Ravens U, Link S, Gath J, Noble M I
Department of Pharmacology, University of Essen, Germany.
Pharmacol Toxicol. 1995 Jan;76(1):9-16. doi: 10.1111/j.1600-0773.1995.tb00095.x.
The effects of various inotropic interventions on post-rest potentiation and its decay were investigated in isolated cardiac muscle. The inotropic interventions studied were: reduced extracellular Na+ and elevated extracellular Ca2+ concentration; exposure to ouabain, monensin, isoprenaline, phenylephrine and cirazoline. Force of contraction (stimulation frequency 2 Hz) was measured isometrically in left atria and right ventricular strips of rat hearts. Maximum post-rest potentiation was reached after 10 sec. of rest and amounted to 245 +/- 26% of pre-rest control in ventricle and 192 +/- 15% in atria. Ca(2+)-recirculation fraction was calculated from the decay of post-rest potentiation after resumption of regular stimulation, it was 0.77 +/- 0.01 in 11 control ventricular strips. High concentrations of caffeine (3 mmol/l) completely abolished post-rest potentiation in both tissues. The development of post-rest potentiation was accelerated in the presence of most of the inotropic agents. However, with the exception of ouabain and only in atrial muscle, none of the inotropic interventions produced higher post-rest contraction amplitudes than during controls. In rat heart muscle, the inotropic interventions studied are not any more effective in augmenting force of contraction than prolonged stimulation intervals. This suggests that (1) the distribution of Ca2+ into the sarcoplasmic reticulum is at a maximum during post-rest potentiation; (2) modifications of signal transduction pathways cannot further increase post-rest potentiation; and therefore that (3) shifts in Ca2+ distribution act as a limiting factor.
在离体心肌中研究了各种变力干预对静息后增强及其衰减的影响。所研究的变力干预措施包括：降低细胞外Na⁺浓度和升高细胞外Ca²⁺浓度；暴露于哇巴因、莫能菌素、异丙肾上腺素、去氧肾上腺素和可乐定。在大鼠心脏的左心房和右心室条带上等长测量收缩力（刺激频率2Hz）。静息10秒后达到最大静息后增强，心室中达到静息前对照的245±26%，心房中为192±15%。根据恢复正常刺激后静息后增强的衰减计算Ca(2+)再循环分数，在11个对照心室条带中为0.77±0.01。高浓度咖啡因（3mmol/L）完全消除了两种组织中的静息后增强。在大多数变力药物存在的情况下，静息后增强的发展加速。然而，除了哇巴因且仅在心房肌中，没有一种变力干预措施产生的静息后收缩幅度高于对照期间。在大鼠心肌中，所研究的变力干预措施在增强收缩力方面并不比延长刺激间隔更有效。这表明：（1）在静息后增强期间，Ca²⁺向肌浆网的分布达到最大值；（2）信号转导途径的改变不能进一步增加静息后增强；因此（3）Ca²⁺分布的变化是一个限制因素。
