Exerimental Study On The Pathogenic Mechanism Of Damp-Heat Syndrome Of Seasonal Febrile Disease Stagnating At Qi-level

The Damp-Heat Syndrome (DHS) of Seasonal Febrile Disease (SFD) is the common clinical syndrome, which arises and develops relaxedly. The pathological changes of DHS of SFD more usually occurs in the Qi-level and little in Ying or Blood-level. This item of research tries to explore the mechanism of the pathological character of DHS mentioned above. This experiment observed the manifestation of New Zealand rabbits when subjected to damp-heat environment (DUE), the high-density lipop2rotein diet(HDLD) and endotoxin (ET) separately and unitedly. The results of the symptoms observation is described as: HDLD hardly brings out DHS; DHE can bring about similar manifestation of DHS; while ET can cause the signs and symptoms of the diseases of Warm-heat nature; signs and symptoms caused by the combination between DUE and ET (DHE+ET) are more serious than that by DUE. Then three factors co-operate on the rabbits, it manifested as fever, lassitude, anorexia, mucous stool and so on, stagnating at Qi-level, closely conform to DHS of SFD. To explore the mechanism ulteriorly, we test the lipoprotein, tumor necrosis factor-a (TNF-a) interieukin-l (IL-1), interleukin-6 (JL-6), calcium, endotoxin (ET) in the blood and observed the pathologic change of the liver by optic microscope. It showed HDLD can bring about plasma lipoprotein increasing. Having Compared the content of ET, TNF-a,IL-6. and lL-6 in the four group model rabbits, we found cytokines level in HDLD group rabbits are much more lower than that of the standard group, as well as El is; liver trauma is slightest;Cytokines content reduce much slowlier after their peak value than the standard and damp-heat environment groups rabbits. To explain the experiment results: the pathogenic mechanisms of DHE to cause the similar manifestations of DES of SFD are:By promoting endotoxin translocation from intestinal cavity to circulation system, inducing more TNF, IL-1 and IL-6, inducing serious liver putrescence. Once damp-heat environment combining with external ET, the condition could be aggravated, such as developing to tissue and apparatus putrescence, microcirculatory disturbance, DJC or even died. If give HDLD before mainlining LPS or exposing to damp-heat environment, plasma increased and can incomplete reversibly neutralize ET activity, reduce El induced cytokines release such as TNF, IL-1, IL-6,and inhibit the afterward reaction cascade, hinder disease developing to Yingue-1evel. On the other hand, lipoprotein can bind with El and prolong the El half-life, delay ET clearance make the disease conditions cant alleviate rapidly, hence retain Qi en. To sum up, endotoxin, damp-heat environment and high-density-lipoprotein diet are the necessary factors during the Damp-heat syndrome of Seasonal Febrile disease developing. ET act as pivotal factor and the others act as accessorial factors. Bidirectional effect of the High-density-lipoprotein diet working on LPS metabolizition just is the mechanisms of Damp-heat syndrome of seasonal febrile disease stagnating at Qi-level, slowly developing to Ying-xue level.