Kato Y, Otani H, Tanaka K, Saito Y, Fukunaka M, Imamura H
Department of Thoracic and Cardiovascular Surgery, Kansai Medical University, Osaka, Japan.
Ann Thorac Surg. 1991 Oct;52(4):979-86. doi: 10.1016/0003-4975(91)91264-v.
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.
细胞内钙离子（[Ca2+]i）在心脏功能调节中起关键作用。我们研究了心脏停搏保存对装载荧光钙指示剂（fura-2）的离体灌注豚鼠心脏中[Ca2+]i瞬变的影响。[Ca2+]i瞬变和等容左心室压力的测量结果显示，在常温全心缺血15分钟期间及再灌注后，[Ca2+]i瞬变和对[Ca2+]i的机械反应发生了显著改变。首先，[Ca2+]i瞬变在缺血期间持续存在，但未产生主动收缩力。这种肌丝对Ca2+敏感性降低的表现再灌注后的前5分钟持续存在。其次，[Ca2+]i的幅度在缺血和再灌注期间减小。第三，缺血期间尤其是再灌注开始时舒张期[Ca2+]i升高。静脉推注冷圣托马斯医院溶液可消除[Ca2+]i瞬变和舒张末期水平的左心室压力升高。此外，低温心脏停搏在再灌注期间改善左心室功能的恢复与其调节受损的[Ca2+]i瞬变和对[Ca2+]i的机械反应的能力密切相关；左心室收缩功能的改善似乎是通过恢复肌丝对Ca2+的敏感性和[Ca2+]i瞬变的幅度来实现的，而左心室更好的舒张顺应性则归因于舒张期[Ca2+]i显著降低。这些结果可能为基于[Ca2+]i瞬变的心脏停搏保存机制提供新的见解。
