Mechanisms of substrate preference for oxidative metabolism during early myocardial reperfusion.
Mechanisms of substrate preference for oxidative metabolism during early myocardial reperfusion.
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早期心肌再灌注过程中氧化代谢底物偏好的机制。
DOI：
10.1152/ajpheart.1990.259.2.h317
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Nellis,SH
中科院分区：
文献类型：
--
作者：
Renstrom,B;Liedtke,AJ;Nellis,SH
我们之前报道过，在工作猪心脏中，早期心肌再灌注期间优选使用脂肪酸。这些研究的目的是测试这种底物氧化模式是否是机械恢复过程中能量需求过多的结果。比较两组猪心脏（n = 15）。两人均接受脂肪乳加肝素（血清脂肪酸，1.02 +/- 0.05 mumol/ml）以确保优选的底物可用性，并均接受[2-14C]丙酮酸盐以监测心肌对碳水化合物底物的使用。在一组（n = 8）中，给予奥芬尼辛以抑制脂肪酸的利用。左前降支 (LAD) 冠状动脉流量在 30 分钟内维持在有氧水平，在 45 分钟内减少 60%，并在最后 50 分钟内恢复到有氧水平。缺血导致了预期的整体和区域机械性能下降。接受奥芬尼辛治疗的心脏在复流期间的运动恢复较少（治疗心脏和对照心脏的有氧值收缩期缩短分别减少 73% 和 32%，P 小于或等于 0.01 和 P 小于或等于 0.05）。缺血期间，两组的丙酮酸氧化均显着下降，但恢复情况却不同。在对照心脏中，再灌注期间 CO2 产生量保持低水平（缺血值的 NS），而在治疗心脏中，CO2 产生量增加 5.5 倍（但没有超过需氧值）。组内灌注床（有氧与再灌注）之间乙酰辅酶A和乙酰肉碱的组织水平没有统计学差异。奥芬尼辛降低了两个灌注床中乙酰肉碱的水平。（摘要截断为 250 字）
We previously reported in working swine hearts a preferred use of fatty acids during early myocardial reperfusion. The purpose of these studies was to test whether this pattern of substrate oxidation was the result of excess energy demands during mechanical recovery. Two groups of pig hearts (n = 15) were compared. Both received Intralipid with heparin (serum fatty acids, 1.02 +/- 0.05 mumol/ml) to ensure preferred substrate availability and both received [2-14C]pyruvate to monitor myocardial use of a carbohydrate substrate. In one group (n = 8) oxfenicine was administered to suppress fatty acid utilization. Left anterior descending (LAD) coronary flow was maintained at aerobic levels for 30 min, reduced by 60% for 45 min, and restored to aerobic levels for a final 50 min. Ischemia caused the expected decreased in global and regional mechanical performance. Recovery in motion during reflow was less in oxfenicine-treated hearts (73 vs. 32% decrease in systolic shortening from aerobic values in treated and control hearts, P less than or equal to 0.01 and P less than or equal to 0.05, respectively). Pyruvate oxidation declined dramatically in both groups during ischemia but recovered disparately. In control hearts CO2 production remained depressed during reperfusion (NS from ischemic values), whereas in treated hearts it increased 5.5-fold (but did not exceed aerobic values). Tissue levels of acetyl CoA and acetylcarnitine were not statistically different between perfusion beds (aerobic vs. reperfusion) within groups. Oxfenicine reduced levels of acetyl carnitine in both perfusion beds.(ABSTRACT TRUNCATED AT 250 WORDS)