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作 者:付作林[1] 冯义柏[1] 史春志[1] 谷翔[1] 黎明[1] 张新平[1]
机构地区:[1]华中科技大学同济医学院附属协和医院心内科,邮政编码武汉430022
出 处:《微循环学杂志》2005年第4期14-16,共3页Chinese Journal of Microcirculation
摘 要:目的探讨急性心肌冬眠时心脏交感神经功能的变化。方法采用大鼠离体心脏急性心肌冬眠模型,测定急性心肌冬眠时电场刺激引起心脏去甲肾上腺素(NA)的释放,并观察复灌后的酪胺反应。结果电场刺激引起的NA的溢出在心肌冬眠组、对照组和复灌组分别为3.24±1.27、76.89±27.65和80.30±23.86pmol/g.min,复灌30min时,酪胺引起NA的释放和心率明显增加,而在去甲丙咪嗪存在的情况下,酪胺的这种作用消失。结论本研究表明离体鼠心急性冬眠时,电场刺激引起的心脏NA释放明显减少,复灌后这种释放恢复至对照组水平,心脏对酪胺的NA反应证明心脏交感神经末梢功能的完整性。提示在急性心肌冬眠过程中,心脏的交感神经功能可能也经历了一个类似冬眠即神经冬眠的过程,再灌注后交感神经的功能可部分或全部恢复。Objective: To investigate the function of cardiac sympathetic nerve during acute myocardial hibernation.Method: Hearts were extracted from rats and set up as acute myocardial hibernation model. They were perfused with modified Krebs-Henseleit buffer at controlled perfusion pressure. Electrical field stimulation-evoked noradrenaline release was determined during the control, acute hibernation and reperfusion group in presence of desipramine.Noradrenaline and heart rates responses on tyramine were assessed after reperfusion.Results: The stimulation-evoked noradrenaline release was significantly smaller during hibernation group, but it recovered to control group level after 30 minutes of reperfusion. Tyramine induced significantly increases in noradrenaline release and heart rates after 30 minutes of reperfusion, but this increases were nonsignificantly in presence of desipramine.Conclusion: These studies indicate that stimulation-evoked myocardial noradrenaline release decrease significantly during acute hibernation in the isolated rat heart, but it recovers to control group level after 30 minutes of reperfusion.The preserved noradrenaline response to tyramine indicates functional integrity of sympathetic nerve terminals, suggesting that the function of cardiac sympathetic nerve may also undergo a hibernation or nerve hibernation during acute myocardial hibernation.
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