Circulatory shock最新文献_第3页

Low-molecular-weight TNF biosynthesis inhibitors: strategies and prospectives. 低分子量TNF生物合成抑制剂:策略和前景。

Circulatory shock Pub Date : 1994-11-01

J C Lee, U Prabhakar, D E Griswold, D Dunnington, P R Young, A Badger

引用次数: 0

Role of nitric oxide in ischemia/reperfusion of the rat kidney. 一氧化氮在大鼠肾缺血再灌注中的作用。

Circulatory shock Pub Date : 1994-10-01

F López-Neblina, A J Paez, A H Toledo, L H Toledo-Pereyra

{"title":"Role of nitric oxide in ischemia/reperfusion of the rat kidney.","authors":"F López-Neblina, A J Paez, A H Toledo, L H Toledo-Pereyra","doi":"","DOIUrl":"","url":null,"abstract":"This work studies the role that nitric oxide (NO) plays in ischemia/reperfusion (I/R) of the rat kidney. Sprague-Dawley rats, weighing 250-300 g, were subjected to 75 min of warm ischemia and contralateral nephrectomy. The animals were divided into six groups (n = 12 per group): ischemic control (IC) with normal saline, L-NG-mono-methyl-arginine (L-NMMA) 50 mg/kg, L-arginine (L-Arg) 300 mg/kg, Na-nitroprusside (Na-NP) 2.5 mg/kg, the combination of L-NMMA+Na-NP at the doses used before, and the sham group. All animals received the drug intravenously 60 min prior to ischemia. Survival was evaluated at seven days. Renal damage was assessed by kidney function tests (serum creatinine and blood urea nitrogen) and light histology. Lipid peroxidation was measured in renal tissue using the thiobarbituric acid assay. Significantly better survival was seen in the Na-NP group, as compared to the rest of the study. Serum creatinine at 24 and 48 hr showed a significant difference between the Na-NP group and the other groups. Histological damage was minimal in the Na-NP group. Clearly, the Na-NP had the most beneficial effect in survival and histological structure. Lipid peroxidation was significantly different, with the lower levels seen in the L-NMMA group and the higher levels in the Na-NP group. In base to these results, we conclude that exogenous NO has a beneficial and protective effect of the ischemically damaged rat kidney. This protection is independent of lipid peroxidation. Endogenous NO production does not play a role in I/R injury in our model.","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"44 2","pages":"91-5"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18544044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Agonistic and antagonistic properties of CD40 mAb G28-5 are dependent on binding valency. CD40 mAb G28-5的激动性和拮抗性取决于其结合价。

Circulatory shock Pub Date : 1994-10-01

J A Ledbetter, L S Grosmaire, D Hollenbaugh, A Aruffo, S G Nadler

引用次数: 0

Inhibition of LPS-mediated cell activation in vitro and in vivo by gangliosides. 神经节苷类对脂多糖介导的细胞活化的体外和体内抑制作用。

Circulatory shock Pub Date : 1994-10-01

J J Mond, K Witherspoon, R K Yu, P Y Perera, S N Vogel

{"title":"Inhibition of LPS-mediated cell activation in vitro and in vivo by gangliosides.","authors":"J J Mond, K Witherspoon, R K Yu, P Y Perera, S N Vogel","doi":"","DOIUrl":"","url":null,"abstract":"Addition of purified GM1 gangliosides inhibited lipopolysaccharide (LPS)-stimulated proliferation of purified B cells by greater than 90%. Addition of gangliosides to B cells as late as 120 min after the addition of LPS still inhibited B-cell proliferation, suggesting that inhibition did not simply reflect direct binding of LPS to gangliosides. Gangliosides also inhibited proliferation of B cells stimulated by anti-Ig antibodies, albeit to a lesser degree than inhibition of the LPS-stimulated response. The finding that B-cell proliferation stimulated by the combination of PMA+ionomycin was also inhibited by gangliosides suggests that its inhibitory activity did not reflect interference with binding of the B-cell stimuli to membrane receptors. The inhibitory effect of gangliosides was not restricted to B cells, since LPS-induced TNF production by macrophages was also inhibited in vitro. The inhibitory activity of gangliosides was also seen in vivo, and mice injected with soluble gangliosides or implanted with slow-release pellets impregnated with gangliosides showed reduced TNF production in vivo in response to LPS. Mice that were implanted with these slow-release pellets were also protected from LPS-induced lethality. Thus, while only 10% of control mice survived injection with LPS+galactosamine, the experimental group showed a 64% survival. It is likely that this protective effect reflects the ability of gangliosides to suppress LPS-mediated TNF production. This model provides a basis for studying a regulatory role for gangliosides in B-cell activation in vitro and macrophage activation in vitro and in vivo. Furthermore, it suggests new approaches to suppress the toxic effects induced by LPS in vivo.","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"44 2","pages":"57-62"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18744241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mechanisms of tumor necrosis factor cytotoxicity and the cytotoxic signals transduced by the p75-tumor necrosis factor receptor. 肿瘤坏死因子细胞毒性机制及p75-肿瘤坏死因子受体转导的细胞毒性信号。

Circulatory shock Pub Date : 1994-10-01

T Reid, P Louie, R A Heller

引用次数: 0

Potentiation of the toxicity of tumor necrosis factor by tumors in mice. 肿瘤坏死因子对小鼠毒性的增强作用。

Circulatory shock Pub Date : 1994-10-01

F Nishigaki, K Miyayasu, S Tsujimoto, T Manda, K Shimomura

{"title":"Potentiation of the toxicity of tumor necrosis factor by tumors in mice.","authors":"F Nishigaki, K Miyayasu, S Tsujimoto, T Manda, K Shimomura","doi":"","DOIUrl":"","url":null,"abstract":"Tumor necrosis factor-alpha (TNF-alpha) was reported to be important in the induction of septic shock. After i.v. injection of recombinant TNF-alpha (rTNF-alpha), BALB/c mice bearing Meth A fibrosarcoma (Meth A), but not normal mice, died of shock. Tumor cells are known to release many biological components. In this study, we examined the role of the tumor in the toxicity of rTNF-alpha in mice. Meth A cells maintained i.p. in mice were cultured for 24 hr in vitro. Conditioned medium (CM) obtained from the Meth A cells was given i.v. to mice, and 2 to 7 days later, i.v. injection of rTNF-alpha induced death in the animals. rTNF-alpha treatment 4 days after Meth A CM gave the maximum effect. rTNF-alpha did not induce death in mice treated with CM from spleen cells. However, after the Meth A cells were passaged 2 or 3 times in in vitro culture, the CM did not potentiate the toxicity of rTNF-alpha in mice. rTNF-alpha induced symptoms of disseminated intravascular coagulation (DIC) on coagulation parameters in the blood, and high plasma tissue factor (TF) activity in Meth A CM-treated mice and Meth A tumor-bearing mice. These results suggest that factor(s) are released from tumor cells activated by interaction with host cells, and injection of rTNF-alpha and the factor(s) results in the induction of DIC syndrome leading to host death.","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"44 2","pages":"77-83"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18744172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Phenotypic analysis of TNFR1-deficient mice and characterization of TNFR1-deficient fibroblasts in vitro. tnfr1缺陷小鼠的表型分析及体外tnfr1缺陷成纤维细胞的表征。

Circulatory shock Pub Date : 1994-10-01

J Rothe, F Mackay, H Bluethmann, R Zinkernagel, W Lesslauer

引用次数: 0

Biology of Fas. Fas生物学。

Circulatory shock Pub Date : 1994-10-01

D H Lynch

引用次数: 0

Regulation of immune responses by the ligands for CD27, CD30, and 4-1BB. CD27、CD30和4-1BB配体对免疫应答的调控。

Circulatory shock Pub Date : 1994-10-01

M R Alderson