Abstract

In dog left ventricular muscle made ischaemic by coronary artery occlusion, cardiac contractility declines immediately. This immediate decline in contractility is accompanied by a raised cellular Na + and a reduction in the ability of cardiac muscle to accumulate Ca 2+ at membrane-located binding sites. Short periods of hypoxia similarly result in a reduction in the ability of cardiac muscle to accumulate Ca 2+ at membrane-located binding sites. Microsomal ATPase activity and the Ca 2+-binding and -accumulating activity of cardiac microsomes is not changed after short periods of ischaemia (5 min), at a time when contractility is maximally depressed. Prolonged ischaemia results in a raised cellular Na + and reduced K +, and in a diminution in the Ca 2+-binding capacity of cardiac microsomes. The ability of cardiac microsomes to accumulate Ca 2+ in the presence of oxalate is, however, not altered by prolonged periods of ischaemia. These results indicate that the altered cardiac contractility found after short periods of either hypoxia or ischaemia may be due, in part at least, to a diminution in the amount of Ca 2+ stored at membrane-located binding sites.

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