Simon R P, Bayne L L
Ann Neurol. 1984 Feb;15(2):188-94. doi: 10.1002/ana.410150213.
The role of intracranial hypertension in the genesis of neurogenic pulmonary edema was studied in 25 sheep; cardiopulmonary hemodynamics (aortic, pulmonary arterial, and left atrial pressures and cardiac output) and fluid and protein movement across the pulmonary capillary bed (efferent pulmonary lymph flow and lymph/plasma protein ratio) were monitored. Only when intracranial pressure was raised to equal the baseline mean systemic pressure (75 to 120 Torr) did we observe the expected Cushing response of increased aortic pressure, or any alteration in pulmonary hemodynamics or fluid movement. When pulmonary changes did occur, they included an increase in pulmonary arterial pressure of between 5 and 15 Torr without any notable rise in left atrial pressure, and a sustained doubling of the pulmonary lymph flow with no dilution of the lymph/plasma protein ratio. In 3 additional animals cerebral ischemia alone produced an elevation in systemic pressure (74 Torr over baseline) without change in pulmonary arterial pressure, left atrial pressure, or pulmonary lymph flow. Thus, intracranial hypertension and ischemia both affect systemic pressure, but only the elevated intracranial pressure is followed by changes in the pulmonary circuit. We suggest that these changes in pulmonary vascular pressure, independent of changes in left atrial pressure, produce increased pulmonary transcapillary fluid flux that may result in neurogenic pulmonary edema.
在25只绵羊身上研究了颅内高压在神经源性肺水肿发生过程中的作用；监测了心肺血流动力学（主动脉压、肺动脉压、左心房压和心输出量）以及液体和蛋白质通过肺毛细血管床的移动情况（肺传出淋巴流量和淋巴/血浆蛋白比率）。只有当颅内压升高到等于基线平均体循环压力（75至120托）时，我们才观察到预期的主动脉压升高的库欣反应，或肺血流动力学或液体移动的任何改变。当肺部确实发生变化时，包括肺动脉压升高5至15托，而左心房压没有明显升高，以及肺淋巴流量持续增加一倍，而淋巴/血浆蛋白比率没有稀释。在另外3只动物中，单独的脑缺血导致体循环压力升高（比基线高74托），而肺动脉压、左心房压或肺淋巴流量没有变化。因此，颅内高压和缺血都会影响体循环压力，但只有颅内压升高会随后导致肺循环的变化。我们认为，这些肺血管压力的变化，独立于左心房压力的变化，会导致肺毛细血管跨膜液体通量增加，这可能会导致神经源性肺水肿。
