Miller W C, Simi W W, Rice D L
Circ Res. 1978 Oct;43(4):598-600. doi: 10.1161/01.res.43.4.598.
Systemic venous hypertension (SVH) is a frequent finding in pulmonary edema. To study the possible contributory or even causal role of SVH in pulmonary edema, a dog model was developed in which balloon catheters were placed in the left and right atria. Inflation of the left atrial balloon produced a tendency to pulmonary edema by causing pulmonary venous hypertension (PVH) (pulmonary artery wedge pressure of 20 mmHg). Inflation of the right atrial balloon produced SVH (central venous pressure of 15 mm Hg). After 2 hours, dogs with SVH with or without PVH demonstrated a greater amount of lung fluid accumulation (P less than 0.01) compared to controls or PVH alone. There was no significant difference in lung water in SVH dogs with or without PVH. Pulmonary blood flow was not significantly different between the experimental groups, each of which was less than control. Impairment of pulmonary lymphatic flow is one possible mechanism producing the worsening edema; however, bronchial venous hypertension or neurogenic reflexes cannot be excluded. We conclude that the contribution of systemic venous hypertension to the development of pulmonary edema may have therapeutic implications.
体循环静脉高压（SVH）是肺水肿中常见的表现。为了研究SVH在肺水肿中可能的促成甚至因果作用，建立了一种犬模型，在该模型中，将球囊导管置于左心房和右心房。左心房球囊充气通过引起肺静脉高压（PVH）（肺动脉楔压为20 mmHg）导致肺水肿倾向。右心房球囊充气产生SVH（中心静脉压为15 mmHg）。2小时后，与对照组或单纯PVH组相比，伴有或不伴有PVH的SVH犬肺内液体蓄积量更多（P<0.01）。伴有或不伴有PVH的SVH犬肺水含量无显著差异。各实验组的肺血流量均低于对照组，但差异无统计学意义。肺淋巴引流受损是导致水肿加重的一种可能机制；然而，不能排除支气管静脉高压或神经反射的作用。我们得出结论，体循环静脉高压对肺水肿发展的作用可能具有治疗意义。
