Alto L E, Dhalla N S
Am J Physiol. 1979 Dec;237(6):H713-9. doi: 10.1152/ajpheart.1979.237.6.H713.
Myocardial cation contents were measured in isolated rat hearts perfused under various conditions. Reperfusion of Ca2+-deprived hearts produced marked increases in myocardial Ca2+ and Na+ and decreases in Mg2+ and K+ contents. These changes were dependent on the Ca2+ concentration and duration of perfusion during the periods of Ca2+ deprivation and reperfusion. The loss of Ca2+ and K+ contents normally seen after Ca2+-free exposure as well as the reperfusion-induced changes were prevented if the Ca2+-free medium contained low (35 mM) Na+ or was cooled to 21 degrees C. Reperfusion with normal Ca2+, low Na+ medium augmented the increase in myocardial Ca2+ content, while reducing K+ or Mg2+ or increasing Mg2+ in the reperfusion medium had no effect. Addition of verapamil, D600, or propranolol to the reperfusion solution did not alter the reperfusion-induced cation changes observed using control medium. These data suggest that during Ca2+ depletion, the mechanisms responsible for regulating calcium influx are either lost or inactivated, so that reperfusion-induced changes are governed solely by the driving force favoring calcium influx. The occurrence of Ca2+ overload under this condition has been implicated in the irreversible damage to myocardium and contractile failure.
在各种条件下灌注的离体大鼠心脏中测量心肌阳离子含量。钙缺乏心脏的再灌注导致心肌钙和钠显著增加，而镁和钾含量降低。这些变化取决于钙缺乏和再灌注期间的钙浓度和灌注持续时间。如果无钙培养基含有低（35 mM）钠或冷却至21摄氏度，则可防止通常在无钙暴露后以及再灌注诱导的钙和钾含量损失。用正常钙、低钠培养基进行再灌注可增加心肌钙含量的增加，而在再灌注培养基中降低钾或镁或增加镁则没有效果。向再灌注溶液中添加维拉帕米、D600或普萘洛尔不会改变使用对照培养基观察到的再灌注诱导的阳离子变化。这些数据表明，在钙耗竭期间，负责调节钙内流的机制要么丧失要么失活，因此再灌注诱导的变化仅由有利于钙内流的驱动力控制。在这种情况下发生的钙超载与心肌的不可逆损伤和收缩功能衰竭有关。
