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糖尿病酮症酸中毒中的酸碱平衡

Acid-base balance in diabetic ketoacidosis.

作者信息

Sestoft L, Folke M, Bartels P D, Marshall M O

出版信息

Ciba Found Symp. 1982;87:254-72. doi: 10.1002/9780470720691.ch14.

DOI:10.1002/9780470720691.ch14
PMID:6804192
Abstract

Acid-base balance during development of diabetic ketoacidosis was reappraised on the basis of old studies on urinary excretion of ions. Circulatory collapse with impaired urinary excretion of acids is a prominent feature of the late phase of diabetic ketoacidosis, in which pathophysiological measurements are difficult to make. To elucidate the balance between hepatic uptake of carboxylic acids (free fatty acids and lactate plus pyruvate) and hepatic release of carboxylic acids (ketone bodies and lactate plus pyruvate) during the late phase of diabetic ketoacidosis, perfused livers from normal and streptozotocine-diabetic rats, fasted for 48 h, were subjected to high perfusate glucose concentrations, low perfusate pH and low perfusate flow rates. Provided that flow was kept normal, there was always a net uptake of carboxylic acids. At normal flow, a low pH and a high glucose concentration in the perfusate did not affect the hepatic uptake of lactate plus pyruvate or the flux of carbon from lactate to glucose. Reduction of the perfusate flow rate by two-thirds invariably turned the liver into a state of net carboxylic acid production. The net uptake of lactate plus pyruvate was greatly reduced, mainly due to initiation of a glycolytic flux.

摘要

基于以往关于离子尿排泄的研究,对糖尿病酮症酸中毒发展过程中的酸碱平衡进行了重新评估。伴有酸尿排泄受损的循环衰竭是糖尿病酮症酸中毒晚期的一个突出特征,在此阶段进行病理生理学测量很困难。为了阐明糖尿病酮症酸中毒晚期肝脏对羧酸(游离脂肪酸、乳酸加丙酮酸)的摄取与肝脏释放羧酸(酮体、乳酸加丙酮酸)之间的平衡,对禁食48小时的正常大鼠和链脲佐菌素诱导的糖尿病大鼠的灌注肝脏施加高灌注液葡萄糖浓度、低灌注液pH值和低灌注液流速。只要流速保持正常,羧酸总会有净摄取。在正常流速下,灌注液中的低pH值和高葡萄糖浓度不会影响肝脏对乳酸加丙酮酸的摄取或碳从乳酸到葡萄糖的通量。将灌注液流速降低三分之二则总会使肝脏转变为羧酸净产生状态。乳酸加丙酮酸的净摄取量大幅减少,主要是由于糖酵解通量的启动。

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