Imamura S, Matsuoka R, Hiratsuka E, Kimura M, Nishikawa T, Takao A
Pediatric Cardiology, Heart Institute of Japan, Tokyo Women's Medical College, Japan.
Circ Res. 1990 Apr;66(4):1067-73. doi: 10.1161/01.res.66.4.1067.
It is uncertain whether the shift of cardiac myosin heavy chain (MHC) during pressure overload can be induced by some intrinsic factors or by the stress imposed directly on the individual myocytes. To study whether the changes in cardiac MHC gene expression produced by one-sided overload are limited to the involved ventricle or extend to the other ventricle, we examined MHC gene expression and isozyme transition in the left and right ventricles in aortic coarctated and pulmonary artery-banded rats. It has been confirmed that the pressure overload is indeed limited to the loaded ventricle. The results showed that, compared with sham-operated rats, there was no significant induction of the beta-MHC messenger RNA and corresponding protein in the unloaded ventricle, whereas significant induction was observed in the overloaded ventricle. These results demonstrated that the changes in MHC gene expression and isozyme produced by one-sided ventricular overload are limited to the involved ventricle. We conclude that the MHC gene regulation during hemodynamic overload may not be induced by intrinsic factors, such as hormones, catecholamine, or atrial natriuretic peptide, but is induced by direct local response to increased load.
压力超负荷期间心肌肌球蛋白重链（MHC）的转变是由某些内在因素引起，还是由直接施加于单个心肌细胞的应激所导致，目前尚不确定。为了研究单侧超负荷引起的心脏MHC基因表达变化是仅限于受累心室还是扩展至另一心室，我们检测了主动脉缩窄和肺动脉束扎大鼠左、右心室的MHC基因表达及同工酶转变。现已证实压力超负荷确实仅限于负荷心室。结果显示，与假手术大鼠相比，未负荷心室中β-MHC信使核糖核酸及相应蛋白质未出现明显诱导，而在超负荷心室中则观察到明显诱导。这些结果表明，单侧心室超负荷引起的MHC基因表达及同工酶变化仅限于受累心室。我们得出结论，血流动力学超负荷期间的MHC基因调控可能不是由激素、儿茶酚胺或心房利钠肽等内在因素诱导，而是由对负荷增加的直接局部反应所诱导。
