Gustin P, Urbain B, Prouvost J F, Ansay M
Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Liège, Belgium.
Toxicol Appl Pharmacol. 1994 Mar;125(1):17-26. doi: 10.1006/taap.1994.1044.
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)
在一个专门设计的空气污染物暴露舱中，研究了大气氨对暴露于四种浓度（0、25、50和100 ppm）氨气6天的猪的体细胞生长、血浆皮质醇和氨浓度以及血细胞计数的影响。还使用离体灌注肺标本评估了这种气体对肺血管血流动力学和通透性以及对内毒素诱导的血管反应的影响。肺总血流阻力（Rt）被分为四个部分：动脉（Ra）、毛细血管前（Ra'）和后（Rv'）以及静脉（Rv）。毛细血管滤过系数（Kf,c）通过重量法进行评估。没有任何氨浓度能显著改变血浆皮质醇和氨浓度或白细胞分类百分比及白细胞总数，这表明不存在与氨相关的应激反应。在暴露的动物中，观察到嗜睡以及与浓度相关的体细胞生长抑制。将暴露期间记录的体重增加变化平均值表示为初始体重的百分比（y）与氨浓度（x）绘制的回归线方程为：y = 3.204 - 0.177x + 0.001x2（r = 0.99；p≤0.013）。向未暴露动物的肺灌注液中注入内毒素180分钟，导致Rt显著增加208%（p < 0.001），这可归因于Ra'和Rv'分别增加338%和180%。内毒素注入还导致Kf,c增加62%（p≤0.001）。猪暴露于任何浓度的氨均未改变任何血流动力学或通透性参数的基线值。然而，暴露于100 ppm氨气的猪的肺对内毒素的血流动力学反应发生了显著改变。如Rt的有限变化（+34.9%）所示，未暴露猪中观察到的Rt、Ra'和Rv'的增加完全被消除。暴露于50 ppm氨气的猪出现中等程度的反应（+131.7%）。氨的这种抑制作用通过线性回归与气体浓度密切相关（r = 0.99；p≤0.037）。暴露于氨并未改变对照组记录的Kf,c变化。得出的结论是，猪暴露于0至100 ppm的空气中氨浓度6天对肺微血管血流动力学和通透性没有直接影响，也不会诱导应激反应。（摘要截断于400字）
