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心之络病“孙络绌急”模型大鼠血浆ET-1、TXB_2、6-keto-PGF_(1α)及AngⅡ的动态变化研究 被引量:2

Study of dynamic change on ET-1,TXB_2,6-keto-PGF_(1α) and AngⅡ in rats model of ‘constriction of tertiary collaterals' of collateral disease in heart
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摘要 目的探讨心之络病"孙络绌急"模型大鼠血浆微血管舒缩因子内皮素-1(ET-1)、血栓素B2(TXB2)、6-酮-前列腺素F1α(6-keto-PGF1α)、血管紧张素Ⅱ(AngⅡ)的变化规律。方法将30只雄性SD大鼠随机分为正常组、造模5 min组、造模10min组、造模20 min组、造模30 min组。采用股静脉注射垂体后叶素(Pit)方法制备心之络病"孙络绌急"模型,正常组注射等量生理盐水。放射免疫法检测血浆ET-1、TXB2、6-keto-PGF1α、AngⅡ水平。结果与正常组比较",孙络绌急"各模型组血浆ET-1水平均显著升高(P<0.01),且于5 min时达到高峰。血浆TXB2在造模5 min组显著升高(P<0.01),而在30 min组其水平明显下降(P<0.05)。血浆6-keto-PGF1α水平在造模10 min后开始显著下降(P<0.05或P<0.01),并在30 min时达到低峰(P<0.01)。TXB2/6-keto-PGF1α在造模后5 min至20 min显著升高(P<0.01或P<0.05),并于5 min时达到高峰,而在30 min时恢复至正常水平。AngⅡ水平在造模后5 min内并无显著变化,而在造模后10 min开始其水平显著升高(P<0.05),并呈递增趋势,且于30min时达到高峰(P<0.01)。结论微血管舒缩因子表达异常、动态平衡破坏提示微血管内皮细胞功能紊乱在"孙络绌急"急性期病理变化过程中发挥着重要作用。血浆AngⅡ显著升高亦提示肾素-血管紧张素系统(RAS系统)在"孙络绌急"早期即可被激活,从而参与并加剧缺血心肌的进一步损害。 Objective To explore the change rule of endothelin-1 (ET-1), thromboxane B2 (TXB2), 6-keto-prostaglandinl st (6-keto-PGF1α) and angiotensin Ⅱ (Ang Ⅱ ) in rats model of ' constriction of tertiary collaterals' of collateral disease in heart. Methods Thirty male SD rats were randomly divided into a normal group, a 5 min-model group, a 10 rain-model group, a 20 min-model group and a 30 min-model group. The model of 'constriction of tertiary collaterals' of collateral disease in heart was established by injection of pituitrin (Pit) into femoral vein, while the normal group was injected with the same volume of normal saline. The level of ET-1, TXB2, 6-keto-PGF1α and Ang Ⅱ was detected with radioimmunoassay. Results Compared with the normal group, the level of ET-1 in all the model groups was increased obviously (P 〈0.01), and reached the peak at 5 min. The level of TXBz was apparently increased in the 5 rain-model group (P 〈0.01), while decreased obviously in the 30 min-model group (P 〈0.05). The level of 6-keto-PGF1α began to decrease significantly 10 rain after modeling (P 〈0.05 or P 〈0.01), and reached the bottom at 30 min (P 〈0.01). TXB2/6-keto-PGF1α was significantly increased from 5 min to 20 min after modeling (P 〈0.01 or P 〈0.05), and reached peak at 5 min while returned to normal level at 30 min. The level of Ang IT had insignificant difference within 5 min after modeling, while obviously increased from 10 min after modeling (P 〈0.05) with an ascending trend and peaked at 30 min (P 〈0.01). Conclusion The abnormal expression and destruction of dynamic balance for microvascular vasomotor factor indicates that dysfunction of microvascular endothelial cells exert an important effect during the process of pathological change in acute phase of ' constriction of tertiary collaterals'. The significant increase of Ang Ⅱ indicates renin angiotensin system (RAS) could be activated at the early stage of ' constriction of
出处 《北京中医药》 2013年第10期789-792,共4页 Beijing Journal of Traditional Chinese Medicine
基金 国家重点基础研究发展计划(973计划)资助项目(2012CB518601)
关键词 孙络绌急 内皮素-1 血栓素B2 6-酮-前列腺素F1Α 血管紧张素Ⅱ 大鼠 constriction of tertiary collaterals endothelin-1 thromboxane B2 6-keto-prostaglandin1α angiotensin Ⅱ rat
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