Evaluation of methods for estimating infarct size by myosin LC2: comparison with cardiac enzymes.

Evaluation of methods for estimating infarct size by myosin LC2: comparison with cardiac enzymes.
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肌球蛋白 LC2 估计梗塞面积方法的评估:与心肌酶的比较。

DOI:
10.1152/ajpheart.1983.245.3.h413
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发表时间:
1983
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Y. Yazaki
Y. Yazaki
中科院分区:
--
文献类型:
--
作者:
R. Nagai;C. Chiu;K. Yamaoki;Y. Ohuchi;S. Ueda;K. Imataka;Y. Yazaki

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研究了组织学确定的梗死面积与循环心肌酶和肌球蛋白轻链2(LC 2)的释放或峰值水平之间的关系。在18只清醒闭胸犬上,结扎冠状动脉左前降支造成心肌梗塞。连续测量肌酸磷酸激酶(CPK)、血浆中天冬氨酸转氨酶的胞浆和线粒体同工酶(sAST和mAST)以及血清中的LC 2,直至梗死后10天,此时通过组织学确定梗死面积[范围为左心室重量的4.0-38.8%(%LV)]。CT大小与LC 2释放最密切相关(r = 0.82,P <0.001),与峰值sAST(r = 0.59,P <0.01)、峰值mAST(r = 0.49,P <0.05)、峰值CPK(r = 0.22)和CPK释放(r = 0.14)的相关性较低。通过限制对梗死面积小于20%LV的犬的分析,改善了梗死面积和CPK释放之间的相关性(n = 11,r = 0.53,P小于0.1)。因为,心肌酶和LC 2,CPK活性衰减最快的淋巴液中孵育时,在体外,CPK在淋巴流中的变性可能有助于梗死面积和CPK释放之间的非线性关系。
The relationship between histologically determined infarct size and release or peak levels of circulating cardiac enzymes and myosin light chain 2 (LC2) was studied. Myocardial infarction was produced by ligating the left anterior descending coronary artery in 18 conscious closed-chest dogs. Creatine phosphokinase (CPK), cytosolic and mitochondrial isozymes of aspartate transaminase (sAST and mAST) in the plasma, and LC2 in the serum were measured serially until 10 days after infarction, when infarct size was determined histologically [range 4.0-38.8% of the left ventricular weight (%LV)]. Infarct size correlated most closely with LC2 release (r = 0.82, P less than 0.001) and less closely with peak sAST (r = 0.59, P less than 0.01), peak mAST (r = 0.49, P less than 0.05), peak CPK (r = 0.22), and CPK release (r = 0.14). The correlation between infarct size and CPK release was improved by limiting the analysis to the dogs with infarct size of less than 20% LV (n = 11, r = 0.53, P less than 0.1). Because, among cardiac enzymes and LC2, CPK activity decayed most rapidly in the lymph fluid when incubated in vitro, degeneration of CPK in the lymph stream may contribute to the nonlinear relationship between infarct size and CPK release.