ABSTRACT
This chapter presents procedures used to implement the animal model. It details the issue preparation for morphologic assessment of lungs and pulmonary macrophages and morphometric and physiologic methods used to determine the nature of the disease. The chapter summarizes data and discusses the possible mechanism for the development of the disorder, future direction of the research, and limitation of the model. It shows that cigarette smoke inhalation by an animal would result in pulmonary disfunction since, especially at present, "veryone knows" smoking is harmful. Total lung volume, rate of compliance change, CO-diffusing capacity, and diffusing capacity per unit lung were significantly reduced in the old smoke-treated mice when compared to all other animal groups. Smoke inhalation by young animals had no apparent effect on pulmonary functions. The present animal model indicates a relationship between cigarette smoke inhalation, the lung macrophage system, and pulmonary fibrosis and implicates kaolinite in the development of the disorder.
