The Possible Machanism Of Multiple Organ Dysfunction Syndrome In Exertional Heatstroke

Heatstroke, also known as fatal heat stroke, at present, divided into two categories: non-exertional heat radiation (classic / nonexertional heat stroke, CHS), and exertional heat-stroke (exertional heat stroke, EHS). CHS caused by the exposure to high temperatures, oc-curs in the young, the elderly, have underlying disease; and EHS is due to hot and humid environment caused by high levels of physical work, more than occurred in healthy young people, athletes, military personnel . In previous studies, mostly non-exertional heatstroke main areas of study related to the pathogenesis, clinical research, pathology, pathophysiol-ogy and other aspects, but on exertional heatstroke pathogenesis has not been reported at home and abroad .ObjectiveEstablished animal model to observe the rats kidney, liver, lung, heart, small intestine, skeletal muscle morphology, by hematoxylin - eosin staining to observe the pathological changes, in order to understand the various organs of three groups of rats form And pathological changes; enzyme reaction for the detection by the immune serum endotoxin, interleukin -6, IL -10, tumor necrosis factorα, were detected by laboratory serum creatinine, urea nitrogen, ALT, AST, muscle Kinase, CK-MB, blood clotting mechanism, observed the change of indicators in each group, analyzed the correlation between each other. From the above experimental anatomy, pathology and immunology of exertional heatstroke caused the beginning of each organ dysfunction and the possible occurrence of dynamic link mechanism.Method1, By six computer-controlled multi-functional treadmill established animal model, the establishment of rats in control group, experimental group 1 (35min), group 2 (70min);2, By hematoxylin - eosin staining observed three groups of rats, liver, lung, kidney, small intestine, the heart of the pathological changes; 3, The levels of endotoxin, interleukin -6, IL -10, tumor necrosis factorαand interleu-kin-1βin blood were detected by immunization ELISA in the three groups. CRE, BUN, ALT, AST, CK, CK-MB, PLT, FB, D-Dimer were detected by laboratory. the indicators observed in each group the changes in rat serum, analyzed the correlation between each other.Result1, Compared with the control group:Small intestine: experimental group 1 mild wall thickening, villous atrophy and some loss, experimental group 2 showed marked mucosal thickening, edema, showed segmental changes, the lesion shows infiltration of inflammatory cells; Kidney: experimental group 1 no significant change in the ball, visible light tubulointerstitial edema, scattered hemorrhage, experimental group 2 showed no abnormal ball, shows extensive interstitial hemorrhage, tubular compression deformation, stenosis, intravascular visible thrombosis;Lungs: experimental group 1 shows focal infiltration of inflammatory cells, bronchial epithelial cells shrivel and fall off the bronchial lumen expansion deformation, scattered interstitial lung hemorrhage; experimental group 2 bronchial epithelial cells appeared atrophic, shedding, and bronchial lumen narrow deformation , a remarkable expansion of alveoli, alveolar septa narrow and broken into large cysts adjacent alveolar fusion, there may be diffuse pulmonary interstitial infiltration of inflammatory cells and extensive bleed-ing.Liver: experimental group 1 can be seen in the portal area inflammatory cell infiltration, no significant swelling of liver cells, showing focal hemorrhage; experimental group 2 cell swelling seen extensive liver cells, liver cells arranged in disorder, showing flaky bleeding. Skeletal muscle: experimental group 1 had mild muscle disorder, muscle fiber hypertrophy, showing a small amount of inflammatory cell infiltration; experimental group 2 significant disordered muscle fibers, muscle fiber hypertrophy with extensive structural breakdown.Cardiomyopathy: three groups of no obvious abnormalities.2, Compared with the control group, experimental group 1 was significantly higher LPS, significant difference, with an extremely statistically significant (P <0.01), IL-10, IL-6, IL-1β, TNF-αlevels are different ; experimental group 2 LPS, IL-10, IL-6, IL-1β, TNF-αwere significantly increased, a significant difference. Compared with the control group, experimental group 1 CK, CK-MB, ALT, AST, BUN, CRE, PLT, FB, D-Dimer no change, no significant difference; experimental group 2 CK, CK-MB, ALT, AST, BUN, CRE, D-Dimer were significantly higher, PLT significantly de-creased, a significant difference,, FB no significant change.Conclusion1, Compared with the experimental group, the pathological changes in various organs in the small intestine of early inflammatory cell infiltration and re-emerged, and kidney, lung and liver by cell edema, hemorrhage based, no significant inflammatory Cell infiltra-tion, myocardial no significant pathological changes.2, This study shows blood endotoxin with significantly increased, IL-10, IL-6, IL-1β, TNF-αalso will increase, both have significant positive correlation.3, This study showed that early in the disease, CK, CK-MB, ALT, AST, BUN, CRE, PLT, FB, D-Dimer no change, no significant difference; with the progression of the gradual emergence of CK, CK-MB , ALT, AST, BUN, CRE, D-Dimer were significantly higher, PLT was significantly decreased with the increase of endotoxin were positively correlated.These conclusions suggest exertional heatstroke can occur in the early reduction of small intestinal mucosa barrier, leading to endotoxemia stimulate massive release of inflammatory mediators, causing damage to various organs and abnormal clotting mechan-ism, leading to multiple organ Failure and DIC.