Reddy Y S, Wyborny L, Lewis R M, Schwartz A
Cardiovasc Res. 1976 Jan;10(1):129-35. doi: 10.1093/cvr/10.1.129.
Experimentally-induced ischaemia in the dog heart was produced by ligating the left circumflex artery. Myosin B isolated from the ischaemic portion of the myocardium differed from myosin B isolated from control tissue in its diminished response to the calcium chelator ethyleneglycol bis (beta-amino-ethylether)-N, N'-tetraacetic acid (EGTA). In the presence of EGTA, ischaemic myosin B required 2.5 +/- 0.5 min for completion of superprecipitation, whereas control myosin B required 6.6 +/- 2.5 min. Likewise, the Mg++ -activated ATPase activity of ischaemic myosin B was inhibited by EGTA to a lesser degree than control myosin B. Experiments with reconstituted myosin B using desensitized control myosin B and regulatory proteins suggest that ischaemia induces changes in the regulatory proteins (troponin and tropomyosin).
通过结扎左旋支动脉在犬心脏中诱导实验性缺血。从心肌缺血部分分离出的肌球蛋白B与从对照组织分离出的肌球蛋白B不同,其对钙螯合剂乙二醇双(β-氨基乙醚)-N,N'-四乙酸(EGTA)的反应减弱。在EGTA存在的情况下,缺血性肌球蛋白B完成超沉淀需要2.5±0.5分钟,而对照肌球蛋白B需要6.6±2.5分钟。同样,EGTA对缺血性肌球蛋白B的Mg++激活的ATP酶活性的抑制程度低于对照肌球蛋白B。使用脱敏对照肌球蛋白B和调节蛋白对重组肌球蛋白B进行的实验表明,缺血会诱导调节蛋白(肌钙蛋白和原肌球蛋白)发生变化。