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首页> 外文期刊>Life sciences >Effect of thymol on calcium handling in mammalian ventricular myocardium
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Effect of thymol on calcium handling in mammalian ventricular myocardium

机译：百里酚对哺乳动物心室钙离子处理的影响

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Concentration-dependent effects of thymol on calcium handling were studied in canine and guinea pig cardiac preparations (Langendorff-perfused guinea pig hearts, canine ventricular trabeculae, canine sarcoplasmic reticular vesicles and single ryanodine receptors). Thymol induced a concentration-dependent negative inotropic action in both canine and guinea pig preparations (EC50=297+/-12 muM in dog). However, low concentrations of thymol reduced intracellular calcium transients in guinea pig hearts without decreasing contractility. At higher concentrations both calcium transients and contractions were suppressed. In canine sarcoplasmic reticular vesicles thymol induced rapid release of calcium (V-max=0.47+/-0.04 nmol s(-1), EC50=258+/-21 muM, Hill coefficient=3.0+/-0.54), and decreased the activity of the calcium pump (EC50=253+/-4.7 muM, Hill coefficient=1.62+/-0.05). Due to the less sharp concentration-dependence of the ATPase inhibition, this effect was significant from 50 muM, whereas the thymol-induced calcium release only from 100 muM. In single ryanodine receptors incorporated into artificial lipid bilayer thymol induced long lasting openings, having mean open times increased with 3 orders of magnitude, however, the specific conductance of the channel remained unaltered. This effect of thymol was not voltage-dependent and failed to prevent the binding of ryanodine. In conclusion, the negative inotropic action of thymol can be explained by reduction in calcium content of the sarcoplasmic reticulum due to the combination of the thymol-induced calcium release and inhibition of the calcium pump. The calcium-sensitizer effect, observed at lower thymol concentrations, indicates that thymol is likely to interact with the contractile machinery also. (C) 2003 Elsevier Inc. All rights reserved. [References: 35]
机译：在犬和豚鼠心脏制剂（Langendorff灌注的豚鼠心脏，犬心室小梁细胞，犬肌浆网状囊泡和单个莱诺碱受体）中研究了百里酚对钙处理的浓度依赖性作用。百里酚在犬和豚鼠的制剂中都诱导了浓度依赖性的负性肌力作用（狗的EC50 = 297 +/- 12μM）。但是，低浓度的百里酚可降低豚鼠心脏内细胞内钙瞬变，而不会降低收缩力。在较高的浓度下，钙瞬变和收缩均被抑制。在犬肌质网状囊泡中，百里酚诱导钙的快速释放（V-max = 0.47 +/- 0.04nmol s（-1），EC50 = 258 +/-21μM，Hill系数= 3.0 +/- 0.54），并降低了钙泵的活性（EC50 = 253 +/- 4.7μM，希尔系数= 1.62 +/- 0.05）。由于ATPase抑制作用的浓度依赖性较弱，因此从50μM起这种作用是显着的，而百里酚诱导的钙仅从100μM起释放。在掺入人工脂质双层百里酚的单个瑞丹碱受体中，诱导了长效的开放，其平均开放时间增加了3个数量级，但是，通道的比电导保持不变。百里香酚的这种作用不是电压依赖性的，并且不能阻止ryanodine的结合。总之，百里香酚的负性肌力作用可以解释为由于百里香酚诱导的钙释放和钙泵抑制的结合而导致的肌浆网钙含量降低。在较低的百里酚浓度下观察到的钙敏化作用表明百里酚也可能与收缩机制相互作用。 （C）2003 Elsevier Inc.保留所有权利。 [参考：35]

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