犬重型脑损伤后神经源性肺水肿的实验研究

目的 探讨犬重型脑损伤后神经源性肺水肿（NPE）的血流动力学发生机制及多巴酚丁胺（Dobutamine)的治疗作用。方法 采用自由落体致犬重型脑损伤模型，24h动态监测血儿茶酚胺（CA）、血流动力学参数及血气变化，测定肺含水量及伊文思蓝透入量，观察肺脏病理改变，并用多巴酚丁胺进行实验治疗。结果 犬脑外伤后30min血CA显著增高，此后3h、8h、12h观察：血CA始终维持于高水平，体循环血管指数（SVRI）、肺循环血管阻力指数（PVRI）、中心静脉压（CVP）持续上升，心脏指数（CI）、左室每搏作功指数（LVSWI）、右室每搏作功指数（RVSWI）呈进行性下降，肺动脉楔压（PAWP）上升，血氧分压（PaO2)下降，至24h CI、PaO2降至最低，PAWP达最高值。统计分析显示：脑外伤组肺含水量和伊文思蓝透入量显著高于对照组。相关分析显示：脑外伤组24h时相CI与PaO2呈显著正相关、与肺含水量呈显著负相关。治疗组使用多巴酚丁胺后，CI趋于正常，PAWP明显下降，PaO2迅速好较。统计分析显示：治疗组肺含水量及伊文思蓝透入量显著低于脑外伤组。结论 1、重型脑损伤后血CA升高引起心脏前、后负荷持续增加，导致心功能失代偿引发急性心功能障碍。2、急性左心功能障碍可直接导致或加重神经源性肺水肿。3、多巴胺丁胺治疗有效。

Experimental Study on Neurogenic Pulmonary Edema Following Severe Brain Injury in Dogs

Objective To study the effects of hemodynamic changes in NPE following severe brain injury in dogs and the therapeutic effects with dobutamine.Methods The severe brain injury model of the dog was made by dropping weight. The changes of catecholamine in serum, hemodynamic parameter and PaO2 were observed at six differenttime points in 24 hours after injury. Water and Evans blue contents of the lungs were measured and pulmonary pathology was also examined.Results The catecholamine in serum rose dramatically at 30 min after injury. Observed at 3 hours, 8 hours, 12 hours and 24 hours time points, the catecholamine remained high level, SVRI, PVRI, CVP increased markedly, CI, LVSWI, RVSWI decreased significantly, PAWP increased dramatically and PaO2 fell down substantially. Statistical analysis showed that water and Evans blue contents of the lungs in brain injury group were more than those in controll group significantly. There was a significantly positive correlation between CI and PaO2,and significantly negative correlation between CI and water content of the lungs. The administration of dobutamine led to normalization of the CI and subsequent improvement in PAWP and PaO2. Statistical analysis showed that water and Evans blue contents of the lungs in treatment group were less than those in brain injury group significantly.Conclusions 1.Both systemic and pulmonary vasoconstriction by sudden massive catecholamine released from severe brain injury created a tremendous increase in ventricular preload and afterload, which caused acute ventricular dysfunction. 2.Acute left ventricular dysfunction was the primary cause of creating or aggravating NPE. 3.Dobutamine is effective.