Severe acute respiratory syndrome (SARS) pertains to the doctrine of febrile disease in Traditional Chinese Medicine(TCM). The prevention and treatment of SARS can be under the guidance of doctrine of febrile disease, treating acorrding to different symptoms and finding effective formulas and herbs. As a subject with a long history, doctrine of febrile disease in TCM accumulated a lot of precious clinical experience in treating and preventing infectious diseases or epidemic diseases,which plays a positive role in the prevention and treatment of SARS. Basically the clinical manifestations of SARS are the same with symptom differentiation according to defensive phase, qi phase, nutrient phase and blood phase in doctrine of febrile disease, among which the manifestation and treatment in the qi phase are the most important. So the qi phase is a key point of controlling disease. As one of the therapeutic principles of febrile disease, letting out heat and pathogenic factors is suitable for treating SARS. During the period of treatment, strengthening body resistance must accompany with letting out pathogenic factors, and timely modification of herbal ingredients according to symptoms changes is also important. In the aspect of SARS prevention, doctrine of febrile disease attaches importance to disinfection and isolation. In the post pneumonic stage, doctrine of febrile disease is good at helping recovery, accelerating absorption and preventing fibrosis by using proper foods and herbs.

Objective To explore the mechanism of QHR (main ingredients:Gypsum, Anemarrhema Asphodeloides Bge, Paeonia Lactiflora Pall) on secretive function of vaso-endothelial cells in rabbits with of endotoxemia. Methods Endotoxemia model was induced by colibacillary endotoxin via auricular intravenous injection in rabbits. The changes on pathomorphology and secretive function of vaso-endothelial cells in the model and QHR group were observed. Results It showed the existence of microthrombus in the lung via microscope in the model. The balance destruction of t-PA/PAI, NO/ET, TXB2/6-K-PGF1? in the model (P