Theoretical Study On Syndrome Of Accumulation Of Cold Fluid In The Lung And The Gene Expressions Of INOS And TNF α In The Lung Tissues Of Pathologic Rabbit Models

This thesis expounds systematically the theoretic problems about the syndrome of accumulation of cold fluid in the lung, such as the conception of fluid-retention and the forming mechanism of fluid-retention syndrome, the conception and fundamental pathogenesis of the syndrome of accumulation of cold fluid in the lung, the lung yang's role in the function of the lung's promoting water metabolism, the key pathogenesis and the mechanism of the incidence of diseases related to the syndrome, the diagnosis and treatment of the syndrome as well as the differentiations of similar syndromes, so as to enrich the theory of the syndrome. Based on the understanding of the pathogenesis of the syndrome, the former study and the current progress about animal model study of syndrome in pulmonary diseases, pathologic rabbit models with the syndrome of accumulation of cold fluid in the lung were set up with the methods of smoke stimulation, infusion of physiologic saline and controlling the ventilating volume in the cold environment. The models were prevented and treated by "Yang-Warming and Fluid-Dispersing Formula". To approach the internal mechanisms of the syndrome of accumulation of cold fluid in the lung and the functional mechanisms of "Yang-Warming and Fluid-Dispersing Formula" so as to understand further the theory of the lung's promoting water metabolism in TCM, the relevant indexes including arterial blood gas, the levels of ET and NO in blood and lung tissues, the expressions of iNOS, iNOSmRNAand TNF a mRNA in lung tissues, etc. were detected. The results of the experiment showed that not only general syndromes of the rabbits in the model group were in accord with clinical symptoms of patients with the syndrome of accumulation of cold fluid in the lung but also the changes of microcosmic indexes coincided with those of pulmonary diseases related to the syndrome. For examples, the levels of ET and NO in blood and lung tissues in the model group were higher than those in the control group, the expressions of iNOS, iNOSmRNA and TNF a mRNA in lung tissues were significantly reinforced and lung tissues were inflammatorily damaged, while the above indexes in the treatment group were improved in varying degrees. These results suggest that the development of pathologic rabbit models with the syndrome of accumulation of cold fluid in the lung is comparatively successful and reliable. TNF α , NO, iNOS and ET participate the forming mechanisms of the syndrome of accumulation of cold fluid in the lung respectively, furthermore, these indexes promote the forming of the syndrome by interaction. "Yang-Warming and Fluid-Dispersing Formula" has marked curative effect on the syndrome. The mechanisms of the effect are probably that it can maintain the levels of TNF a , ET and NO in lung tissues stable so as to reduce permeability of pulmonary vessels and inhibit hyperemia, edema and inflammatory effusing in lung tissues to protect lung tissues and regulate diastolization and contraction of airway to improve ventilation of the lung by controlling the gene expressions of iNOS and TNF a in lung tissues. That is, the functions of warming yang and dispersing cold fluid and improving ventilation of the lung of "Yang-Warming and Fluid-Dispersing Formula" have close relationship with its controlling ET, NO, iNOS, TNF a etc., and this is probably part microcosmic mechanism of the lung's promoting water metabolism.