• 作者： 黃廷飛；張丙龍；陳樹仁
• 作者服務機構： 國立臺灣大學醫學院生理學科; 國立臺灣大學醫學院解剖學科
• 中文摘要： 採取貓健全心室肌，急性(一小時)及慢性(六天)乏血心室肌各做離體標本灌流。使用微小電極記錄心肌細胞電位。乏血心肌靜止動作電位減小。后者平頂部消失，並其期間縮短。分析藥物對健全及乏血心肌細胞電位作用差異。其結果Tetrodotoxin 1-2μg/ml灌流30分鐘，對健全或乏血心肌無顯著作用2?4 mM MnCl2及verapamil 1μg/ml灌流30分鐘，乏血心肌靜止動作電位減小。Acetylcholine 5μg/ml灌流3?5分鐘，乏血心肌動作電位減小。Adrenaline 0.5?1μg/ml灌流3?5分鐘，乏血心肌動作電位增大，但對健全心肌無顯著作用。Deslanoside 2μg/ml灌流30分鐘，乏血心肌靜止及動作電位減小。根據結果可知乏血心肌對藥物尤其自主神經傳遞物質靈敏性增加，可能易促生心律不整。
• 英文摘要： The ventricular muscles (VM) of cats were dissected from the normal hearts or from hearts with acute (1-hr) or chronic (6-day) infarction produced by the coronary ligation. The glass microelectrode technique was employed to record the transmembrane potentials of the isolated myocardiums. Decrease in resting potential and action potential lacking of the plateau phase was recorded from the ischemic zone of either the acute or the chronic infarction. Effects of various drugs on the transmembrane potentials of the normal and the ischemic VM were tested. Perfusion of tetrodotoxin 1-2μg/ml for 30min had no effect on either the normal or the ischemic VM. Perfusion of 2-4 mM MnCl2 or verapamil 1μg/ml for 30min decreased resting and action potentials of the ischemic VM. Acetylcholine, (5μg/ml, 3-5 min) decreased the action potential of the ischemic VM, while adrenaline, (1μg/ml, 3-5 min) increased the potential. Deslanoside, (2μg/ml, 30 min) also depressed the resting and action potentials of the ischemic VM. The increased sensitivity of the ischemic VM to acetylcholine and adrenaline may facilitate genesis of the arrhythmia following the myocardial infarction.
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