Bowers R E, McKeen C R, Park B E, Brigham K L
Am Rev Respir Dis. 1979 Apr;119(4):637-41. doi: 10.1164/arrd.1979.119.4.637.
After reviewing the characteristics of neurogenic pulmonary edema, Theodore and Robin suggested that it was probably due to rupture of lung vessels by marked but transitory pulmonary hypertension. In this study, we have determined the effects of increased intracranial pressure in a sheep model in which we could measure the flow rate and protein content of lung lymph, and thus detect changes in pulmonary vascular permeability. We found that increasing intracranial pressure to amounts near systemic arterial pressure produced a 3-fold increase in the flow of protein-rich lymph, which indicates increased lung vascular permeability. The high permeability often developed, and always persisted, without extraordinary increases in pulmonary vascular pressure. We conclude that increased lung vascular permeability may follow intracranial hypertension and that extreme pulmonary hypertension is not a prerequisite. Our data do not permit us to exclude barotrauma to exchanging vessels as a cause of capillary damage, but do suggest that other factors, perhaps local release of permeability mediators, may be involved.
在回顾了神经源性肺水肿的特征后，西奥多和罗宾认为，它可能是由于显著但短暂的肺动脉高压导致肺血管破裂所致。在本研究中，我们在绵羊模型中测定了颅内压升高的影响，在此模型中我们可以测量肺淋巴的流速和蛋白质含量，从而检测肺血管通透性的变化。我们发现，将颅内压升高至接近体动脉压的水平会使富含蛋白质的淋巴流量增加3倍，这表明肺血管通透性增加。高通透性常常出现且始终存在，而肺动脉压并未异常升高。我们得出结论，颅内高压可能会导致肺血管通透性增加，而极端的肺动脉高压并非必要条件。我们的数据不允许我们排除交换血管的气压伤作为毛细血管损伤的原因，但确实表明可能涉及其他因素，也许是通透性介质的局部释放。
