去甲肾上腺素对心肌细胞内氢离子浓度的影响。

Effect of norepinephrine on myocardial intracellular hydrogen ion concentration.

作者信息

Riegle K M, Clancy R L

出版信息

Am J Physiol. 1975 Aug;229(2):344-9. doi: 10.1152/ajplegacy.1975.229.2.344.

DOI:10.1152/ajplegacy.1975.229.2.344

Abstract

The effect of norepinephrine (NE) on the intracellular hydrogen ion concentration [H+]i of isolated rat hearts perfused with a modified Krebs-Henseleit solution (SHS) was determined. The [H+]i was calculated with the [14C]-dimethyloxazolidinedione method. Respiratory or metabolic acidosis was produced by equilibrating the KHS with 20% C02 or decreasing the [HC03-] of the KHS, respectively. Three types of experiments were carried out: 1) beta blockade--MJ 1999 (Sotalol) was added to the KHS; 2) control--no pharmacological treatment; and 3) NE-norepinephrine was added to the KHS. The effective CO2 buffer values (delta[HC03-]i/deltapHi) during respiratory acidosis were: beta blockade, 11; control, 35; and NE, 84. The production of metabolic acidosis resulted in the following [H+]i changes: beta blockade, 52 mM; control, 60 nM; and NE 7 nM. These results suggest that NE markedly attenuates the changes in [H+]i accompanying respiratory and metabolic acidosis and may account in part for previous observations that the effective C02 buffer value of cardiac muscle in vivo is greater than that in vitro.

摘要

测定了去甲肾上腺素（NE）对用改良的克雷布斯 - 亨泽莱特溶液（SHS）灌注的离体大鼠心脏细胞内氢离子浓度[H⁺]i的影响。[H⁺]i采用[¹⁴C] - 二甲基恶唑烷二酮法计算。分别通过用20% CO₂平衡KHS或降低KHS的[HCO₃⁻]来产生呼吸性或代谢性酸中毒。进行了三种类型的实验：1）β受体阻断——向KHS中加入MJ 1999（索他洛尔）；2）对照——不进行药物治疗；3）向KHS中加入NE——去甲肾上腺素。呼吸性酸中毒期间的有效CO₂缓冲值（δ[HCO₃⁻]i / δpH i）分别为：β受体阻断组为11；对照组为35；NE组为84。代谢性酸中毒的产生导致以下[H⁺]i变化：β受体阻断组为52 mM；对照组为60 nM；NE组为7 nM。这些结果表明，NE显著减弱了伴随呼吸性和代谢性酸中毒的[H⁺]i变化，这可能部分解释了先前的观察结果，即体内心肌的有效CO₂缓冲值大于体外。