Pathogenesis of hemodynamic pulmonary edema
Belov, I.V.
Patologicheskaia Fiziologiia i Eksperimental'naia Terapiia 1982(3): 16-21
1982
ISSN/ISBN: 0031-2991 PMID: 7122134 Document Number: 192449
Circulation dynamics and the state of the pulmonary tissue during the development of hemodynamic pulmonary edema as well as occulsion of the inferior vena cava (VCI) at the peak of edema were studied experimentally in 32 dogs. Pulmonary edema was induced by continuous noradrenalin infusion after preliminary infusion of isotonic NaCl solution and ligation of the pulmonary vein. The development of pulmonary edema was associated with a sharp increase of hydrostatic pressure in pulmonary circulation in intensified blood filling of the lungs. Intracaval VCI occlusion was conducted distal and proximal to the renal veins for 1 h. In response to the occlusion, venous return to the heart decreased and hydrostatic pressure in the pulmonary vessels reduced, causing pulmonry edema to diminish. The role of venous return in the pathogenesis of pulmonary edema is demonstrated. A scheme of hemodynamic pulmonary edema development mechanisms is suggested.