ACh诱导的脐带血管收缩效应及其机制研究
发布时间:2019-01-16 04:32
【摘要】:[目的]研究毒蕈碱受体激动剂乙酰胆碱(ACh, acetylcholine)对正常人脐带血管的舒缩功能的影响及其相应机制并与其对大鼠和羊血管舒缩功能的作用进行比较研究。 [方法](1)临床收集正常足月新生儿脐带;(2)收集孕21天胎鼠脐带,分别分离活性离体动静脉脐带血管;(3)收集正常成年雄性大鼠胸主动脉、肠系膜动脉,孕晚期胎羊颈动脉,肠系膜动脉和股动脉。分别将分离后的血管剪成3-5mm长度的血管环,置于5ml Krebs37℃恒温水浴槽内,进行大血管和微血管功能实验测定ACh对血管张力的影响。同时,本实验采用RT-PCR技术检测了人脐血管中M受体亚型的分布。 【结果】ACh、卡巴胆碱cabarchol (10-11-10-3mol/L)对脐带血管表现为较强的剂量依赖性收缩作用,而且在低浓度时也并未观察到其对脐带血管的舒张作用。ACh、cabarchol对脐带血管的收缩作用可被阿托品(10-6mo1/L)完全阻断,在基础血管张力下,尼古丁(nicotine,10-11-10"3mol/L)对脐带血管张力没有明显影响,但通过抑制血管内皮NO合成可使脐带血管对ACh的收缩反应增强,而PKC通路阻断剂和L-Ca通道阻断剂则可降低ACh的收缩反应。RT-PCR结果显示,除M1受体在脐带血管中表达量较少以外,M2-M5的rn-RNA表达水平基本相似。 【结论】ACh对正常人脐带血管表现为较强的收缩作用而不是舒张作用,实验表明ACh对脐带血管的收缩作用与M受体下游的L-Ca、PKC通路有关。
[Abstract]:[objective] to study the effects of muscarinic receptor agonist acetylcholine (ACh, acetylcholine) on the systolic and diastolic function of normal umbilical cord blood vessels in rats and sheep. [methods] (1) normal umbilical cord of full-term newborns was collected clinically, (2) umbilical cord of 21 day pregnant rats was collected, and active isolated umbilical cord blood vessels were isolated. (3) the thoracic aorta, mesenteric artery, fetal goat carotid artery, mesenteric artery and femoral artery were collected from normal adult male rats. The isolated blood vessels were cut into 3-5mm long vascular rings and placed in the 5ml Krebs37 鈩,
本文编号:2409465
[Abstract]:[objective] to study the effects of muscarinic receptor agonist acetylcholine (ACh, acetylcholine) on the systolic and diastolic function of normal umbilical cord blood vessels in rats and sheep. [methods] (1) normal umbilical cord of full-term newborns was collected clinically, (2) umbilical cord of 21 day pregnant rats was collected, and active isolated umbilical cord blood vessels were isolated. (3) the thoracic aorta, mesenteric artery, fetal goat carotid artery, mesenteric artery and femoral artery were collected from normal adult male rats. The isolated blood vessels were cut into 3-5mm long vascular rings and placed in the 5ml Krebs37 鈩,
本文编号:2409465
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