30 Sprague-Dawley rats were used and divided into 3 groups:simple burned (n=12), saline-treated (n=6) and dialysis-treated group (n=12). The trunk below lumbar region and hind extremities of each animal were scalded with 80℃ water for 30 seconds to produce burn shock. In the compensatory stage of shock the blood pressure was not decreased apparently yet microcirculation and electrocardiogram had already been disturbed and becoming severe with the course of disease. When the average arterial blood pressure had lowered to near half of original level after 5 hr of burn, the animals were given abdominal dialysis with balance Krebs solution. In dialysis-treated group, blood pressure and heart rate increased, stagnant capillaries opend up, electrocardiogram partly recovered to near normal and survival time of animals extended significantly as compared with that of simple control or saline-treated group. These indicated that some toxic factors which could be dialysed were prodced after burn and involved in the pathogenesis of burn shock.

The lumbo-abdominal area and lower extremities of rat were scalded with 80℃ water for 30 seconds (covering about 35—400% TBS) in order to reproduce a model of burn shock. The serum level of malondialdehyde, which is the secondary products of lipid peroxidation, has been measured after burning. The level of products resulting from lipid peroxidation gradually rose up 1-2 hr following scalding. It increased significantly at 3.5 hr and reached to the top level 5 hr after burning. Then it returned down but was still significantly higher than normal at 7 hr post-burn. The administration of peritoneal dialysis with balanced Kreb's solution started just before the appearance of top level (4.5 hr after scalding). The serum level of products fron lipid peroxidation returned to near normal 1.5 hr following peritoneal dialysis. The time course of the change of lipid peroxidation products was similar to that of the development of burn shock, which indicated that the tissue damage from the effect of free radicals might play an important role in the pathogenesis of burn shock.

An irreversible hemorrhagic shock model was produced on dog. The effect of external counterpulsation on systemic circulation and microcireulation was observed by using a model CN-1821 colour microscopic TV set (Hitachi Denshia Ltd.) and a YKMICAS multiple parameters computer analysis system of microcirculation image. It was shown that 10 min after external counterpulsation treatment the decreased central venous pressure and mean arterial pressure during hemorrhagic shock rose and 120 min after treatment the microcirculatory disorder of conjunctiva in shock state, including vessel diameter, blood velocity, and blood flow, nearly returned to normal. Half of the animals survived more than 3 days. These results indicated that the application of external counterpulsation could improve the circulatory disturbance markedly in hemorrhagic shock, which led to increased survival rate.

Objective To study the effectiveness of interventional chemotherapy in combination with embolization for bulky cervical carcinoma in stage Ⅱb.Methods Cases divided into preoperative interventional group(A)and preoperative radiotherapy group(B).Radical surgery for uterine and pelvic lymph node was performed in each group 2～ 4 weeks after treatment.Results The 3 year survival rates were 91.0% and 88.48%,and 5 year survival rates were 81.79% and 73.37% in A and B,respectively.The recurrence rates were 21.7% in A and 48.6% in B(P

Microscopic studies of the skin and visceral microcirculation were made in rabbits with burn shock. Based upon the observations, the development of burn shock can be divided into 3 stages, namely: stage of excitation, stage of relative compensation and stage of decompensation. In the stage of relative decompensation, there is dilatation of the venules, margination of the WBC, agglomeration of RBC, stagnation of blood flow in the microcirculation. Margination of WBC increases the post-capillary resistance, and agglomeration of RBC hinders the blood flow in the microcirculation.Consequently, the stage of decompensation ensues. Histologically, extensive congestion of the heart, liver, spleen, lungs and kidneys was found. Hemorrhage in the lungs and thrombi in the pulmonary and renal venules were found as well.We suspected that the masses of the agglomerated cells or small thrombi obstructing pulmonary vessels might be one of the direct causes leading to the temporary stagnation or slowing down of the blood flow. As the shear velocity of the blood flow increases, dissociation of the agglomerated cell masses occurs, blood pressure will be lowered temporarily and blood flow will slow down. Obstruction of the pulmonary vessels by the cell masses, therefore, may play an important part in the development of burn shock.

AIM: To investigate the variation of nitric oxide(NO) and NO synthase(NOS) in rats during the early stage of severe burn and their possible relation with prognosis of severe burns.METHODS: Levels of NO - 2/NO - 3, the metabolic products of NO, nNOS and iNOS protein in brain, lung and duodenum of rats were measured before and after burns. Survival times of rats in each group were also measured.RESULTS: Levels of NO - 2/NO - 3 in rats after burn increased remarkably, selective inducible NOS( iNOS) inhibitor aminoguanidine (AG), and nonselective NOS inhibitor L-NAME can inhibit this increasing. Levels of neuronal NOS(nNOS) protein in normal rats were low, and iNOS could not be detected. Levels of nNOS protein increased mildly in all observed tissues and the levels of iNOS protein increased remarkably after burn. Administration of L-NAME and AG made the increase of nNOS more apparently but could not affect the level of iNOS. Survival time of rats decreased in L-NAME group and increased in AG group compared to control group.CONCLUSION: Symptoms such as vascular ralaxation and hypotension in burn shock are connected mainly with over-increased iNOS. [

AIM: To identify the effects of nitric oxide synthase (NOS) inhibitor on NO production, expression of NOS and mean artery pressure (MAP) in rats with severe burns. METHODS: After administration of non-selective NOS inhibitor, L-NAME, and selective inducible NOS (iNOS) inhibitor, aminoguanidine (AG), to rats with severe burns, levels of NO - 2/NO - 3 in blood, mRNA expression of nerve NOS (nNOS) in lung and duodenum, MAP in each group were calculated. RESULTS: Levels of NO - 2/NO - 3 in blood of rats increased significantly post burn, which could be inhibited by L-NAME and AG, especially by L-NAME. Expression of nNOS mRNA in lung and duodenum of rats increased post burn, which could be enhanced by AG and L-NAME. MAP of rats decreased gradually post burn and administration of AG could slow down this process significantly. CONCLUSION: cNOS and iNOS could play different roles in the pathophysiology of burn shock. Over-expression of iNOS could be closely related to the pathogenesis of burn shock.

OBJECTIVETo investigate the source, transmission route and risk factors of an outbreak of severe fever with thrombocytopenia syndrome (SFTS).

METHODSCase definition was made and suspected cases were searched. A standardized questionnaire was used to collect information on demographic features (age, gender, occupation, residential address), history of exposure, clinical signs and symptoms etc. Blood samples were collected from 12 suspected cases while index patient's blood samples were collected from walls of the residence. All samples were detected for SFTS virus using RT-PCR. Sero-prevalence rates of SFTS virus IgG were also conducted among healthy people, host and vectors.

RESULTSA total of 13 cases including 6 male and 7 female were identified during this outbreak in May 2014. Index patient developed illness onset on April 23 and died on May 1. Secondary patients would include 8 family members, 3 neighborhoods, 1 individual who lived in the same village, developing illness onset between May 10 and 16, with a peak on May 13. The incubation period was 9-15 days. Clinical signs and symptoms appeared as fever (100%), chill (92%), anergy (92%), body aches (92%), anorexia (92%), headache (77%), nausea (69%) etc. Neutropenia and thrombocytopenia also appeared. History of the index patient showed that she collected tea leaves in her hometown 1 month before the illness onset. After index patient died on May 1, 9 secondary patients had directly contacted the blood of the deceased. Data from the retrospective cohort study showed that 'direct contact with blood' was an important risk factor (RR = 43.36, 95% CI: 13.66-137.63, P = 0.000).

CONCLUSIONMajority of the secondary patients of these clusters contracted the SFTS virus infection through exposure to the blood of the index patient. However, aerosol transmission could not be ruled out, suggesting that precaution should be taken for doctors, nurses and family members when looking after the patients with SFTS virus infection.

China ; epidemiology ; Disease Outbreaks ; Environment ; Female ; Fever ; epidemiology ; Humans ; Male ; Retrospective Studies ; Risk Factors ; Severity of Illness Index ; Syndrome ; Thrombocytopenia ; epidemiology