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酸碱平衡对离体灌注豚鼠肝脏胆汁碳酸氢盐分泌的影响。

Effect of acid-base balance on biliary bicarbonate secretion in the isolated perfused guinea pig liver.

作者信息

Blot-Chabaud M, Dumont M, Corbic M, Erlinger S

机构信息

Unité de Recherches de Physiopathologie Hépatique, Institut National de la Santé et de la Recherche Médicale, Hôpital Beaujon, Clichy, France.

出版信息

Am J Physiol. 1990 Jun;258(6 Pt 1):G863-72. doi: 10.1152/ajpgi.1990.258.6.G863.

Abstract

Secretin-induced choleresis is of ductal origin and involves bicarbonate transport. Its mechanism is unknown. To determine the relative effects of systemic pH, PCO2, and bicarbonate concentration on secretin-stimulated bicarbonate transport, states of acute metabolic and respiratory acidosis or alkalosis were created in isolated perfused guinea pig livers with or without secretin infusion. During spontaneous secretion conditions, biliary bicarbonate secretion was not correlated with perfusate pH (7.19-7.62) or perfusate PCO2 (23.9-59.7) but was significantly correlated with perfusate bicarbonate concentration (17.5-37.9 mM). Under secretion infusion (25 mU/min), bile flow and biliary bicarbonate concentration increased significantly (109 and 51%, respectively). Biliary bicarbonate secretion was not correlated with perfusate pH (7.19-7.60) but was significantly correlated both with perfusate bicarbonate concentration (14.6-36.8 mM) and PCO2 (25.8-54.3 mmHg). Spontaneous and secretin-induced bile flow were correlated with biliary bicarbonate concentration. The correlation between biliary bicarbonate secretion and PCO2 during secretin-induced choleresis supports the hypothesis that secretin-induced biliary bicarbonate secretion could, at least in part, involve a transport of H+ (or OH-) rather than HCO3- itself and that intracellular pH could play a role in the regulation of this secretion. Amiloride (5 X 10(-4) M) did not influence secretin-induced biliary bicarbonate secretion. This result suggests that the Na(+)-H+ exchange is not involved in bicarbonate secretion by ductular cells.

摘要

促胰液素诱导的胆汁分泌源于胆管,涉及碳酸氢盐转运。其机制尚不清楚。为了确定全身pH值、PCO2和碳酸氢盐浓度对促胰液素刺激的碳酸氢盐转运的相对影响,在有或没有输注促胰液素的情况下,对分离灌注的豚鼠肝脏造成急性代谢性和呼吸性酸中毒或碱中毒状态。在自发分泌条件下,胆汁碳酸氢盐分泌与灌注液pH值(7.19 - 7.62)或灌注液PCO2(23.9 - 59.7)无关,但与灌注液碳酸氢盐浓度(17.5 - 37.9 mM)显著相关。在输注促胰液素(25 mU/分钟)时,胆汁流量和胆汁碳酸氢盐浓度显著增加(分别增加109%和51%)。胆汁碳酸氢盐分泌与灌注液pH值(7.19 - 7.60)无关,但与灌注液碳酸氢盐浓度(14.6 - 36.8 mM)和PCO2(25.8 - 54.3 mmHg)均显著相关。自发和促胰液素诱导的胆汁流量与胆汁碳酸氢盐浓度相关。促胰液素诱导胆汁分泌期间胆汁碳酸氢盐分泌与PCO2之间的相关性支持了这样的假设,即促胰液素诱导的胆汁碳酸氢盐分泌至少部分可能涉及H +(或OH -)的转运而非HCO3 -本身,并且细胞内pH值可能在这种分泌的调节中起作用。氨氯吡脒(5×10^(-4) M)不影响促胰液素诱导的胆汁碳酸氢盐分泌。该结果表明,钠氢交换不参与胆管细胞的碳酸氢盐分泌。

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