Effect of cardioplegic preservation on intracellular calcium transients.

Author(s): Kato Y, Otani H, Tanaka K, Saito Y, Fukunaka M, Imamura H

Affiliation(s): Department of Thoracic and Cardiovascular Surgery, Kansai Medical University, Osaka, Japan.

Publication date & source: 1991-10, Ann Thorac Surg., 52(4):979-86.

Publication type:

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.