CALCIUM EXCHANGE IN RABBIT MYOCARDIUM DURING AND AFTER HYPOXIA - ROLE OF SODIUM CALCIUM EXCHANGE

Calcium uptake was measured using 47Ca2+ in the isolated and arterially perfused interventricular septum of the rabbit. Experiments were undertaken to determine whether calcium uptake on reoxygenation in linked to recovery of mechanical function and whether calcium uptake is through the sodium-calcium exchange mechanism. During substrate-free hypoxia for 45 min total tissue calcium remained unchanged but immediately upon reoxygenation there was a substantial net gain of calcium. Recovery of mechanical function upon reoxygenation was inversely related to the increase in tissue calcium. Activation of sodium-calcium exchange by perfusion with a low-sodium, zero-potassium, sucrose solution also increased tissue calcium and the relation to mechanical recovery was similar to that observed on reoxygenation. The sodium-calcium exchange mechanism was not affected by hypoxia and could be demonstrated during perfusion with a substrate-free hypoxic solution. Lithium (100 mm) substitution for sucrose prevented the calcium influx induced by a low-sodium and zero-potassium perfusate under normoxic conditions. Lithium substitution early during hypoxia or on reoxygenation did not affect the increase in myocardial calcium on reoxygenation. Amiloride (10-4 m), presumed to inhibit sodium-hydrogen exchange during hypoxia, had no effect upon reoxygenation induced calcium uptake. It is concluded that the increase in calcium uptake that occurs on reoxygenation after a period of substrate-free hypoxia is related to mechanical recovery. Sodium-calcium exchange may contribute to calcium uptake on reoxygenation in this experimental model but is not the major mechanism. © 1990.