AJP - Heart and Circulatory Physiology, Vol 247, Issue 5 874-H879, Copyright © 1984 by American Physiological Society
Calcium paradox of the heart: a role for intracellular sodium ions
R. A. Chapman, G. C. Rodrigo, J. Tunstall, R. J. Yates and P. Busselen
Hearts that have been perfused in low calcium fluids suffer, on return to
normal calcium solutions, an impairment of function which can be
irreversible-- the "calcium paradox." In hypothermic mammalian, amphibian,
and fish heart the strong contracture, which is a typical first stage in
the development of the calcium paradox, is reversible and appears to depend
on a large rise in intracellular Na concentration ([Na]i), which occurs
during the period of Ca deprivation. This rise is mainly due to a
maintained inward Na flux through the Ca channels and causes a
depolarization of the membrane potential, which stabilizes at about -20 mV.
In frog atrial muscle if the membrane potential is clamped to values more
negative than -50 mV during the period of Ca deprivation, no contracture
develops on the restoration of the extracellular Ca concentration ([Ca]o).
In all tissues the depolarization, the rise in [Na]i, and the Ca addition
contracture are blocked by Ca channel blockers, antiarrhythmic drugs, and
Mg ions if present in the Ca-free fluid. These agents are ineffective,
however, if applied after a period of Ca deprivation when [Na]i has already
risen. The influx of Ca ions, on Ca repletion, is therefore unlikely to be
via the Ca channels and would seem to be through the Na-Ca exchange.
