Effects of prostaglandin E1 and hydralazine on the longitudinal distribution of pulmonary vascular resistance during vasoconstrictor pulmonary hypertension in sheep

Pulmonary capillary pressure (Ppc) is dependent upon left atrial pressure, pulmonary venous resistance, and cardiac output. The effects of pulmonary vasodilators on Ppc will therefore depend upon any alterations in the longitudinal distribution of pulmonary vascular resistance (precapillary [arteria...

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Bibliographic Details
Published in:Anesthesiology (Philadelphia) 1992, Vol.76 (1), p.106-112
Main Authors: PEARL, R. G, SIEGEL, L. C
Format: Article
Language:English
Subjects:
Alprostadil - pharmacology
Animals
Biological and medical sciences
Cardiovascular system
Hydralazine - pharmacology
Hypertension, Pulmonary - chemically induced
Hypertension, Pulmonary - physiopathology
Lung - blood supply
Male
Medical sciences
Pharmacology. Drug treatments
Prostaglandin Endoperoxides, Synthetic
Random Allocation
Sheep
Vascular Resistance - drug effects
Vasodilation
Vasodilator agents. Cerebral vasodilators
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Summary:Pulmonary capillary pressure (Ppc) is dependent upon left atrial pressure, pulmonary venous resistance, and cardiac output. The effects of pulmonary vasodilators on Ppc will therefore depend upon any alterations in the longitudinal distribution of pulmonary vascular resistance (precapillary [arterial] and postcapillary [venous] components). We therefore studied the effects of two pulmonary vasodilators (prostaglandin E1 and hydralazine) on Ppc and the longitudinal distribution of pulmonary vascular resistance. Pulmonary hypertension was produced in sheep by the continuous administration of the thromboxane A2-mimetic U46619. Ppc was measured by analysis of pulmonary artery occlusion pressure decay curves. U46619 increased Ppc by 9 mmHg and increased both the arterial and venous components of pulmonary vascular resistance. Subsequent administration of prostaglandin E1 decreased Ppc by 5 mmHg and decreased both the arterial and venous components of pulmonary vascular resistance (by 50 and 69% respectively). Hydralazine produced smaller decreases in the arterial and venous components of pulmonary vascular resistance (by 35 and 49% respectively) and did not significantly reduce Ppc. We conclude that prostaglandin E1 but not hydralazine is effective in decreasing Ppc in this experimental model of pulmonary hypertension.
ISSN:0003-3022
1528-1175
DOI:10.1097/00000542-199201000-00016