肝脏在低血流状态下乳酸酸中毒发生过程中的作用。
The role of the liver in the development of lactic acidosis in low flow states.
作者信息
Schröder R, Gumpert J R, Pluth J R, Eltringham W K, Jenny M E, Zollinger R M
出版信息
Postgrad Med J. 1969 Aug;45(526):566-70. doi: 10.1136/pgmj.45.526.566.
The role of the liver in lactate metabolism in an experimental low flow state induced by cardiac tamponade was investigated in dogs. Arterial and venous lactate, and pyruvate levels and arterio-venous oxygen content differences were measured for the liver, gut, forequarter and hind limbs. Cardiac output and regional blood flows were determined by electromagnetic flow probes. The contribution of the liver to the development of lactic acidosis was found to be variable. When hepatic oxygen consumption was decreased, the liver was documented as the major site of lactate production with an associated increase in the lactate-pyruvate ratio of hepatic venous blood. In some experiments, however, the hepatic oxygen consumption was maintained, or even increased slightly; in these circumstances the liver was, in part, responsible for the development of lactic acidosis by impaired lactate consumption.
在犬类中研究了肝脏在心脏压塞诱发的实验性低流量状态下乳酸代谢中的作用。测量了肝脏、肠道、前肢和后肢的动脉血和静脉血中的乳酸、丙酮酸水平以及动静脉氧含量差值。通过电磁流量探头测定心输出量和局部血流量。发现肝脏对乳酸酸中毒发展的作用是可变的。当肝脏耗氧量降低时，肝脏被证明是乳酸产生的主要部位，同时肝静脉血中乳酸与丙酮酸的比值会相应增加。然而，在一些实验中，肝脏耗氧量保持不变，甚至略有增加；在这些情况下，肝脏部分地由于乳酸消耗受损而导致乳酸酸中毒的发展。
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