Research On Pathology Mechanisms Of "Pulmonary Diseases Transferring To Large Intestine" Based On Pathology Changes About Rat Model Of Pulmonary Disease And Related Active Substances Content Of SP, VIP, INOS

ObjectiveThrough the observation of lung disease and the general behavior of the rat model of performance, and select three points in time dynamic observation of the pathophysiology of the lung and gastrointestinal tissue, pathology, and its related active substances of SP, VIP, and iNOS in expression and association, to explore lung and intestinal pathological mass change mechanism.MethodsIn our study,60SD rats, SPF grade male. Randomly divided into2groups: control group,24, model36. Blank rats reared in a smoke-free environment, the model group were simply smoked law model, each smoked50min, three times a day (9:00in the morning, afternoon2o’clock and6o’clock), a total of smoke smoked70d. Detected after the end of the modeling rat lung function, gastrointestinal function, pathophysiology indicator light microscopy observation of the lung, stomach, duodenum, jejunum, ileum, colon, rectal tissue HE staining and electron microscopy of lung and colon tissue ultra-change of the micro-structure of pathological morphology, immunohistochemistry assay organs and tissues of SP, VIP, and the expression of iNOS in.Results1. PathophysiologyRat weight:normal control group rats weight in natural growth, rats weight of model group in slow growth. Compared with blank control group, model group, the20th day,50th day,70th day were respectively significant different (p＜0.01). Model group, compared with the20th day,50th day and70th day were different (p＜0.05) or significant differences (p＜0.01). Pulmonary function testing:compared with the control group, model group were respiratory rate to accelerate, tidal volume and minute ventilation than the blank group (p＜0.05) or significant differences (P<0.01). Compared with20th day, the model the50th day and70th day of the model group were tidal volume, minute ventilation decreased, there are significant differences (p＜0.01).Gastrointestinal function testing:compared with blank control group, model group, intragastric residual rate increased rates lower small intestine, there are significant differences (p＜0.01). Compared with the20th day of modeling, the model rats modeling the50th day and70th day the residual rate of increase of the stomach, small intestine lower rate, there are differences (p＜0.05) or significant differences (P<0.01). Compared with50th day, the70th day increased intragastric residue rate, small intestinal propulsion rates lower, a significant difference (P<0.01).2. PathomorphologyLight microscopy:bronchial epithelial cell degeneration, necrosis, inflammatory cell infiltration of rat lungs about model group could be observed to various degrees in the20th day50th day and70th day; a large number of inflammation, intestinal mucosa and submucosa cell infiltration, to various degrees, were emerged from colon tissue, which focal wall to attach the skin cell degeneration, necrosis, inflammatory cell infiltration, multiple small focal and sheet erosion, the remnants of the epithelial cells and other pathological changes could also be observed; significant changes have not found about stomach, duodenum, jejunum, ileum, rectum tissue biopsy of rats.Electron microscopy:in the model group the20th day I alveolar epithelial cell structural damage; no significant changes in the rat colon tissue. Pulmonary capillary wall incrassation, a large number of phagocytic vacuoles in alveolar epithelial cells have been appeared on the50th day; intestinal mucosa microvillihas disappeared of a part of colon issue, accompanying with mitochondrial swelling and nuclide damage. Reduction of lung mesenchymal cells ingredients swelling of the vascular endothelial cells, cells collapse, nuclear expansion, mitochondrial swelling, cristae disappear, type II alveolar epithelial cell microvilli loss, swelling of the endoplasmic reticulum have been emerged on the70th day; intestinal microvilli arranged in sparse disorder submucosal lamina propria gap collagen fibers, as shown in fibroblasts.3. neuropeptide substance contentCompared with the control group, lung tissue of SP, the VIP, the expression of iNOS were increased and different about model rats on the20th day,50th day and70th day,(P<0.05).In model group, the rats lung tissue, SP, VIP, the expression of iNOS were increased with the time of modeling (P＜0.05or p＜0.01). Compared with the20th day of modeling, the50th day and the70th day manifest diffetences (P<0.05) or significant differences (p＜0.01). Compared with the50th day, the70th day were different (p＜0.05) or significant different (p＜0.01); SP, VIP, iNOS expression of rats colon were increased with modeling time increased (p＜0.05or p＜0.01), and compared with the20th day, the50th day and the70th day shows differences(p＜0.05) or significant differences (p＜0.01). Compared with the50th day, the70th day shows differences (p＜0.05) or significant differences (p＜0.01) difference.ConclusionPulmonary disease in rats change gastrointestinal function, reveals that the "pulmonary disease can affect large intestine"Pulmonary disease in rats led to pathological damage of the large intestine, and the main position is on colon.Primary experiment result about SP, VIP, and iNOS in the neuropeptide substance between the lung and intestine reveal a correlation trend, which may become the material basis of lung disease transferring to large intestine.In this model, that pulmonary disease transfers to large intestine is on the model50th day.