Firth J D, Raine A E, Ledingham J G
Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford.
Lancet. 1988 May 7;1(8593):1033-5. doi: 10.1016/s0140-6736(88)91851-x.
Contemporary theories of oedema formation are often based on the idea that "effective" blood volume is reduced, and that sodium retention and oedema are a result of the kidney responding, as in haemorrhage, to a perception by receptors in the circulation that blood volume is inadequate. This idea has enhanced understanding of the pathophysiology of such conditions as cardiac failure and cirrhosis, but has obscured the fact that blood volume is almost always increased in oedematous states. Evidence is presented that an increase in renal venous pressure can cause sodium retention by a direct action on the kidney: a rise in venous pressure could thereby initiate a vicious circle by causing sodium retention, expansion of plasma volume, and further increase in venous pressure. This sequence of events may be crucial in the pathophysiology of cor pulmonale, and an exacerbating factor in other oedematous states.
“有效”血容量减少，钠潴留和水肿是肾脏的反应结果，就像在出血时一样，循环中的感受器察觉到血容量不足，肾脏做出响应。这一观点增进了对诸如心力衰竭和肝硬化等病症病理生理学的理解，但却掩盖了水肿状态下血容量几乎总是增加这一事实。有证据表明，肾静脉压力升高可通过对肾脏的直接作用导致钠潴留：静脉压力升高进而可能通过引起钠潴留、血浆量扩张以及静脉压力进一步升高而引发恶性循环。这一系列事件在肺心病的病理生理学中可能至关重要，并且是其他水肿状态下的一个加重因素。
