二丁酰环磷酸腺苷和胰高血糖素对心肌细胞pH1的影响

The effect of dibutyryl cyclic AMP and glucagon on the myocardial cell pH1.

作者信息

Fenton R A, Gonzalez N C, Clancy R L

出版信息

Respir Physiol. 1978 Feb;32(2):213-23. doi: 10.1016/0034-5687(78)90111-1.

Abstract

DBcAMP or crystalline glucagon was utilized to elevate the intracellular cyclic AMP concentration in isolated rat hearts. Butyric acid, a metabolite of DBcAMP, was also investigated. Their effect on the intracellular pH (pHi) as determined by the distribution of [14C]DMO was investigated. Rat hearts, perfused with a recirculated modified Krebs-Henseleit solution maintained at 30 degrees C, were exposed to respiratory acidosis by bubbling the perfusate with 20% CO2. alpha- and beta-receptor antagonists were used to block the effects of endogenous catecholamines. Hypercapnia decreased the pHi from 7.09 to 6.82. A similar degree of hypercapnia decreased the pHi to only 6.95 in the presence of DBcAMP and to only 6.96 in the presence of glucagon. The effective buffer values (delta[HCO-3]i/deltapHi) were: control, 19; butyric acid, 16; DBcAMP, 139; glucagon, 148. These data suggest that cAMP mediates the effect of norepinephrine, which has been shown to diminish the change in pHi accompanying respiratory acidosis.

摘要

二丁酰环磷腺苷（DBcAMP）或结晶胰高血糖素被用于提高离体大鼠心脏细胞内的环磷腺苷浓度。同时也研究了DBcAMP的代谢产物丁酸。研究了它们对通过[14C]二甲基氧芐脒（DMO）分布测定的细胞内pH（pHi）的影响。用在30℃下循环的改良克雷布斯-亨泽莱特溶液灌注的大鼠心脏，通过向灌注液中鼓入20%的二氧化碳使其暴露于呼吸性酸中毒环境中。使用α和β受体拮抗剂来阻断内源性儿茶酚胺的作用。高碳酸血症使pHi从7.09降至6.82。在存在DBcAMP的情况下，类似程度的高碳酸血症仅使pHi降至6.95，在存在胰高血糖素的情况下仅降至6.96。有效缓冲值（δ[HCO-3]i/δpHi）分别为：对照组19；丁酸16；DBcAMP 139；胰高血糖素148。这些数据表明环磷腺苷介导去甲肾上腺素的作用，而去甲肾上腺素已被证明可减少伴随呼吸性酸中毒的pHi变化。