Brooks W W, Conrad C H, Morgan J P
Veterans Affairs Medical Center, MA, USA.
Cardiovasc Res. 1995 Apr;29(4):536-42.
The aim was to test the hypothesis that reperfusion induced arrhythmias are associated with major alterations in intracellular calcium ([Ca2+]i) regulation.
Intracellular calcium, epicardial electrical potentials, and isovolumetric left ventricular pressure were simultaneously recorded in isolated perfused intact rat hearts during ischaemia (10 min) and reperfusion. [Ca2+]i was measured using the bioluminescent calcium indicator aequorin.
Neither ventricular tachycardia nor ventricular fibrillation occurred during ischaemia. However, during the first minute of reperfusion ventricular tachycardia or fibrillation were frequently observed. Cellular calcium was altered by varying the perfusate calcium ([Ca2+]o; 0.5, 1.0, and 3.0 mmol.litre-1). 0% (0/6), 50% (5/10), 91% (10/11), respectively, of hearts showed ventricular tachycardia, ventricular fibrillation, or both upon reperfusion (P < 0.001, 0.5 v 3.0 mmol.litre-1). At all [Ca2+]o values examined, early ischaemia was associated with a rapid decrease in developed pressure and transient increase in the peak calcium transient followed by a gradual decline and subsequent increase in diastolic calcium during late ischaemia. The initiation of ventricular tachycardia/fibrillation upon reperfusion was immediately preceded by large increases in the amplitude of the calcium transient. These increases in systolic calcium were not seen in hearts in which ventricular arrhythmias did not occur.
The association between reperfusion induced abrupt increases in peak calcium and the occurrence of ventricular tachycardia or fibrillation suggests that intracellular calcium transients may have a significant role in initiating these ventricular arrhythmias.
旨在验证再灌注诱导的心律失常与细胞内钙（[Ca2+]i）调节的重大改变相关这一假说。
在离体灌注的完整大鼠心脏缺血（10分钟）和再灌注期间，同时记录细胞内钙、心外膜电位和等容左心室压力。使用生物发光钙指示剂水母发光蛋白测量[Ca2+]i。
缺血期间未发生室性心动过速或室颤。然而，在再灌注的第一分钟内，经常观察到室性心动过速或室颤。通过改变灌注液钙浓度（[Ca2+]o；0.5、1.0和3.0 mmol·升-1）来改变细胞钙。再灌注时，分别有0%（0/6）、50%（5/10）、91%（10/11）的心脏出现室性心动过速、室颤或两者皆有（P<0.001，0.5与3.0 mmol·升-1相比）。在所有检测的[Ca2+]o值下，早期缺血与舒张末压力快速下降以及钙瞬变峰值短暂升高相关，随后在晚期缺血期间逐渐下降并随后舒张期钙升高。再灌注时室性心动过速/室颤的起始之前，钙瞬变幅度立即大幅增加。在未发生室性心律失常的心脏中未观察到收缩期钙的这些增加。
再灌注诱导的钙峰值突然增加与室性心动过速或室颤的发生之间的关联表明，细胞内钙瞬变可能在引发这些室性心律失常中起重要作用。
