Effects of amiloride on metabolism and contractility during reoxygenation in perfused rat hearts.

Myocardial recovery after hypoxia may be determined not only by the extent of metabolic depression during the hypoxic period but also by changes in cation contents as well. Calcium overload during reoxygenation, mediated in part by Na-Ca exchange and supported by the rise in cell sodium during hypoxia, may be one factor. The effects of amiloride (0.1 mM), a diuretic that inhibits Na(+)-H+ and Na-Ca exchanges in cardiac sarcolemma and mitochondria preparations, were studied during hypoxia-reoxygenation in the isovolumic, isolated rat heart. During hypoxia, cell sodium, measured using potassium ethylenediamine tetraacetate cobaltate as an extracellular marker, increased in amiloride and amiloride-free hearts, but there was no increase in cell calcium (3.3 +/- 0.3 vs. 3.6 +/- 0.9 mumol/g dry wt; p = NS). Amiloride did not alter developed pressure (DP), end-diastolic pressure (EDP), pH, or integrated areas of adenosine triphosphate (ATP) and phosphocreatine (PCr) (determined by phosphorus-31-nuclear magnetic ...