Altona J C, van der Laarse A
Cardiovasc Res. 1982 Mar;16(3):138-43. doi: 10.1093/cvr/16.3.138.
The effects of energy-deprivation on composition and permeability of the sarcolemmal membrane of cardiac cells was studied using monolayer cultures of neonatal rat heart cells incubated in the absence of oxygen and metabolic substrates for 0 to 10 h at 37 degrees C. In the course of anoxia the cells were analysed for cholesterol content, a sarcolemmal sterol, and L-leucyl-naphthylamidase (LNA) activity, a sarcolemmal protein. In addition, sarcolemmal permeability was studied by measuring the efflux of alpha-hydroxybutyrate dehydrogenase (HBDH) activity from the incubated cells. To test whether cholesterol and LNA are indeed markers of sarcolemmal membrane of the heart cells used, sarcolemmal preparations were obtained using an isolation method with cation-coated beads. The results of this study indicate that during anoxia and substrate depletion, changes in sarcolemmal cholesterol content precede sarcolemmal LNA liberation and cytoplasmic HBDH release. It is concluded that energy-deprivation in cardiac cells destroys sarcolemmal structure and function, secondary to the loss of cholesterol.
利用新生大鼠心脏细胞单层培养物,在37℃下于无氧及无代谢底物的条件下孵育0至10小时,研究了能量剥夺对心脏细胞肌膜组成和通透性的影响。在缺氧过程中,分析细胞的胆固醇含量(一种肌膜固醇)和L - 亮氨酰萘胺酶(LNA)活性(一种肌膜蛋白)。此外,通过测量孵育细胞中α - 羟丁酸脱氢酶(HBDH)活性的流出量来研究肌膜通透性。为了检验胆固醇和LNA是否确实是所用心脏细胞肌膜的标志物,采用阳离子包被珠分离法获得肌膜制剂。本研究结果表明,在缺氧和底物耗尽期间,肌膜胆固醇含量的变化先于肌膜LNA释放和细胞质HBDH释放。得出的结论是,心脏细胞中的能量剥夺会破坏肌膜结构和功能,这是胆固醇丢失的继发结果。