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短链脂肪酸和二氧化碳作为离体绵羊瘤胃黏膜中钠和氯吸收的调节剂。

Short-chain fatty acids and CO2 as regulators of Na+ and Cl- absorption in isolated sheep rumen mucosa.

作者信息

Gäbel G, Vogler S, Martens H

机构信息

Institut für Veterinärphysiologie, Freie Universität Berlin, Federal Republic of Germany.

出版信息

J Comp Physiol B. 1991;161(4):419-26. doi: 10.1007/BF00260803.

Abstract

Unidirectional 22Na+ and 36Cl- fluxes were determined in short-circuited, stripped rumen mucosa from sheep by using the Ussing chamber technique. In both CO2/HCO3(-)-containing and CO2/HCO3(-)-free solutions, replacement of gluconate by short-chain fatty acids (SCFA, 39mM) significantly enhanced mucosal-to-serosal Na+ absorption without affecting the Cl- transport in the same direction. Short-chain fatty acid stimulation of Na+ transport was at least partly independent of Cl- and could almost completely be abolished by 1 mM mucosal amiloride, while stimulation of Na+ transport was enhanced by lowering the mucosal pH from 7.3 to 6.5. Similar to the SCFA action, raising the PCO2 in the mucosal bathing solution led to an increase in the amiloride-sensitive mucosal-to-serosal Na+ flux. Along with its effect on sodium transport, raising the PCO2 also stimulated chloride transport. The results are best explained by a model in which undissociated SCFA and/or CO2 permeate the cell membrane and produce a raise in intracellular H+ concentration. This stimulates an apical Na+/H+ exchange, leading to increased Na+ transport. The stimulatory effect of CO2 on Cl- transport is probably mediated by a Cl-/HCO3- exchange mechanism in the apical membrane. Binding of SCFA anions to that exchange as described for the rat distal colon (Binder and Mehta 1989) probably does not play a major role in the rumen.

摘要

采用尤斯灌流小室技术,测定了绵羊短路剥离瘤胃黏膜中单向的(^{22}Na^+)和(^{36}Cl^-)通量。在含(CO_2/HCO_3^-)和不含(CO_2/HCO_3^-)的溶液中,用短链脂肪酸(SCFA,39mM)替代葡萄糖酸盐可显著增强黏膜到浆膜的(Na^+)吸收,而不影响同向的(Cl^-)转运。短链脂肪酸对(Na^+)转运的刺激至少部分独立于(Cl^-),且几乎可被1mM黏膜阿米洛利完全消除,而将黏膜pH从7.3降至6.5可增强对(Na^+)转运的刺激。与短链脂肪酸的作用类似,提高黏膜灌流液中的(PCO_2)会导致阿米洛利敏感的黏膜到浆膜的(Na^+)通量增加。除了对钠转运的影响外,提高(PCO_2)还刺激了氯转运。这些结果最好用一个模型来解释,即未解离的短链脂肪酸和/或(CO_2)透过细胞膜,导致细胞内(H^+)浓度升高。这刺激了顶端的(Na^+/H^+)交换,导致(Na^+)转运增加。(CO_2)对氯转运的刺激作用可能是由顶端膜中的(Cl^-/HCO_3^-)交换机制介导的。如对大鼠远端结肠所描述的那样,短链脂肪酸阴离子与该交换的结合(Binder和Mehta,1989年)在瘤胃中可能不起主要作用。

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