Lung injury edema in dogs. Influence of sympathetic ablation.
Open Access
- 1 December 1983
- journal article
- research article
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 72 (6) , 1977-1986
- https://doi.org/10.1172/jci111162
Abstract
Increased vascular permeability characterizes lung injury pulmonary edema and renders fluid balance in the injured lung especially sensitive to changes in hydrostatic pressure. Pulmonary edema is often associated with increased sympathetic nervous system activity which can lead to pulmonary venoconstriction. This postcapillary venoconstriction could raise microvascular pressure and might therefore increase edema in the injured lung. We produced lung injury edema in dogs with oleic acid and directly measured small (less than 2 mm) pulmonary vein pressure. We found that the small pulmonary vein pressure was increased from 9.8 +/- 0.5 mmHg to 12.6 +/- 0.5 mmHg (n = 10) by oleic acid injury edema. The increase was not due to a rise in left atrial pressure since the small pulmonary vein-left atrial pressure gradient also increased. To test if this increase in the postcapillary pressure gradient was sympathetically mediated, we either unilaterally ablated the stellate ganglion or produced unilateral alpha adrenergic blockade with phenoxybenzamine before giving oleic acid. Both of these "antisympathetic" interventions prevented the increase in pulmonary vein pressure caused by oleic acid edema in the protected lung but not in the intact contralateral lung. These interventions produced a 30 +/- 6.8% reduction in the amount of edema caused by oleic acid. Restoring the increase in small vein pressure by inflating a balloon in the left atrium of dogs with bilateral stellate ganglion ablations abolished the reduction in edema produced by antisympathetic treatment. However, the decrease in edema was not significantly correlated with the reduction in pulmonary vein pressure. Thus, the mechanism of the effects of these antisympathetic interventions remains unclear. We conclude that lung injury edema causes sympathetically mediated pulmonary venoconstriction and that antisympathetic interventions significantly reduce lung injury edema and microvascular pressure.This publication has 40 references indexed in Scilit:
- Treatment of Acute Low Pressure Pulmonary Edema in DogsJournal of Clinical Investigation, 1981
- Effect of furosemide in canine low-pressure pulmonary edema.Journal of Clinical Investigation, 1979
- Effects of Prostaglandin Cyclic Endoperoxides on the Lung Circulation of Unanesthetized SheepJournal of Clinical Investigation, 1979
- Influence of sympathetic stimulation and vasoactive substances on the canine pulmonary veins.Journal of Clinical Investigation, 1975
- Increased Sheep Lung Vascular Permeability Caused by Pseudomonas BacteremiaJournal of Clinical Investigation, 1974
- Urinary Catecholamine Excretion in Myocardial InfarctionCirculation, 1969
- Pressure Changes in the Dog Lung Secondary to Hemorrhagic ShockAnnals of Surgery, 1969
- Respiratory and hemodynamic changes after injection of free fatty acidsJournal of Surgical Research, 1968
- Modification by Beta-Adrenergic Blockade of the Circulatory Responses to Acute Hypoxia in Man*Journal of Clinical Investigation, 1967
- Neurohemodynamics of Pulmonary EdemaCirculation, 1952