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机构地区:[1]成都医学院第一附属医院麻醉科,成都610500
出 处:《成都医学院学报》2015年第2期165-169,共5页Journal of Chengdu Medical College
摘 要:目的观察机械通气对糖尿病小鼠肾素-血管紧张素系统及肺微血管通透性的影响。方法选取SPF级C57/BL6小鼠32只,随机分为4组:对照组(C组)、糖尿病组(D组)、机械通气组(V组)和糖尿病机械通气组(DV组),每组8只。采用链脲佐菌素制作糖尿病动物模型。C组和D组气管切开后自主呼吸;V组和DV组使用0.125g氯唑沙宗进行呼吸阻断,之后接呼吸机行机械通气。观察肺组织结构改变,检测小鼠肺湿/干重比、髓过氧化物酶(MPO)活性和肺微血管通透性,检测Ang、AT1和ACE的mRNA表达水平及AngⅡ的含量。结果与C组比较,其余3组肺组织病理改变明显,肺微血管通透性显著增加(P〈0.05);肺湿/干重比、MPO活性、Ang、AT1和ACE的mRNA表达水平及AngⅡ含量均显著增高(P〈0.05);与V组比较,D组和DV组上述指标均显著增高(P〈0.05);与D组比较,DV组上述指标明显提高(P〈0.05)。结论糖尿病小鼠机械通气后,肺微血管通透性增加,肾素-血管紧张素系统被激活,而肾素-血管紧张素系统的激活可能是其致病机制之一。Objective To investigate the effect of mechanical ventilation on the expression changes of renin- angiotensin system and lung microvascular endothelial cell permeability in diabetes mice. Methods Thirty two SPF grade C57/BL6 mice were used and streptozocin was used to produce diabetic mice. Mice were anesthesized with 1% pentobarhital intraperitoneal injection of 100 mg/kg, followed by tracheotomy in fixed endotracheal tube and were divided into the control group (C group), diabetic group (D group) and spontaneous breathing, mechanical ventilation group (V group) and diabetic mechanical ventilation group (DV group) received 0. 125 g chlorzoxazone respiratory blocking,and used the animal ventilator for mechanical ventilation for 4 hours, and mice were sacrificed to collect blood specimens. Detection of mouse lung wet to dry weight ratio, lung tissue structure change, myeloperoxidase activity, pulmonary microvascular permeability and the content of angiotensin Ang Ⅱ receptor, AT1, angiotensin converting enzyme (ACE) mRNA expression levels and Ang Ⅱ . Results Compared with group C, group V,D,and DV showed pathological changes with increased lung wet-dry ratios,MPO activities and increased mRNA expression of Ang Ⅱ , AT1, and ACE (P〈0. 05); compared with group V, Group D and DV had more increases (P〈0.05) ; compared with group D,group DV was significantly higher (P〈0.05). Conclusion Diabetic mice with mechanical ventilation made the renin-angiotensin system activated and pulmonary microvascular permeability increased. Renin-angiotensin system activation may be one of ways leading to the pathogenicity.
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