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The Annals of Thoracic Surgery, Vol 52, 979-986, Copyright © 1991 by The Society of Thoracic Surgeons
Y Kato, H Otani, K Tanaka, Y Saito, M Fukunaka and H Imamura
Intracellular Ca2+ ([Ca2+]i) plays a pivotal role in the regulation of
cardiac function. We investigated the effect of cardioplegic preservation
on [Ca2+]i transients in the isolated and perfused guinea pig heart loaded
with a fluorescent Ca2+ indicator (fura-2). The measurements of [Ca2+]i
transients and isovolumetric left ventricular pressure revealed that
[Ca2+]i transients and mechanical responses to [Ca2+]i were markedly
altered during 15 minutes of normothermic global ischemia and after
reperfusion. First, [Ca2+]i transients remained during ischemia without
generation of active force of contraction. Such a manifestation of
depressed sensitivity of the myofilaments to Ca2+ persisted for the first 5
minutes after reperfusion. Second, the amplitude of [Ca2+]i was diminished
during ischemia and reperfusion. Third, diastolic [Ca2+]i was increased
during ischemia and especially at the onset of reperfusion. Bolus infusion
of cold St. Thomas' Hospital solution abolished [Ca2+]i transients and left
ventricular pressure development at an end-diastolic level. Moreover,
improved recovery of left ventricular function during reperfusion afforded
by the hypothermic cardioplegia was intimately related to its ability to
modulate impaired [Ca2+]i transients and mechanical responses to [Ca2+]i;
improvement of systolic left ventricular function appears to be produced by
restoration of Ca2+ sensitivity of the myofilaments and the amplitude of
[Ca2+]i transients, whereas better diastolic compliance of the left
ventricle is ascribed to significantly lower diastolic [Ca2+]i. These
results may provide new insight into the mechanism of cardioplegic
preservation on the basis of [Ca2+]i transients.
ARTICLES
Effect of cardioplegic preservation on intracellular calcium transients
Department of Thoracic and Cardiovascular Surgery, Kansai Medical University, Osaka, Japan.
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