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作 者:屈正[1] 孙衍庆[1] 董培青[1] 任发成[1]
机构地区:[1]首都医科大学附属北京安贞医院心外科,100029
出 处:《心肺血管病杂志》1997年第3期231-233,共3页Journal of Cardiovascular and Pulmonary Diseases
摘 要:对6只犬建立单侧(右)肺通气+阻断降主动脉+左心转流模型。分为正常左房压转流组(对照)和左心转流期间短暂左房压增高组(实验)各3只。结果示实验组出现以美陷侧肺明显的含水量增多,肺泡腔内不同程度出血,上皮细胞变性、线粒体肿胀等形态学改变,以及肺组织血管紧张素转换酶活性减低。认为肺美陷时肺泡压减低为零,肺血管壁周围的对抗力被削弱,肺血管跨壁压增大,加之美陷侧肺组织因缺氧而耐受性差,当左房压升高时,易发生肺水肿和肺出血的病理改变。In 6 canine models under left heart bypass (LHB) and one lung ventilation performng for 120minutes, the changes in angiotension converting enzyme (ACE) activity and morphology of the lung tissues were investigated. The left atrial pressure was controlled less than 1. 6kPa in 3 cases (group A) and elevated to 2. 80~3. 60kPa for 20 min utes during LHB in another 3 cases (group B). The results showed that there were no clear pathological or ultrasturctural changes observed in either ventilated or collapsed lung in group A. But in group B, pulmonary congestion, interstitial edema and intrapulmonary hemorrhage were mere obvious in the collapsed lung that theventilated lung. ACE activity of collapsed lung decreased significanly in group B than in group A. The injury of collapsed lung resulted by high left atrial pressure minght be associated with reduction of counteration to alveoli vascularwall due to the pulmonary atelectasis and hypoxia.
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