Beresewicz A, Mistarz K, Demkow M
Department of Clinical Physiology, Medical Center of Postgraduate Education, Warszawa, Poland.
Biomed Biochim Acta. 1990;49(10):1039-48.
The duration of ischemia resulting in 50% post-ischemic recovery of hemodynamic functions was 25 min in the control isolated working rat hearts and increased to 45 min in the hearts subjected to normothermic cardioplegia plus normothermic global ischemia (36 degrees C) and to 180 min in the hearts subjected to hypothermic cardioplegia and hypothermic ischemia (22 degrees C). Addition of 10(-6) M trifluoperazine to the normothermic St. Thomas' cardioplegic solution considerably improved the protective properties of the solution as assessed by the functional recovery of the heart. Under conditions of hypothermic ischemic arrest the drug failed to improve the protective properties of cardioplegic solution, suggesting a common modality between hypothermia and trifluoperazine-induced protection.
在对照的离体工作大鼠心脏中，导致血流动力学功能缺血后恢复50%的缺血持续时间为25分钟；在接受常温心脏停搏加常温全心缺血（36摄氏度）的心脏中，该时间增加到45分钟；而在接受低温心脏停搏和低温缺血（22摄氏度）的心脏中，该时间增加到180分钟。在常温圣托马斯心脏停搏液中添加10^(-6) M三氟拉嗪，根据心脏功能恢复情况评估，显著改善了该溶液的保护特性。在低温缺血性停搏条件下，该药物未能改善心脏停搏液的保护特性，提示低温和三氟拉嗪诱导的保护之间存在共同机制。
