Deaciuc I V, Bagby G J
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112-1393.
Circ Shock. 1988 Jul;25(3):165-72.
Liver perfusion experiments were performed to further investigate the origin of hypertriacylglycerolemia associated with endotoxemia in rats. For this purpose male rats were treated with E. coli endotoxin in a dose of 0.5 mg/100 g b.w. intravenously, deprived of food (with free access to water), and used 18 h later for liver perfusion experiments. Livers were isolated and perfused for 4 h with a medium consisting of Krebs-Ringer bicarbonate buffer containing bovine serum albumin (4%, w/v), glucose, 5 mM, oleate, 0.7-0.8 mM, and aged human erythrocytes, 20% (v/v). The rates of triacylglycerol (TAG) output, oleate uptake, and ketogenesis were measured. Endotoxin treatment did not induce changes of the rate of either TAG output or ketogenesis in the perfused liver. The data give further support to the contention that hypertriacylglycerolemia associated with endotoxicosis is unlikely to originate in an overproduction of TAG by the liver.
进行肝脏灌注实验以进一步研究大鼠内毒素血症相关的高三酰甘油血症的起源。为此，将雄性大鼠静脉注射剂量为0.5 mg/100 g体重的大肠杆菌内毒素，禁食（可自由饮水），18小时后用于肝脏灌注实验。分离肝脏并用含有牛血清白蛋白（4%，w/v）、5 mM葡萄糖、0.7 - 0.8 mM油酸和20%（v/v）衰老人红细胞的 Krebs - Ringer碳酸氢盐缓冲液组成的培养基灌注4小时。测量三酰甘油（TAG）输出率、油酸摄取率和生酮率。内毒素处理未引起灌注肝脏中TAG输出率或生酮率的变化。这些数据进一步支持了与内毒素血症相关的高三酰甘油血症不太可能起源于肝脏TAG过度产生的观点。
