Haemodynamic changes in adrenaline-induced acute massive lung oedema.
During the production of adrenaline-induced acute massive lung oedema in the dog, plumonary arterial, pulmonary venous, systemic arterial, and bronchial arterial blood pressures all increase markedly. Pulmonary arterial and venous blood flows fall steeply after initial transient rises. Systemic arterial blood flow also declines, with or without an initial transient increase. The bronchial arterial blood flow shows an initial fall followed by a rise of late onset. The main determinant for the pathogenesis of adrenaline-induced lung oedema is apparently the enormously increased hydrostatic pressure in the pulmonary vascular bed.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001981:Bronchial Arteries; D002339:Carotid Arteries; D004285:Dogs; D055590:Electromagnetic Phenomena; D004837:Epinephrine; D005263:Femoral Artery; D011651:Pulmonary Artery; D011654:Pulmonary Edema / Q000139:chemically induced / Q000503:physiopathology*; D011667:Pulmonary Veins; D012039:Regional Blood Flow / Q000187:drug effects; D012212:Rheology; D014690:Venous Pressure / Q000187:drug effects
D004837:Epinephrine