Steinberg J B, Doherty N E, Munfakh N A, Geffin G A, Titus J S, Hoaglin D C, Denenberg A G, Daggett W M
Department of Surgery, Massachusetts General Hospital, Boston 02114.
Ann Thorac Surg. 1991 Apr;51(4):620-9. doi: 10.1016/0003-4975(91)90322-h.
Reports differ as to the efficacy of glucose and insulin as cardioplegic additives. Although deliberate oxygenation of crystalloid cardioplegic solutions improves myocardial protection, little is known about the protection afforded by glucose and insulin in such oxygenated solutions. In the isolated working rat heart, we studied the addition of oxygen, glucose, and insulin, separately and together, to a cardioplegic solution. The solution was equilibrated with O2 or N2, with glucose added as a substrate or sucrose as a nonmetabolizable osmotic control, with or without insulin. Hearts were arrested for 2 hours at 8 degrees C by multidose infusions. Oxygenation decreased lactate production and improved high-energy phosphate and glycogen preservation during arrest, prevented ischemic contracture, and improved functional recovery. The addition of glucose to the oxygenated solution increased the level of adenosine triphosphate at end-arrest from 10.5 +/- 0.5 to 13.9 +/- 0.6 nmol/mg dry weight and glycogen stores from 18.7 +/- 2.5 to 35.7 +/- 5.5 nmol/mg dry weight. The further addition of insulin did not better preserve these metabolites. Improvements in functional recovery due to glucose or insulin in the oxygenated solution attained statistical significance when both additives were included. Glucose increased lactate production significantly only when the solution was nitrogenated. Insulin added to the nitrogenated glucose-containing solution increased adenosine triphosphate and glycogen levels after 1 hour of arrest; and, although insulin did not prevent ischemic contracture from developing during the latter part of arrest with profound depletion of these metabolites, functional recovery was improved. The mechanism of improved functional recovery by insulin is not clear.(ABSTRACT TRUNCATED AT 250 WORDS)
关于葡萄糖和胰岛素作为心脏停搏添加剂的疗效,各报告说法不一。尽管对晶体心脏停搏液进行蓄意氧合可改善心肌保护,但对于葡萄糖和胰岛素在这种氧合溶液中所提供的保护作用却知之甚少。在离体工作的大鼠心脏中,我们研究了分别或共同向心脏停搏液中添加氧气、葡萄糖和胰岛素的情况。该溶液用氧气或氮气平衡,添加葡萄糖作为底物或蔗糖作为不可代谢的渗透对照,同时添加或不添加胰岛素。通过多次输注使心脏在8摄氏度下停搏2小时。氧合可减少乳酸生成,改善停搏期间高能磷酸盐和糖原的保存,预防缺血性挛缩,并改善功能恢复。向氧合溶液中添加葡萄糖可使停搏末期三磷酸腺苷水平从10.5±0.5纳摩尔/毫克干重增加到13.9±0.6纳摩尔/毫克干重,糖原储备从18.7±2.5纳摩尔/毫克干重增加到35.7±5.5纳摩尔/毫克干重。进一步添加胰岛素并不能更好地保存这些代谢产物。当同时包含这两种添加剂时,氧合溶液中葡萄糖或胰岛素对功能恢复的改善具有统计学意义。仅当溶液用氮气平衡时,葡萄糖才会显著增加乳酸生成。添加到用氮气平衡的含葡萄糖溶液中的胰岛素在停搏1小时后可增加三磷酸腺苷和糖原水平;并且,尽管胰岛素在停搏后期这些代谢产物严重耗竭时并不能阻止缺血性挛缩的发生,但功能恢复得到了改善。胰岛素改善功能恢复的机制尚不清楚。(摘要截选至250字)