Increased pulmonary vascular permeability following acid aspiration

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Abstract
The effect of HCl aspiration on transvascular fluid and protein flux and lung water content was studied in 21 anesthetized dogs. Steady-state lung lymph flow, pulmonary arterial and left atrial pressures and the concentration of total protein and albumin in lymph and plasma after intratracheal instillation of 2 ml/kg 0.1 N HCl was measured. Acid injury produced a 2-fold increase in lung lymph flow and lymph protein clearance when compared with control. This indicated an increase in pulmonary microvascular permeability. In dogs given 25 g concentrated human albumin and 1 mg/kg furosemide 10 min after acid injury, the acid-induced increase in fluid filtration was prevented. The decrease in fluid filtration was not attributed to an increase in the transvascular protein osmotic pressure gradient but to a more direct effect of furosemide. Treatment with furosemide alone prevented increased lung lymph flow induced by acid injury but albumin alone did not. In all acid-injured animals there was an increase in lung water when compared with control. Acid aspiration produced localized areas of damage to filtration vessels that led to increased leakage of protein and water. Furosemide treatment prevented much of this increased fluid and protein flux by an undefined mechanism.