Circulatory shock最新文献_第8页

Increase in the plasma concentration of reduced glutathione observed in rats with liver damage induced by lipopolysaccharide/D-galactosamine: effects of ulinastatin, a urinary trypsin inhibitor. 脂多糖/ d -半乳糖胺所致肝损伤大鼠血浆还原性谷胱甘肽浓度升高:尿胰蛋白酶抑制剂乌司他丁的作用

Circulatory shock Pub Date : 1993-12-01

H Okabe, K Irita, K Kurosawa, K Tagawa, A Koga, M Yamakawa, J Yoshitake, S Takahashi

{"title":"Increase in the plasma concentration of reduced glutathione observed in rats with liver damage induced by lipopolysaccharide/D-galactosamine: effects of ulinastatin, a urinary trypsin inhibitor.","authors":"H Okabe, K Irita, K Kurosawa, K Tagawa, A Koga, M Yamakawa, J Yoshitake, S Takahashi","doi":"","DOIUrl":"","url":null,"abstract":"The changes in plasma concentrations of reduced glutathione were investigated in rats with endotoxin hepatitis. An increase in serum alanine aminotransferase activity and in serum total bilirubin concentration was observed 12 hr after the intraperitoneal co-administration of small doses of Escherichia coli lipopolysaccharide and D-galactosamine in starved rats. At the same time, an increase in the plasma concentration of reduced glutathione was also observed. The increase in reduced glutathione from 14 +/- 2 to 20 +/- 9 microM (n = 11, P < 0.05) correlated well with that in serum alanine aminotransferase activity. Ulinastatin, a potent inhibitor of polymorphonuclear leukocyte elastase, partially counteracted all of these changes. Ulinastatin also reduced histological liver damage induced by endotoxin. We conclude that the increase in the plasma concentration of reduced glutathione reflects hepatocellular damage associated with endotoxin hepatitis. The partial reversal of the damage by ulinastatin is consistent with the proposal that the activation of polymorphonuclear leukocytes is involved in endotoxin hepatitis.","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"41 4","pages":"268-72"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19134505","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

Electrophysiologic properties of isolated adult cardiomyocytes from septic rats. 脓毒症大鼠离体成年心肌细胞的电生理特性。

Circulatory shock Pub Date : 1993-12-01

S N Wu, S I Lue, S L Yang, H K Hsu, M S Liu

{"title":"Electrophysiologic properties of isolated adult cardiomyocytes from septic rats.","authors":"S N Wu, S I Lue, S L Yang, H K Hsu, M S Liu","doi":"","DOIUrl":"","url":null,"abstract":"In this study, we examined the effect of sepsis on the electrical properties of isolated ventricular myocytes. Sepsis was induced by cecal ligation and puncture (CLP). The control rats were sham-operated. Membrane potentials and ionic currents in isolated cardiac myocytes were measured by the tight-seal, whole-cell patch-clamp technique. The results show that the resting membrane potentials of heart cells were significantly lower in the septic group (18 hr post-CLP) than those in the control group. However, there was no significant difference in action potential duration of 50% and 90% repolarization between the two groups of cells. In voltage-clamp experiments, isoproterenol (10 nM), a beta-adrenergic agonist, caused an increase in L-type calcium current (ICa,L) in a similar magnitude in myocytes isolated from the control and septic rats. Furthermore, isoproterenol failed to modify the time constants for ICa,L inactivation and the overall shape of current-voltage relationship for both groups of cells. These results indicate that formation of a G omega seal and subsequent tight-seal whole-cell recording with patch-clamp technique can be performed in heart cells derived from CLP-induced septic rats, and that septic rat heart is capable of responding effectively to beta-adrenergic stimulation.","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"41 4","pages":"239-47"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19134502","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

Macrophage treatment in suckling rat endotoxic shock. 巨噬细胞治疗哺乳大鼠内毒素休克。

Circulatory shock Pub Date : 1993-12-01

M Goto, R C Lichtenberg, M E Gottschalk, C L Anderson, H L Mathews, W P Zeller

引用次数: 0

Ketoisocaproate infusion improves survival from experimental sepsis by an antioxidant mechanism. 酮异己酸输注通过抗氧化机制提高实验性败血症的生存率。

Circulatory shock Pub Date : 1993-12-01

T Yonekura, S Matsusue, M Walser

引用次数: 0

Subcutaneous and gut tissue perfusion and oxygenation changes as related to oxygen transport in experimental peritonitis. 实验性腹膜炎的皮下和肠组织灌注和氧合变化与氧转运的关系。

Circulatory shock Pub Date : 1993-12-01

J B Antonsson, K Kuttila, J Niinikoski, U H Haglund

{"title":"Subcutaneous and gut tissue perfusion and oxygenation changes as related to oxygen transport in experimental peritonitis.","authors":"J B Antonsson, K Kuttila, J Niinikoski, U H Haglund","doi":"","DOIUrl":"","url":null,"abstract":"Peritonitis and septic shock may lead to tissue hypoxia, but this risk is not identical in all organ systems. This study was undertaken to measure changes in tissue oxygenation and perfusion in the gut wall and subcutaneous tissue, respectively, and to examine their relation to oxygen delivery and consumption. Twelve pigs were anesthesized and mechanically ventilated. An ultrasonic flow probe was placed around the superior mesenteric artery for registration of blood flow. A mesenteric vein was cannulated for blood sampling. For calculation of gut intramural pH (pHi), a Silastic balloon (Tonomitor) was placed in the lumen of the midileum. pHi was calculated from tonometrically measured PCO2 and arterial bicarbonate concentration. The subcutaneous PO2 was measured by means of an oxygen-permeable Silastic tube implanted in the subcutis of the abdominal wall. Oxygen delivery (DO2) and consumption (VO2) were determined for the gut as well as for the whole body. In six randomly allocated animals, peritonitis was induced after a stabilization period of at least 1 hr, by instillation of autologous faeces into the abdominal cavity, while the other six animals served as controls. The animals were then followed for 5 hr. pHi remained stable in the control group, whereas a drop from 7.37 to 7.02 took place in the peritonitis group. In the test group, subcutaneous oxygen tension (PscO2) already began to fall 1 hr after the induction of peritonitis, and gained the minimum at the end of the study. In peritonitis, a moderate correlation was seen between pHi and DO2 (r = 0.51 +/- 0.16); no statistical difference was noted if pHi was correlated to gut DO2 (r = 0.56 +/- 0.18).(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"41 4","pages":"261-7"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19134504","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

Transmigration routes and a delayed systemic hypotension in rats after intraperitoneal injection of endotoxin from Escherichia coli. 腹腔注射大肠杆菌内毒素后大鼠的转运途径和迟发性全身性低血压。

Circulatory shock Pub Date : 1993-11-01

K Sugimoto, M Kawamura, M Katori, M Shindo, T Ohwada

{"title":"Transmigration routes and a delayed systemic hypotension in rats after intraperitoneal injection of endotoxin from Escherichia coli.","authors":"K Sugimoto, M Kawamura, M Katori, M Shindo, T Ohwada","doi":"","DOIUrl":"","url":null,"abstract":"An intraperitoneal injection of endotoxin (ETX; 3 mg/kg) to rats caused gradual decrease in the systemic arterial blood pressure for up to 3 hr, together with decrease in heart rate, increase in hematocrit, and changes in the core temperature (an initial increase and a subsequent decrease). Pretreatment of rats with indomethacin (10 mg/kg, p.o.) prevented the decrease in the systemic blood pressure and the changes in other three parameters. The intraperitoneal injection of ETX also induced a gradual increase in exudation of plasma for up to 3 hr, with increased levels of prostaglandin (PG) E2 and 6-keto-PGF1 alpha in the peritoneal exudate. Indomethacin inhibited the exudation of plasma. The levels of ETX in the arterial and portal venous plasmas began to increase 5 min after the intraperitoneal injection of ETX, and reached levels on the order of micrograms per milliliter plasma 10-20 min after the injection. The levels of ETX in the right and left thoracic lymph nodes, but not in the mesenteric lymph nodes, increased in parallel with those in the systemic arterial plasma. In conclusion, the delayed hypotension may be attributable to the mesenteric vasodilatation induced by PGs generated in the peritoneal cavity, and the ETX injected entered the systemic circulation mainly through lymphatic vessels, but in the initial stage, a part of ETX may be transmigrated into portal vein through damaged intestine.","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"41 3","pages":"185-96"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19257020","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

Recombinant amino terminal fragment of bactericidal/permeability-increasing protein prevents hemodynamic responses to endotoxin. 抗菌/通透性增加蛋白的重组氨基末端片段阻止内毒素对血流动力学的反应。

Circulatory shock Pub Date : 1993-11-01

W S Ammons, A H Kung

{"title":"Recombinant amino terminal fragment of bactericidal/permeability-increasing protein prevents hemodynamic responses to endotoxin.","authors":"W S Ammons, A H Kung","doi":"","DOIUrl":"","url":null,"abstract":"We sought to determine if a recombinant amino terminal fragment of bactericidal/permeability increasing protein (rBPI23) alters the hemodynamic responses to endotoxin. Experiments were performed on Sprague Dawley rats anesthetized with Ketamine and xylazine. In rats challenged with a 30 min infusion of 0.25 mg/kg lipopolysaccharide (LPS; Escherichia coli 0111:B4), there were early (30-90 min), significant increases in cardiac index, heart rate, and stroke volume, accompanied by significant decreases in blood pressure and total peripheral resistance. For the remainder of the 210 min observation period, cardiac index, and stroke volume progressively declined to levels significantly below those of control rats receiving only vehicles. At the same time, blood pressure and total peripheral resistance steadily increased above the vehicle control group. Infusion of 3 mg/kg of rBPI23 abolished these LPS-induced hemodynamic responses. A dose of 1.0 mg/kg of rBPI23 was associated with a modest, significant inhibition of changes evoked by LPS, whereas 0.3 mg/kg was without significant effect. Thaumatin, a control cationic protein with molecular weight and isoelectric point similar to those of rBPI23, failed to alter any responses to LPS. These results indicate that rBPI23 produces a dose-dependent inhibition of hemodynamic changes, associated with endotoxemia, and provides further support for the potential utility of rBPI23 as a therapeutic agent in the treatment of gram-negative sepsis and infection.","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"41 3","pages":"176-84"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19257731","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

Lipopolysaccharide induces interleukin-6 release from rat peritoneal macrophages in vitro: evidence for a novel mechanism. 脂多糖诱导大鼠腹腔巨噬细胞释放白细胞介素-6:一个新机制的证据。

Circulatory shock Pub Date : 1993-11-01

R M Wright, C S Holladay, B L Spangelo

{"title":"Lipopolysaccharide induces interleukin-6 release from rat peritoneal macrophages in vitro: evidence for a novel mechanism.","authors":"R M Wright, C S Holladay, B L Spangelo","doi":"","DOIUrl":"","url":null,"abstract":"Interleukin-6 (IL-6) is a cytokine involved in the terminal differentiation of B-cells, T-cell activation, and secretion of hepatic acute phase proteins. The production of IL-6 is regulated by many factors, including IL-1 and lipopolysaccharide (LPS). Because IL-6 may be an important contributor to the effects of LPS in inflammation and septic shock, we investigated the ability of LPS to induce IL-6 release from peritoneal macrophages (m phi) in vitro. M phi were isolated from male Long-Evans rats, and cultured in 96-well tissue culture plates at 1 x 10(5) cells/well in serum-free RPMI-1640 medium. Following a 2-hr attachment period, the cells were rinsed twice to remove the nonadherent cells. LPS (0.006-100 ng/ml) stimulated IL-6 release by six- to 12-fold during a 4 hr incubation. In contrast, IL-1 beta (0.006-100 ng/ml) had no effect. Because cyclooxygenase metabolites of arachidonic acid are increased by LPS, we determined the effects of indomethacin (a cyclooxygenase inhibitor) and CGS8515 (a 5-lipoxygenase inhibitor) on LPS-induced IL-6 release. Neither indomethacin (10 microM) nor CGS8515 (2.5 microM) had any effect on basal or LPS-induced IL-6 release. Very low concentrations of LPS (0.01-1,000 pg/ml) stimulated IL-6 by two- to threefold. Pertussis toxin (10 ng/ml), which inactivates Gi protein, had no effect on LPS-induced IL-6 release from mø. Thromboxane B2 (TXB2) concentrations were also elevated with as little as 0.1 pg/ml LPS; however, pertussis toxin inhibited LPS-stimulated TXB2 release.(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"41 3","pages":"131-7"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18513892","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

Priming of phagocytes for reactive oxygen production during hepatic ischemia-reperfusion potentiates the susceptibility for endotoxin-induced liver injury. 在肝缺血-再灌注过程中，吞噬细胞激活活性氧产生，增强了内毒素诱导的肝损伤的易感性。

Circulatory shock Pub Date : 1993-11-01 DOI: 10.1016/0891-5849(93)90492-D

P. Liu, S. Vonderfecht, M. Fisher, G. McGuire, H. Jaeschke

引用次数: 39

Fluid shifts induced by the administration of 7.5% sodium chloride in 6% dextran 70 (HSD) in dehydrated swine. 在6%葡聚糖70 (HSD)中添加7.5%氯化钠引起脱水猪的体液转移。

Circulatory shock Pub Date : 1993-11-01

C B Matthew, M J Durkot, D R Patterson

引用次数: 0