Lopaschuk G D, Spafford M A, Davies N J, Wall S R
Department of Pediatrics, University of Alberta, Edmonton, Canada.
Circ Res. 1990 Feb;66(2):546-53. doi: 10.1161/01.res.66.2.546.
Alterations in energy substrate utilization during reperfusion of ischemic hearts can influence the functional recovery of the myocardium. Energy substrate preference by the reperfused myocardium, however, has received limited attention. Therefore, we measured oxidation rates of glucose and palmitate during reperfusion of ischemic hearts. Isolated working rat hearts were perfused with 1.2 mM palmitate and 11 mM [14C]glucose, 1.2 mM [14C]palmitate and 11 mM glucose, or 11 mM [14C]glucose alone, at an 11.5 mm Hg preload and 80 mm Hg afterload. Hearts were subjected to 60-minute aerobic perfusion or 25-minute global ischemia followed by 60-minute aerobic reperfusion. Steady-state oxidative rates of glucose or palmitate were determined by measuring 14CO2 production. In hearts perfused with glucose alone, oxidative rates during reperfusion were not significantly different than nonischemic hearts (1,008 +/- 335 vs. 1,372 +/- 117 nmol [14C]glucose oxidized/min/g dry wt, respectively). In the presence of palmitate, glucose oxidation was markedly reduced in reperfused and nonischemic hearts (81 +/- 11 and 101 +/- 15 nmol [14C]glucose oxidized/min/g dry wt, respectively). Palmitate oxidation rates were not significantly different in reperfused compared with nonischemic hearts (369 +/- 55 and 455 +/- 50 nmol [14C]palmitate oxidized/min/g dry wt, respectively). [14C]Palmitate was incorporated into myocardial triglycerides to a greater extent in reperfused ischemic hearts than in nonischemic hearts (26.0 and 13.8 mumol/g dry wt, respectively). Under the perfusion conditions used, palmitate provided over 90% of the ATP produced from exogenous substrates. Addition of the carnitine palmitoyltransferase I inhibitor, ethyl 2-[6-(4-chlorophenoxy)hexyl]oxirane-2-carboxylate (Etomoxir, 10(-6) M), during reperfusion stimulated glucose oxidation and improved mechanical recovery of ischemic hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
缺血心脏再灌注期间能量底物利用的改变会影响心肌的功能恢复。然而,再灌注心肌对能量底物的偏好受到的关注有限。因此,我们测量了缺血心脏再灌注期间葡萄糖和棕榈酸的氧化速率。将离体工作大鼠心脏在11.5 mmHg前负荷和80 mmHg后负荷下,用1.2 mM棕榈酸和11 mM [14C]葡萄糖、1.2 mM [14C]棕榈酸和11 mM葡萄糖或仅11 mM [14C]葡萄糖进行灌注。心脏先进行60分钟有氧灌注或25分钟全心缺血,然后进行60分钟有氧再灌注。通过测量14CO2生成量来测定葡萄糖或棕榈酸的稳态氧化速率。在仅用葡萄糖灌注的心脏中,再灌注期间的氧化速率与非缺血心脏无显著差异(分别为1,008±335和1,372±117 nmol [14C]葡萄糖氧化/min/g干重)。在有棕榈酸存在的情况下,再灌注和非缺血心脏中的葡萄糖氧化均显著降低(分别为81±11和101±15 nmol [14C]葡萄糖氧化/min/g干重)。与非缺血心脏相比,再灌注心脏中棕榈酸的氧化速率无显著差异(分别为369±55和455±50 nmol [14C]棕榈酸氧化/min/g干重)。与非缺血心脏相比,[14C]棕榈酸在再灌注缺血心脏中更多地掺入心肌甘油三酯中(分别为26.0和13.8 μmol/g干重)。在所使用的灌注条件下,棕榈酸提供了超过90%的外源性底物产生的ATP。在再灌注期间添加肉碱棕榈酰转移酶I抑制剂乙基2-[6-(4-氯苯氧基)己基]环氧乙烷-2-羧酸盐(依托莫司,10(-6) M)可刺激葡萄糖氧化并改善缺血心脏的机械恢复。(摘要截断于250字)