Effects of atmospheric ammonia on pulmonary hemodynamics and vascular permeability in pigs: interaction with endotoxins.

The influence of atmospheric ammonia on the somatic growth, the plasma cortisol and ammonia concentrations, and cell blood counts was investigated in pigs exposed to four concentrations (0, 25, 50, and 100 ppm) for 6 days in a specifically designed air-pollutants exposure chamber. The effects of this gas on pulmonary vascular hemodynamics and permeability and on the endotoxin-induced vascular response were also assessed using an isolated perfused lung preparation. The total pulmonary blood flow resistance (Rt) was partitioned into four components: arterial (Ra), pre-(Ra') and post-(Rv') capillary and venous (Rv). The capillary filtration coefficient (Kf,c) was evaluated by using a gravimetric technique. None of the concentrations of ammonia significantly modified the plasma cortisol and ammonia concentrations or the differential leukocyte percentages and total white blood cell count, suggesting an absence of stress related to ammonia. In exposed animals, lethargy and a concentration-related depression of the somatic growth were observed. The equation of the regression line plotted relating the mean values of the changes in body weight gain recorded over the exposure period expressed as percentages of the initial body weight (y) and ammonia concentrations (x) was: y = 3.204 - 0.177x + 0.001x2 (r = 0.99; p < or = 0.013). Endotoxin infused in the perfusion liquid of lungs from unexposed animals for 180 min induced a significant 208% increase in Rt (p < 0.001) which can be ascribed to a 338 and 180% increase in Ra' and Rv', respectively. Endotoxin infusion also induced a 62% (p < or = 0.001) increase in the Kf,c. Exposure of pigs to ammonia at any concentration did not modify the baseline values of any hemodynamic or permeability parameters. However, the hemodynamic response to endotoxins in lungs from pigs exposed to 100 ppm was significantly altered. The increase in Rt, Ra', and Rv' observed in unexposed pigs was completely abolished as shown by the limited changes in Rt (+34.9%). An intermediate reaction (+131.7%) was obtained in pigs exposed to 50 ppm. This inhibiting effect of ammonia was closely correlated with gas concentration by a linear regression (r = 0.99; p < or = 0.037). The changes in the Kf,c recorded in the control group were not modified by exposure to ammonia. It was concluded that exposure of pigs to aerial ammonia concentrations from 0 to 100 ppm for 6 days has no direct effect on the pulmonary microvascular hemodynamics and permeability and induces no stress response.(ABSTRACT TRUNCATED AT 400 WORDS)