AIM: To study protective effects and mechanism of heat shock response (HSR) on cardiovascular system in rats after heat exposure. METHODS: The study was divided into 2 experiments: ① Protective effects of HSR on cardiovascular system in rats after heat exposure. SD rats randomly allocated into 2 groups: heat shock group (HS group), sham control group (SC group). HS group were treated with heat shock, but SC group weren't. After recovering for 20 h at room temperature, two groups exposed to death in thermal environment, and blood pressure and electrocardiogram were measured continuously. Through Chart software mean arterial pressure(MAP), existent time etc were acquired. ② SD male rats randomly allocated into 3 groups: HS group, SC group and normal temperature control group (NC group). NC group weren't treated. The treatment in HS and SC group was identical with in the first experiment, but it would be terminated at 73 min after heat exposure, meanwhile content of MDA of myocardium were measured. RESULTS: ① Existent time in HS group was longer than that in SC group and shock arrived later; ② During earlier period after heat exposure MAP had no significant changes between HS and SC group, but after 60 mins MAP in HS group were higher than that in SC group; ③ Compared with NC group, content of MDA in myocardium in SC group was higher significantly at 73 min after heat exposure. Howerer, content of MDA in HS group was lower than in SC group, and had no significant changes with NC group. CONCLUSION:Through decreasing production of MDA in myocardium, HSR has a protective effect on cardiovascular system in rats after heat exposure.

The purpose of this study was to investigate and analyze the high frequency electrocardiogram (HFECG) for middle-aged and elderly people.138 subjects were chosen in our study.The mean age was 60.38 years.Among them,72.1 per cent were between 50 and 69 years.The results showed that (1) the differences were not significant between male and female groups in the mean number of high frequency notches (HFN).(2) For an increase in high frequency notches in the leads V1 and V2,we should consider the possibility of pathological changes of the anterior medial wall of heart,which was supplied by the dessending rami of the right anterior coronary artery,on the one hand,and it might remind us to pay great attention to posteromedian wall of heart,on the other hand.(3) Looking at all age groups in this study,we preliminarily found that the age peak of ischemic heart disease was between 50 and 70 years,according to the number of high frequency notches in the leads of HFECG.(4) The sensitivity of HFECG for diagnosing ischemic heart disease is 40 per cent higher than that of the conventional ECG.(5) In addition,nine leads were used in this examination,which not only preserved sensitivity of six leads but also could provide a localizing value for the diagnosis of heart disease.

Objective To investigate the effects of co-exposure to LPS and heat on plasma tumor necrosis factor-? (TNF-?) and interleukin-6 (IL-6) in rats. Methods Eighty male pathogen-free Wistar rats were randomly assigned to 4 groups: saline-injected normothermic control (group C), saline-injected heat exposed (group H), LPS-injected normothermic control (group L), LPS-injected heat exposed (group HL). Rectal temperature (Tr), heart rate (HR), mean arterial pressure (MAP), and respiratory rate (RR) were continually monitored. Plasma levels of TNF-? and IL-6 were determined at 0, 40, 80, 120 min after treatment. Results The rats in group HL displayed significantly higher values of Tr , HR , and RR and lower values of MAP than that of group C at 120 min. There was a significant difference in the values of HR and MAP between group HL and the other 3 groups at the same time point. The rats in group HL displayed an early rise in levels of plasma TNF-?, IL-6 at 40 min. The significant elevation of the peak TNF-? level at 80 min in group HL was observed. Plasma IL-6 hyperexpression was shown in rats in group HL which was significantly higher than the other 3 groups at the same time point. Conclusion Co-exposure to LPS and heat induces the rat to develop and augment systemic inflammatory response syndrome.

AIM: To study the preventive effects of Keningfang decoction on the experimental influenza virus pneumonia in mice and its mechanism. METHODS: Fifty NIH mice were divided into five groups randomly (ten mice in each group), normal control group, model group, virazole treatment group, Keningfang I treatment group, Keningfang II treatment group. The FM 1 virus strain that kept in frozen condition were revived and cultured in chick embryo. The mice in every group that were lightly anesthetized by aether, and infected by dropping FM 1 15 LD 50 into the nose, except for the normal control group, by equal volume distilled water. Mice were treated with drugs or distilled water two days before the model was made (0 3 mL, 2 times a day). The mice were treated with drug for six days, then was killed, the lungs were collected, and kept in -70 ℃. HSP70 was measured in the lung tissue by Western blot. Pathologic changes of the mice lungs were observed under microscope. RESULTS: Compared with the normal control group, HSP70 in the other groups were increased significantly (P

OBJECTIVETo investigate the variation and the effect of TNF and NO in the process of the creation of protective heat stress model and provide more thoretical basis.

METHODSThe rats were properly treated with heat and then the serum was separated. Radioimmunoassay and nitrate reductase assay were employed to measure the concentration of TNF and NO at different time between 0 h and 24 h after heat stress respectively.

RESULTSCompared with the control, the concentration of TNF increased significantly 2 h, 4 h, 8 h, 12 h after heat stress, of which 2 h, 12 h(P < 0.05), 4 h, 8 h(P < 0.01), but no significant changes 0 h, 24 h after heat stress. The concentration reached the peak 4 h after heat stress[(3.35 +/- 0.20) ng/ml] and increased significantly than 0 h, 2 h, 8 h, 12 h, 24 h after heat stress(P < 0.01, P < 0.05). 24 h after heat stress it recovered to normal standard. Compared with the control, the concentration of NO was higher 2 h, 4 h, 8 h, 12 h, 24 h after heat stress(P < 0.05), but no significance at 0 h. The concentration amounted to peak 8 h after heat stress[(108.21 +/- 27.89) mumol/L] and increased than 0 h, 2 h, 4 h after heat stress(P < 0.01). After 8 h it began to decrease continuously in heat stress group, however it was higher 24 h after heat stress than control.

CONCLUSIONTNF and NO played an important role in the process of the creation of protective heat stress model.

Animals ; Disease Models, Animal ; Heat Stress Disorders ; prevention & control ; Nitric Oxide ; blood ; physiology ; Rats ; Time Factors ; Tumor Necrosis Factor-alpha ; blood ; physiology

OBJECTIVETo establish a animal model of hepatic steatosis induced by chronic viral hepatitis in C(57)BL/6 mice.

METHODSC(57)BL/6 mice were randomly assigned to control group, high-fat diet group, mouse hepatitis virus strain A59 (MHV-A59) virus infection group, and high-fat diet plus virus infection group. At 13 weeks of the experiment, serum samples were collected to detect MHV antibodies and transaminase and lipid levels. The hepatic pathologies of the mice were examined with Oil red O staining of the frozen sections the and HE staining of paraffin-embedded sections.

RESULTSThe mice in the two virus infection groups showed strong positivity of MHV antibodies in the serum. Compared with the control group, the mice in high-fat diet group and the two virus infection groups had significantly increased AST and ALT levels with also elevated TC and LDL-C levels. The two virus infection groups both exhibited obvious pathologies in the liver characteristic of chronic viral hepatitis with increased lipid accumulation in the hepatocytes.

CONCLUSIONWe have successfully established a mouse model of hepatic steatosis induced by chronic viral hepatitis, which provides the basis for further study of the disease mechanism.

Animals ; Antibodies, Viral ; blood ; Chronic Disease ; Diet, High-Fat ; Disease Models, Animal ; Fatty Liver ; virology ; Hepatitis, Chronic ; virology ; Mice ; Mice, Inbred C57BL ; Murine hepatitis virus