Olivoto R R, Damiani C E N, Kassouf Silva I, Lofrano-Alves M S, Oliveira M A, Fogaça R T H
Departamento de Fisiologia, Universidade Federal do Paraná, Curitiba, PR, Brasil.
Braz J Med Biol Res. 2014 Apr;47(4):328-33. doi: 10.1590/1414-431x20143472. Epub 2014 Mar 21.
In cardiac and skeletal muscle, eugenol (μM range) blocks excitation-contraction coupling. In skeletal muscle, however, larger doses of eugenol (mM range) induce calcium release from the sarcoplasmic reticulum. The effects of eugenol are therefore dependent on its concentration. In this study, we evaluated the effects of eugenol on the contractility of isolated, quiescent atrial trabeculae from male Wistar rats (250-300 g; n=131) and measured atrial ATP content. Eugenol (1, 3, 5, 7, and 10 mM) increased resting tension in a dose-dependent manner. Ryanodine [100 µM; a specific ryanodine receptor (RyR) blocker] and procaine (30 mM; a nonspecific RyR blocker) did not block the increased resting tension induced by eugenol regardless of whether extracellular calcium was present. The myosin-specific inhibitor 2,3-butanedione monoxime (BDM), however, reversed the increase in resting tension induced by eugenol. In Triton-skinned atrial trabeculae, in which all membranes were solubilized, eugenol did not change resting tension, maximum force produced, or the force vs pCa relationship (pCa=-log [Ca2+]). Given that eugenol reduced ATP concentration, the increase in resting tension observed in this study may have resulted from cooperative activation of cardiac thin filaments by strongly attached cross-bridges (rigor state).
在心肌和骨骼肌中，丁香酚（微摩尔范围）可阻断兴奋 - 收缩偶联。然而，在骨骼肌中，较大剂量的丁香酚（毫摩尔范围）可诱导肌浆网释放钙。因此，丁香酚的作用取决于其浓度。在本研究中，我们评估了丁香酚对雄性Wistar大鼠（250 - 300克；n = 131）分离的静态心房小梁收缩性的影响，并测量了心房ATP含量。丁香酚（1、3、5、7和10毫摩尔）以剂量依赖性方式增加静息张力。无论细胞外钙是否存在，ryanodine [100 μM；一种特异性ryanodine受体（RyR）阻滞剂]和普鲁卡因（30毫摩尔；一种非特异性RyR阻滞剂）均不能阻断丁香酚诱导的静息张力增加。然而，肌球蛋白特异性抑制剂2,3 - 丁二酮单肟（BDM）可逆转丁香酚诱导的静息张力增加。在所有膜均被溶解的Triton处理的心房小梁中，丁香酚并未改变静息张力、产生的最大力或力与pCa的关系（pCa = -log [Ca2+]）。鉴于丁香酚降低了ATP浓度，本研究中观察到的静息张力增加可能是由于强附着的横桥（强直状态）对心脏细肌丝的协同激活所致。
