Achike F I, Dai S
Department of Pharmacology, Faculty of Medicine, University of Hong Kong.
Eur J Pharmacol. 1991 Apr 10;196(1):77-83. doi: 10.1016/0014-2999(91)90411-i.
Langendorff preparations of Sprague-Dawley rat hearts were perfused with calcium-free Krebs solution of pH 7.48 (control), 7.26 (acidosis) or 7.69 (alkalosis) containing either adrenaline or potassium. The responses of the force of contraction, coronary perfusion pressure and heart rate to graded doses of calcium preceded by a single dose of verapamil were measured. Contractile responsiveness to calcium was reduced during acidosis in both adrenaline- and potassium-stimulated hearts but was increased or reduced during alkalosis with adrenaline- or potassium stimulation, respectively. The efficacy of verapamil as a calcium antagonist increased during acidosis or alkalosis in both adrenaline- and potassium-stimulated hearts. In conclusion, acidosis or alkalosis inhibits potassium-stimulated contractions of the heart and enhances the effects of verapamil on potassium- and adrenaline-mediated contractions. Acidosis inhibits and alkalosis enhances adrenaline-stimulated contractions.
用含有肾上腺素或钾的pH值为7.48（对照）、7.26（酸中毒）或7.69（碱中毒）的无钙Krebs溶液灌注斯普拉格-道利大鼠心脏的Langendorff标本。测量了在单次给予维拉帕米后，收缩力、冠状动脉灌注压和心率对不同剂量钙的反应。在肾上腺素和钾刺激的心脏中，酸中毒时对钙的收缩反应性降低，但在碱中毒时，分别在肾上腺素或钾刺激下，收缩反应性增加或降低。在肾上腺素和钾刺激的心脏中，酸中毒或碱中毒时维拉帕米作为钙拮抗剂的效力均增加。总之，酸中毒或碱中毒抑制心脏的钾刺激收缩，并增强维拉帕米对钾和肾上腺素介导的收缩的作用。酸中毒抑制而碱中毒增强肾上腺素刺激的收缩。
