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[乙醇对不同静息张力下大鼠离体胸主动脉的舒张作用及其机制]

[Vasodilating effect and its mechanism of ethanol on isolated rat thoracic aorta at different resting tension].

作者信息

Ru Xiao-Chen, Qian Ling-Bo, Cui Jie, Qian Yun, Gao Qin, Xia Qiang

机构信息

Department of Physiology, Zhejiang University School of Medicine, Hangzhou 310058, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2008 Aug;24(3):269-73.

PMID:21141580
Abstract

AIM

To investigate the vasodilating effect and its mechanism of ethanol on isolated rat thoracic aorta at different resting tension.

METHODS

The tension of the isolated Sprague-Dawley rat thoracic aorta rings perfused with different concentrations of ethanol was measured using organ bath technique.

RESULTS

At different resting tension (1.0, 1.5, 2.0, 2.5, 3.0, 3.5 and 4.0 g), ethanol (0.1-7.0 per thousand) caused a concentration-dependent relaxation on endothelium-denuded aortic rings precontracted with KCl (6 x 10(-2)mol/L) or phenylephrine (PE, 10(-6) mol/L), and the vasodilating effect was the most potent when the aortic rings were at the resting tension of 3 g. Ethanol had much less vasodilating effect on endothelium-intact aortic rings. Ethanol at 3 per thousand (the maximum-effect concentration) inhibited the CaCl2 induced contraction and downward shifted concentration-response curve of endothelium-denuded aortic rings pre-contracted with KCI or PE at the resting tension of 3 g. Incubation of aorta with ruthenium red (10(-5) mol/L) or heparin (50 mg/L) decreased the vasodilating effect of ethanol (3.0 per thousand) on endothelium-denuded aorta precontracted with PE at the resting tension of 3 g.

CONCLUSION

Ethanol induces endothelium-independent relaxation on rat thoracic aorta, which is concerned with the resting tension. This effect of ethanol may be mediated by the inhibition of voltage-dependent and receptor-operated Ca2+ channels in the vascular smooth muscle cells. The inhibition of the ryanodine receptor and trisphosphate inositol (IP3) pathway may also contribute to this effect.

摘要

目的

研究乙醇在不同静息张力下对离体大鼠胸主动脉的舒张作用及其机制。

方法

采用器官浴技术,测量用不同浓度乙醇灌注的离体Sprague-Dawley大鼠胸主动脉环的张力。

结果

在不同静息张力(1.0、1.5、2.0、2.5、3.0、3.5和4.0 g)下,乙醇(0.1‰-7.0‰)可使预先用氯化钾(6×10⁻²mol/L)或去氧肾上腺素(PE,10⁻⁶mol/L)预收缩的去内皮主动脉环产生浓度依赖性舒张,且当主动脉环静息张力为3 g时,舒张作用最强。乙醇对完整内皮主动脉环的舒张作用小得多。在静息张力为3 g时,3‰(最大效应浓度)的乙醇可抑制氯化钙诱导的收缩,并使预先用氯化钾或去氧肾上腺素预收缩的去内皮主动脉环的浓度-反应曲线向下移位。用钌红(10⁻⁵mol/L)或肝素(50 mg/L)孵育主动脉可降低3‰乙醇对静息张力为3 g时预先用去氧肾上腺素预收缩的去内皮主动脉的舒张作用。

结论

乙醇可诱导大鼠胸主动脉产生不依赖内皮的舒张,这与静息张力有关。乙醇的这种作用可能是通过抑制血管平滑肌细胞中的电压依赖性和受体操纵性钙通道介导的。对兰尼碱受体和三磷酸肌醇(IP3)途径的抑制也可能有助于这种作用。

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