Robinson F R, Runnels L J, Conrad D A, Teclaw R F, Thacker H L
Animal Disease Diagnostic Laboratory, Purdue University, West Lafayette, IN 47907.
Vet Hum Toxicol. 1990 Dec;32(6):569-72.
The pathologic response of the lung to irritant gases ranges from the acute exudative phase through the subacute proliferative phase to the chronic fibrosing phase. These responses are based on damage to the Type I cells, and possibly endothelial cells, and the subsequent proliferative and repair processes in the surviving animals. Responses to high dose exposures appear at the microscopic level as exudation of protein rich fluids into alveoli (alveolar edema) and subsequent death due to anoxia. Physiologically, this could be described as a mismatch of ventilation with perfusion, resulting in impaired gas exchange. Animals surviving this acute exudative phase resolve the alveolar edema to fibrin, and Type II cells become hypertrophic and hyperplastic in the process of replacing the damaged Type I cells. The acute and subacute responses also elicit inflammatory changes in the interstitium of the lung that may progress to fibrosis in the chronic stage of a survivable exposure. Diagnostic cases in livestock involving irritant gases reflect similar toxic injuries to the lung.
肺对刺激性气体的病理反应范围从急性渗出期到亚急性增殖期,再到慢性纤维化期。这些反应基于对I型细胞以及可能的内皮细胞的损伤,以及存活动物随后的增殖和修复过程。高剂量暴露后的反应在微观层面表现为富含蛋白质的液体渗入肺泡(肺泡水肿),随后因缺氧而死亡。从生理角度来看,这可描述为通气与灌注不匹配,导致气体交换受损。在急性渗出期存活下来的动物会将肺泡水肿消退为纤维蛋白,在此过程中,II型细胞会肥大并增生,以取代受损的I型细胞。急性和亚急性反应还会引发肺间质的炎症变化,在可存活暴露的慢性阶段可能会发展为纤维化。家畜中涉及刺激性气体的诊断病例反映出对肺的类似毒性损伤。