Lipid Alterations in Isolated, Working Rat Hearts During Ischemia and Reperfusion: Its Relation to Myocardial Damage
Lipid Alterations in Isolated, Working Rat Hearts During Ischemia and Reperfusion: Its Relation to Myocardial Damage
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缺血和再灌注期间离体工作大鼠心脏的脂质变化：其与心肌损伤的关系
DOI：
10.1161/01.res.64.2.304
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发表时间：
1989
影响因子：
20.1
通讯作者：
R. Reneman
中科院分区：
文献类型：
--
作者：
M. Bilsen;G. J. van der Vusse;P. Willemsen;W. Coumans;T. Roemen;R. Reneman
脂质代谢紊乱可能在不可逆心肌损伤的发生中起重要作用。为了研究缺血和再灌注对脂质稳态的影响，并描述其对心肌损伤的可能后果，对Krebs-Henseleit灌注的工作大鼠心脏进行了不同时间段的无血流缺血（10至90分钟），有或没有30分钟的再灌注。在缺血期间，非酯化脂肪酸（NEFA）的上升之前，大量的甘油的积累，表明存在一个活跃的三酰甘油-NEFA循环。NEFA的后续增长（90分钟后从0.25至1.64 μmol/g干残留物重量[平均值]）与ATP降低至低于10 μmol/g干重的值和AMP（酰基辅酶A合成酶的有效抑制剂）升高至超过2 μmol/g干重的值相一致，使后者化合物成为在长时间缺血期间阻碍内源性脂质周转的良好候选物。再灌注导致NEFA额外升高（缺血60分钟后高达4.1 μmol/g干残留物重量）。缺血或再灌注均未导致三酰甘油和各种磷脂的组织含量显著降低。在再灌注期间，每搏输出量的恢复在被认为与正常线粒体功能不相容的组织NEFA水平下仍然足够。37在再灌注心脏的NEFA含量和再灌注期间乳酸脱氢酶的累积释放之间发现正相关性（r=0.81）。因此，得出结论：1）再灌注导致心肌脂质稳态的额外变化，2）可能在细胞水平上将累积的NEFA区室化，和3）NEFA的累积是心肌细胞损伤的敏感标志物。
Disturbances in lipid metabolism may play an important role in the onset of irreversible myocardial damage. To investigate the effect of ischemia and reperfusion on lipid homeostasis and to delineate its possible consequences for myocardial damage, Krebs-Henseleit-perfused, working rat hearts were subjected to various periods of no-flow ischemia (10 to 90 minutes) with or without 30 minutes of reperfusion. During ischemia, the rise in nonesterified fatty acids (NEFAs) was preceded by the accumulation of substantial amounts of glycerol, indicating the presence of an active triacylglycerol-NEFA cycle. The subsequent rise in NEFAs (from 0.25 to 1.64 μmol/g dry residue wt after 90 minutes [means]) coincided with the reduction of ATP to values lower than 10 μmol/g dry wt and the rise of AMP, a potent inhibitor of acyl-coenzyme A synthetase, to values exceeding 2 μmol/g dry wt, making the latter compound a good candidate to hamper the turnover of endogenous lipids during prolonged ischemia. Reperfusion resulted in an additional rise in NEFAs (up to 4.1 μmol/g dry residue wt after 60 minutes of ischemia). Neither ischemia nor reperfusion resulted in significant decreases in the tissue content of triacylglycerols and the various phospholipids. During reperfusion recovery of stroke volume was still adequate at tissue NEFA levels thought to be incompatible with normal mitochondrial function.37 A positive correlation (r=0.81) was found between NEFA content of reperfused hearts and cumulative release of lactate dehydrogenase during reperfusion. Accordingly it is concluded that 1) reperfusion results in additional changes in myocardial lipid homeostasis, 2) the accumulating NEFAs are compartmentalized, possibly at the cellular level, and 3) the accumulation of NEFAs is a sensitive marker for myocardial cell damage.
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DOI：
10.1152/ajpheart.1982.243.2.h187
发表时间：
1982
期刊：
The American journal of physiology
影响因子：
--
作者：
Corr,PB;Snyder,DW;Lee,BI;Gross,RW;Keim,CR;Sobel,BE
通讯作者：
Sobel,BE
影响因子：
6.5
作者：
W. R. Morrison;L. Smith
通讯作者：
W. R. Morrison;L. Smith
狗心脏体外完全缺血时溶血磷脂积累与质膜损伤的关系。
影响因子：
5
作者：
Steenbergen,C;Jennings,RB
通讯作者：
Jennings,RB
大鼠心脏磷脂酶 A 的亚细胞定位：胞质磷脂酶 A1 的证据。
影响因子：
6.5
作者：
Nalbone,G;Hostetler,KY
通讯作者：
Hostetler,KY
DOI：
--
发表时间：
1983
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Gross,RW;Sobel,BE
通讯作者：
Sobel,BE