Eskenasy A
Med Interne. 1977 Jan-Mar;15(1):85-91.
The main morphogenetic and pathogenetic elements of pulmonary chronic suppurations were experimentally investigated in rabbits. The animals were sensitized by blood way with complete Freund adjuvant containing serum proteins, which determined a nodular and diffuse granulomatous reaction in the pulmonary tissue. The perturbing agent of the model system was a maintained immediate type hypersensitivity reaction produced by an excess of intrapulmonary antigen accumulation after an intratracheal injection of the same agent with antigens in excess. The animals sacrificed 15, 30 and 45 days after the intratracheal challenge presented a wide and progressive cellulofibrous restructuring of the lung tissue with exclusion of lung areas, persistence of granulocytic foci, release of lactic-dehydrogenase, chronic vascular lesions and diffuse fibrosclerosis. The importance of the persisting antigens which maintain the Arthus type hypersensitivity reaction, of vascular chronic lesions determined by the blood transport of deleterious products and by immunopathologic phenomena, as well as of the cellulo-fibrous proliferation, are emphasized as elements of autoaggressive processes with common and immune components, all contributing to the chronic evolution of pulmonary suppurations.
在兔子身上对肺部慢性化脓的主要形态发生和发病机制因素进行了实验研究。通过静脉途径用含有血清蛋白的完全弗氏佐剂使动物致敏，这在肺组织中引发了结节性和弥漫性肉芽肿反应。模型系统的干扰因素是在气管内注射相同抗原且过量后，肺内抗原积累过多产生的持续速发型超敏反应。在气管内激发后15、30和45天处死的动物，肺组织呈现广泛且进行性的纤维组织重构，伴有肺组织区域的排除、粒细胞灶的持续存在、乳酸脱氢酶的释放、慢性血管病变和弥漫性纤维硬化。强调了持续存在的抗原维持阿瑟斯型超敏反应的重要性、由有害产物的血液运输和免疫病理现象所决定的血管慢性病变以及纤维组织增殖的重要性，这些都是具有共同和免疫成分的自身攻击性过程的要素，都促成了肺部化脓的慢性演变。
