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机构地区:[1]北京大学人民医院心脏外科,100044 [2]北京大学医学部基础药理教研室
出 处:《中华胸心血管外科杂志》2011年第1期39-42,共4页Chinese Journal of Thoracic and Cardiovascular Surgery
摘 要:目的 证实观察犬体外循环模型中肺脏损伤的存在,并试图探讨体外循环下肺损伤肺水肿与水通道aquaporin-1表达之间的联系.方法 杂种犬8只,建立浅低温体外循环模型,停跳90 min,复跳6 h,分别比较其血流动力学指标变化、血浆总渗透压、肺干重/湿重比例以及普通病理与超微病理的各自特点,利用反转录聚合酶链反应半定量测定aquaporin-1的mRNA表达.结果 以体外循环前指标作自身对照,行单因素方差分析和Q检验.体外循环缺血再灌注后,血液动力学相对平稳,肺干重/湿重比例随体外循环时间延长逐渐下降(P<0.001),同时血浆总渗透压有上升趋势(P<0.01).病理证实复跳后3~6 h可以见到明显的肺间质水肿和血管内皮细胞损伤.肺脏内AQP1的mRNA表达随体外循环时间延长而下降,在复跳后3 h和6 h分别降低至术前水平的78.4%和55.5%(P<0.01).结论 体外循环造成的肺脏损伤与水肿在心脏复跳后3~6 h表现严重,同期肺内aquaporin-1的mRNA表达下降,提示肺脏毛细血管内皮损伤.Objective To testify the lung injury induced by cardiopulmonary bypass(CPB) in canine model and observe the influence of CPB on the aquaporin-1 ( AQP1 ) mRNA expression in canine lung. Methods 8 mongrel dogs were used to perform the cardiopulmonary bypass. The hearts arrested for 90 minutes with mild hypothermia and rebeated for 6 hours. The hemodynamics, the ratio of lung dry weight and wet weight, the plasmic osmotic pressure, and the characteristics of light and fine structure were analyzed. The retro-transcription polyase chain reaction ( RT-PCR ) was used to measure the expression of AQP1 mRNA during the CPB. Results The hemodynamic data were stable in different time point during the CPB (P 〉0.05 ). The ratio of lung dry weight and wet weight was getting lower ( P 〈0.001) and the plasmic osmotic pressure was getting higher due to the prolongation of the CPB time and reperfusion time ( P 〈0.01). The light and electron microscopy showed the prominent aggregation of the white blood cell, severe interstitial edema and mild tear of respiratory membrane after 3 hour and 6-hour rebeat. AQP1 mRNA expression in lung was downregulated, 78.4% after 3-hour reperfusion and 55.5% after 6-hour reperfusion respectively, comparing to the level before CPB. Conclusion We recognize that the lung injury and lung edema were severe following 3-hour and 6-hour rebeat in CPB and hypothesize that the down-regulation of lung AQP1 mRNA expression may be a sign of pulmonary interstitial capillary injury induced by CPB.
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