彩色多普勒血流显像观察负压疗法对肢体血供的影响

目的 用彩色多普勒血流显像观察负压对肢体动脉闭塞犬患肢血供的影响 .方法 犬 15只 ,随机分治疗组 10只和对照组 5只 .两组均采用切断犬后肢股动脉分支、动脉腔内置入螺旋状金属丝的方法 ,制作肢体缺血模型 .在模型制作后2 wk,治疗组行患肢负压治疗 10 d,对照组不做负压治疗 .两组均于模型前、模型后 2 wk及治疗结束后 ,用彩色多普勒血流显像 (CDFI)观察患肢股动脉血流的变化 .结果 治疗组在治疗后侧支血流均明显增加 ,7只犬股动脉管腔内出现搏动性血流 (P<0 .0 1) ;对照组无明显变化 .

Failure of P-selectin blockade alone to protect the liver from ischemia-reperfusion injury in the isolated blood-perfused rat liver

AIM： To determine if blockade of P-selectin in the isolated blood-perfused cold ex vivo rat liver model protects the liver from ischemia-reperfusion injury. METHODS： The effect of P-selectin blockade was assessed by employing an isolated blood-perfused cold ex vivo rat liver with or without P-selectin antibody treatment before and after 6 h of cold storage in University of Wisconsin solution. RESULTS： In our isolated blood-perfused rat liver model, pre-treatment with P-selectin antibody failed to protect the liver from ischemia-reperfusion injury, as judged by the elevated aspartate aminotransferase activity. In addition, P-selectin antibody treatment did not significantly reduced hepatic polymorphonuclear leukocyte accumulation after 120 min of perfusion. Histological evaluation of liver sections obtained at 120 min of perfusion showed significant oncotic necrosis in liver sections of both ischemic control and P-selectin antibody-treated groups. However, total bile production after 120 rain of perfusion was significantly greater in P-selectin antibody-treated livers, compared to control livers. No significant difference in P-selectin and ICAM-1 mRNAs and proteins, GSH, GSSG, and nuclear NF-kB was found between control and P-selectin antibody-treated livers. CONCLUSION： In conclusion, we have shown that blockade of P-selectin alone failed to reduced polymorphonuclear leukocyte accumulation in the liver and protect hepatocytes from ischemia-reperfusion injury in the isolated blood-perfused cold-ex vivo rat liver model.

Study on the protective mechanism of remifentanil on mitochondria in rat hepatocytes subjected to ischemia-reperfusion injury

Objective:To explore the protective effect of remifentanil on mitochondria in rat hepatocytes subjected to ischemia-reperfusion injury and their possible mechanism. Methods:The model of rat hepatic ischemia-reperfusion injury was used and the effect of remifentanil on the ultrastructure of mitochondria, calcium homeostasis, MDA level in mitochondria were observed. Results: In contrast with the control group, mitochondrial matrix calcium concentration, calcium concentration after calcium uptake, and the quantity of calcium uptake in low and high remifentanil concentration groups and 5-HD group are lower (P<0. 01), and there is no difference in RHD (5-HD+remifentanil) group. The difference in MDA level between groups is insignificant. Conclusion:Remifentanil at clinical concentrations exerts a protective effect on mitochondria in rat hepatocytes subjected to ischemia-reperfusion injury, in which activating the KATP channel may be involved.

Significant increase in HBV, HCV, HIV and syphilis infections among blood donors in West Bengal, Eastern India 2004-2005: Exploratory screening reveals high frequency of occult HBV infection

AIM: To evaluate the prevalence of markers of hepatitis B virus (HBV) and hepatitis C virus (HCV) and human immunodeficiency virus (HIV) among blood donors in Kolkata, Eastern India for two consecutive years and to conduct a pilot study to explore the presence of HBV DNA among hepatitis B surface antigen (HBsAg) negative but anti-HBc positive blood donors. METHODS: Seroprevalence of HBsAg, anti-HCV and anti-HIV was studied among 113 051 and 106 695 voluntary blood donors screened in 2004 and 2005, respectively. Moreover, a pilot study on 1027 HBsAg negative donors was carried out for evaluating the presence of HBV DNA by PCR on HBsAg negative/anti- HBc positive donors. RESULTS: A statistically significant increase in the prevalence of HBV (1448 vs 1768, P < 0.001), HIV (262 vs 374, P < 0.001), HCV (314 vs 372, P = 0.003) and syphilis (772 vs 853, P = 0.001) infections was noted among blood donors of Kolkata West Bengal in 2005 as compared to 2004. Moreover, the exploratory study on 1027 HBsAg negative donors revealed that 188 (18.3%)of them were anti-HBc positive out of which 21% were positive for HBV DNA. CONCLUSION: The findings of this study underscore the significantly increasing endemicity of hepatitis viruses, syphilis and HIV among the voluntary blood donors of our community. The pilot study indicates a high rate of prevalence of HBV DNA among HBsAg negative/anti-HBc positive donors and thus emphasizes the need for a more sensitive and stringent screening algorithm for blood donations.

Expression of Toll-like Receptor 2/4 on Alveolar Macrophage in the Model of Total Hepatic Ischemia/Reperfusion Injury in Mice

Objective： To explore the expression and meaning of Toll-like receptor 2/4 in alveolar macrophage during the process of total hepatic ischemia in mice. Methods： BALB/c mice were used in a model of total hepatic ischemia/reperfusion. Alveolar Macrophage were collected at the time point of lh, 6h and 12h by the means of bronchoalveolar lavage （BAL）, and its TLR2/4 mRNA and protein were detected with Flow Cytometry and Real-time PCR. The level of TNF in BAL fluid were measured. The concentration of MPO, the ratio of wet/dry and lung histological scores were used to assess the degrees of lung injuries. Results： At the three time points of hepatic ischemia reperfusion, the expression of TLR2/4 protein of and mRNA were up-regulated and the level of TLR2 was on the rise continually. TLR4 at the time of 6 h reached the peak value （P〈0.01）. The level of TNF-2 in BAL fluid reached the highest point at the time of 6 h （P〈0.01）. The ratio of wet/dry rose continually during hepatic ischemia reperfusion. After 1 h, the level of MPO increased rapidly. Then it reached the peak value during the period of 6 h to 12 h. Conclusion： TLR2/4 on the mice of alveolar macrophage were activated in the process of hepatic ischemia/reperfusion and involved in the injury of lung.