Hedberg P S, Torchiana D F, Reynolds T R, Geffin G A, Titus J S, Daggett W M
Department of Surgery, Massachusetts General Hospital, Boston 02114.
J Surg Res. 1994 May;56(5):439-45. doi: 10.1006/jsre.1994.1069.
Ventricular contracture was produced in isolated perfused rat hearts by a novel method using repeated administration of an anoxic cold hyperkalemic cardioplegia solution. Contracture could be reversed by reperfusion with the same solution, without calcium (Group 1), oxygenated (Group 2), or oxygenated and calcium free (Group 3). Group 1 hearts underwent partial reversal of contracture; in Group 2, contracture was reversed more completely, but the effect was transient. Hearts in Group 3 had contracture reversed completely to a level lower than prearrest end diastolic pressure. Hearts in contracture were profoundly depleted of high-energy phosphates (ATP, 9% of control; creatine phosphate, 27%) and the success of contracture reversal was paralleled by the extent to which each solution repleted ATP and PCr. Ventricular contracture produced by energy depletion is rapidly reversed by restoration of oxygen to the myocardium. Reducing extracellular calcium by acalcemic perfusion is ineffective as an isolated measure but is synergistic with reoxygenation and enhances contracture reversal.
通过一种新方法，即反复给予缺氧冷高钾停搏液，在离体灌注大鼠心脏中诱导心室挛缩。使用相同溶液进行再灌注可使挛缩逆转，该溶液无钙（第1组）、充氧（第2组）或充氧且无钙（第3组）。第1组心脏的挛缩出现部分逆转；第2组的挛缩逆转更完全，但效果是短暂的。第3组心脏的挛缩完全逆转至低于停搏前舒张末期压力的水平。处于挛缩状态的心脏中高能磷酸盐（ATP，为对照的9%；磷酸肌酸，为对照的27%）严重耗竭，挛缩逆转的成功与每种溶液补充ATP和磷酸肌酸的程度平行。能量耗竭所致的心室挛缩可通过恢复心肌氧供迅速逆转。作为单独措施，无钙灌注降低细胞外钙无效，但与再给氧具有协同作用并增强挛缩逆转。
