犬重型脑损伤后神经源性肺水肿的血流动力学发生机制

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。方法：采用自由落体致犬重型脑损伤模型，24h动态监测血肾上腺素（E）、去甲肾上腺素（NE），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。结果：犬脑损伤后30min血NE、E显著增高，此后3，8，12，24h血NE、E始终维持于高水平，体循环血管阻力指数（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）、左室每搏做功指数（LVSWI）、右室每搏做功指数（RVSWI）进行性下降， 肺动脉楔压（PAWP）上升，动脉血氧分压（PaO2)下降，至24hCI、PaO2降至最低，PAWP达最高值；脑损伤组肺含水量和伊文思蓝透入量显著高于对照组；脑损伤组24hCI与PaO2 呈显著正相关、与肺含水量呈显著负相关。结论：重型脑损伤后血NE、E升高引起心脏前、后负荷持续增加，最终导致心功能失代偿引发急性心功能受损；急性左心功能受损可直接导致或加重神经源性肺水肿。

Hemodynamic mechanism of neurogenic pulmonary edema following severe brain injury in dogs

Objective To study the hemodynamic mechanism of neurogenic pulmonary edema following severe brain injury in dogs.Methods The severe brain injury model of the dog was made by dropping weight. The changes of epinephrine (E) and noradrenerge (NE) in serum, hemodynamic parameters and PaO 2 were observed at six different time points in 24 hours after injury. The water and Evans blue contents of the lungs were measured and the pulmonary pathology was also examined. Results E and NE in serum rose dramatically 30 minutes after injury. At 3, 8, 12 and 24 hours, NE and E kept at a high level. Systemic vascular resistance index (SVRI), pulmonary vascular resistance index (PVRI) and central venous pressure (CVP) increased markedly, but cardiac index (CI), left ventricular stroke work index (LVSWI) and right ventricular stroke work index (RVSWI) decreased significantly and gradually. Pulmonary arterial wedge pressure (PAWP) increased dramatically and PaO 2 fell down substantially. At the 24th hour, CI and PaO 2 reached the lowest point but PAWP the peak. Statistical analysis showed that the water and Evans blue contents of the lungs in brain injury group were significantly more than that in control group. There was a significantly positive correlation between CI and PaO 2, and significantly negative correlation between CI and the water content of the lungs. Conclusions Both systemic and pulmonary vasoconstriction by sudden massive catecholamine released from severe brain injury create a tremendous increase in ventricular preload and afterload, which causes acute ventricular dysfunction. Acute left ventricular dysfunction can directly create or aggravate NPE.