Key result
Lactic acid-induced acidemia triggers fulminating pulmonary edema in dogs with LV overload, unlike vasoactive compounds.
Why the study?
The pathogenesis of pulmonary edema in left heart failure involves complex hydrostatic, osmotic, and permeability changes that require further elucidation.
Do hypoxemia, vasoactive compounds, or acidemia precipitate pulmonary edema in dogs with experimental left ventricular overload?
Population
14 dogs with isolated left ventricular overload induced by Teflon graft between aorta and left atrium
Comparison
Breathing 10% O2 vs infusion of histamine, epinephrine, angiotensin, or lactic acid
Design
Preclinical experimental study
Follow-up
3 weeks following surgery prior to acute exposures
Authors
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Acidemia may precipitate pulmonary edema in experimental LV overload; leaves open its role in human HF decompensation.
Do hypoxemia, vasoactive compounds, or acidemia precipitate pulmonary edema in dogs with experimental left ventricular overload?
In a canine model of left ventricular overload, acidemia induced by lactic acid infusion precipitated severe pulmonary edema, highlighting its potential pathogenic role in heart failure.
John S. Baumber (1980) studied Left ventricular overload and pulmonary edema (n=14). Hypoxia, vasoactive compounds, and lactic acid infusion was evaluated on Development of pulmonary edema. In dogs with experimental left ventricular overload, acidemia induced by lactic acid infusion resulted in fulminating pulmonary edema, whereas vasoactive compounds did not.
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