The distribution of calcium in hypoxic cat hearts: the effect of beta 1-blockade.

Abstract

Contractile activity decays rapidly during the first few minutes of hypoxia in the mammalian myocardium. These changes may be the result of redistribution of the Ca involved in the excitation–contraction (E–C) coupling mechanism. It was the purpose of this study to determine if distortions in the Ca pool(s) involved in E–C coupling are responsible for the acute reduction in contractile force in the heart. Working, Langendorff kitten heart preparations were perfused with a Krebs–Henseleit solution equilibrated with 5% O2, 5% CO2, and 90% N2. Within 3 min of initiation of this treatment the Ca content of a pool directly involved in E–C coupling (Ca2) was reduced by approximately one-half, and this was accompanied by an equivalent increase in a slowly exchanging Ca pool (Ca3). A concomitant reduction in contractile force was associated with this redistribution of Ca. The Ca remaining in the heart after contractility had been abolished by Ca-free perfusion (residual tissue Ca) was significantly elevated by hypoxia. The β1 blocking agent practolol (10−5 M), prevented the hypoxia-induced reduction in Ca content of Ca2 produced by hypoxia, but had no effect on contractility under hypoxic conditions or during re-oxygenation. Practolol did not prevent the increase in residual tissue Ca induced by hypoxia. It was concluded that the immediate reduction in contractility caused by hypoxia was not causally related to the reduction in the quantity of Ca in Ca2, the pool involved in E–C coupling, but may be related to a rapid decrease in the supply of energy for contraction.