No beneficial effect of ATP-MgCl2 on impaired transmembrane potential and protein synthesis in liver ischemia.
No beneficial effect of ATP-MgCl2 on impaired transmembrane potential and protein synthesis in liver ischemia.
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发表时间：
1982
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通讯作者：
P. Hasselgren;E. Jennische;J. Fornander;A. Hellman
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作者：
P. Hasselgren;E. Jennische;J. Fornander;A. Hellman
本实验观察了大鼠肝缺血过程中及缺血后一段时间（60 min）肝细胞膜电位（HCMP）和蛋白质合成的变化。ATP-MgCl 2（5 μ mol. 100 g bw-1）或生理盐水在肝缺血期之前或之后缓慢静脉内给药。ATP-MgCl 2对受损的HCMP或蛋白质合成没有有利的影响。与此相反，这些细胞代谢变量的缺血后恢复较慢的动物接受ATP-MgCl 2肝缺血后的一段时间相比，盐水处理的大鼠。在缺血期结束时，肝组织中的ATP、葡萄糖和乳酸与缺血前接受ATP-MgCl 2或生理盐水的动物相同。这些结果表明，先前报道的在肝血流量减少的情况下给予ATP-MgCl 2后的有益作用主要不是由于肝脏中代谢情况的改善。
Hepatic cell membrane potential (HCMP) and protein synthesis were studied in rats during and after a period (60 min) of liver ischemia. ATP-MgCl2 (5 mumol . 100 g bw-1) or saline was administered slowly intravenously before or after the period of liver ischemia. No beneficial effect of ATP-MgCl2 on the impaired HCMP or protein synthesis was observed. On the contrary, the post-ischemic restitution of these cellular metabolic variables was slower in animals receiving ATP-MgCl2 after the period of liver ischemia as compared with saline-treated rats. At the end of the ischemic period, ATP, glucose and lactate in liver tissue were the same in animals receiving ATP-MgCl2 or saline before ischemia. These results suggest that the beneficial effects previously reported after administration of ATP-MgCl2 in conditions with reduced hepatic blood flow are not primarily due to an improved metabolic situation in the liver.