced by permanent occlusion of a coronary artery. However, 40 minutes of ischemia followed by 10 minutes of arterial reflow resulted in an 18-fold increase in Ca uptake in the injured tissue. Tissue (45)Ca increased linearly up through 10 minutes of arterial reflow but did not increase further with an additional 10 minutes of reflow. Myocardium reversibly injured by 10 minutes of ischemia followed by 20 minutes of arterial reflow did not accumulate excess (45)Ca. Calcium uptake is assumed to be an active process associated with mitochondrial accumulation of calcium into dense intramitochondrial granules of calcium phosphate. The uptake is a feature of irreversible cellular injury, but occurs only when arterial blood flow is present. The mechanism of the uptake has not been established. It appears to be related to defects in cellular permeability or mitochondrial function.

Acute Disease↗

PubMed1971