AJP - Heart and Circulatory Physiology, Vol 242, Issue 6 1022-H1030, Copyright © 1982 by American Physiological Society
Contracture of isolated rat heart cells on anaerobic to aerobic transition
C. Hohl, A. Ansel, R. Altschuld and G. P. Brierley
Adult rat heart myocytes prepared by collagenase perfusion show a
progressive loss of adenylate energy charge and total adenine nucleotide as
a function of time of anaerobic incubation in the absence of glucose.
Re-aeration of the rod-shaped anaerobic cells produces a population of
viable rounded cells in hypercontracture. The round cells show extensive
morphological dislocations but remain metabolically competent in that they
1) restore adenosine 5'-triphosphate levels to the extent permitted by the
depleted adenine nucleotide pool: 2) reestablish a low Na+-K+ ratio; and 3)
restore creatine phosphate to 73% of control. The hypercontracture on
re-aeration of anaerobic myocytes closely resembles an analogous
contracture of heart cells in situ produced when hypoxic perfused hearts
are reoxygenated, the so-called "oxygen paradox." Both processes are
eliminated by inclusion of glucose during the anaerobic phase and by
inhibitors of respiration and uncouplers of oxidative phosphorylation added
before reoxygenation. Mitochondria in the hypercontracted myocytes retain
high acceptor control ratios. Contracture on re-aeration occurs to nearly
the same extent in the presence of either mM Ca2+ or 0.1 mM EGTA.
Contracture appears related to dislocations in intracellular Ca metabolism
that result from the declining energy charge and depleted nucleotide pool
produced during anoxic incubation.
