Circulatory shock最新文献_第2页

Functional requirement of the two TNF receptors for induction of apoptosis in PC60 cells and the role of mitochondria in TNF-induced cytotoxicity. 两种TNF受体诱导PC60细胞凋亡的功能要求以及线粒体在TNF诱导的细胞毒性中的作用。

Circulatory shock Pub Date : 1994-12-01

P Vandenabeele, V Goossens, R Beyaert, W Declercq, J Grooten, B Vanhaesebroeck, M Van de Craen, D Vercammen, B Depuydt, G Denecker

引用次数: 0

Effect of cardiogenic shock on pharmacokinetics and tissue distribution of ampicillin-sulbactam. 心源性休克对氨苄青霉素-舒巴坦药代动力学和组织分布的影响。

Circulatory shock Pub Date : 1994-11-01

W A Arden, D E Barker, W E Strodel, K Record, G Leader, M Derbin, G Gellin, R W Schwartz

{"title":"Effect of cardiogenic shock on pharmacokinetics and tissue distribution of ampicillin-sulbactam.","authors":"W A Arden, D E Barker, W E Strodel, K Record, G Leader, M Derbin, G Gellin, R W Schwartz","doi":"","DOIUrl":"","url":null,"abstract":"A reversible cardiogenic shock model in pigs investigated shock-induced changes in the pharmacokinetics and tissue distribution of ampicillin-sulbactam and the efficacy of this antibiotic regimen in eliminating enteric bacterial translocation. Sixteen pigs were randomly allocated to 3 groups: group I (shock, ampicillin-sulbactam, n = 6), group II (no shock, ampicillin-sulbactam, n = 6), and group III (shock, no ampicillin-sulbactam, n = 4). Nalidixic acid-resistant E. coli (60 x 10(6) CFU) were instilled into a jejunal loop created in each pig, and bacterial cultures were taken from thoracic duct lymph, periportal, and mesenteric lymph nodes. Ampicillin-sulbactam was administered intravenously at a standard dose of 3 g. Results showed that 1) ampicillin and sulbactam concentrations generally increase during cardiogenic shock; 2) cardiogenic shock does not increase ampicillin concentrations in jejunum and liver; 3) during resuscitation, thoracic duct lymph ampicillin concentrations decrease; and 4) during and immediately after cardiogenic shock, standard doses of ampicillin-sulbactam appear efficacious in eliminating translocated bacteria.","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"44 3","pages":"138-47"},"PeriodicalIF":0.0,"publicationDate":"1994-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18605130","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

Effect of estradiol on endotoxin-induced changes in steroid hormone levels and lethality in male rats. 雌二醇对内毒素诱导的雄性大鼠类固醇激素水平变化和致死率的影响。

Circulatory shock Pub Date : 1994-11-01

N Christeff, M C Auclair, N Thobie, B Fertil, A Carli, E A Nunez

{"title":"Effect of estradiol on endotoxin-induced changes in steroid hormone levels and lethality in male rats.","authors":"N Christeff, M C Auclair, N Thobie, B Fertil, A Carli, E A Nunez","doi":"","DOIUrl":"","url":null,"abstract":"We examined the effect of exogenous estradiol on the changes in serum steroid hormone levels induced by a nonlethal dose of Escherichia coli endotoxin in male rats and the deaths due to nonlethal and lethal doses of endotoxin. Injection of estradiol 5 min before a nonlethal dose of endotoxin changed the serum sex steroid hormone response of male rats to endotoxin. The serum estrogen concentrations of estradiol + endotoxin-treated rats decreased by 50% (P < 0.001), while those of the endotoxin-treated rats increased (2- to 5-fold). The serum androgen concentrations of estradiol + endotoxin-treated rats did not change significantly, while those of endotoxin-treated rats dropped to 30-40%, P < 0.001. Exogenous estradiol also appeared to influence the percentage of endotoxin-induced deaths in a dose-dependent manner. It reduced the number of deaths induced by nonlethal (2 mg/kg) dose of endotoxin but increased the number of deaths induced by a highly lethal dose (8 mg/kg). These results, together with the known relationships between estrogen and the immune response, suggest that estrogens affect the course of septic shock in a complex fashion and may have either protective or deleterious effect.","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"44 3","pages":"154-9"},"PeriodicalIF":0.0,"publicationDate":"1994-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18605132","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

Ketamine suppresses tumor necrosis factor-alpha activity and mortality in carrageenan-sensitized endotoxin shock model. 氯胺酮抑制卡拉胶致敏内毒素休克模型的肿瘤坏死因子- α活性和死亡率。

Circulatory shock Pub Date : 1994-11-01

K Koga, M Ogata, I Takenaka, T Matsumoto, A Shigematsu

{"title":"Ketamine suppresses tumor necrosis factor-alpha activity and mortality in carrageenan-sensitized endotoxin shock model.","authors":"K Koga, M Ogata, I Takenaka, T Matsumoto, A Shigematsu","doi":"","DOIUrl":"","url":null,"abstract":"We have reported that an intravenous anesthetic, ketamine, has a potent suppressive effect on lipopolysaccharide (LPS)-induced TNF-alpha production in vitro [Takenaka et al., Anesthesiology 80:402-408, 1994]. The purpose of the present study was to investigate the overall effects of ketamine on hemodynamics, serum TNF-alpha level, arterial blood gases (ABGs), blood glucose level, liver function, and lethality in carrageenan (CAR)-sensitized endotoxemic models. All animals were pretreated intraperitoneally with CAR (150 mg/kg) 16 hr before LPS stimulation. The control rats were injected LPS with 0.5 mg/kg intravenously (i.v.). The ketamine-treated rats were injected with 100 mg/kg of ketamine intramuscularly 30 min before LPS (0.5 mg/kg) i.v. injection, followed by an i.v. infusion at 0, 5, or 10 mg/kg/hr. Serum TNF-alpha, ABGs, blood glucose, and hematological studies were determined at 0, 2, and 6 hr after the LPS challenge. Serum hepatocellular enzyme levels were measured at 6 hr after the injection. In CAR-sensitized rats, serum TNF-alpha activity remarkably increased in accordance with the mild decrease of mean arterial pressure (MAP) at 2 hr after LPS stimulation. In addition, severe metabolic acidosis, hypoglycemia as well as severe hepatic injury were induced at 6 hr after the LPS challenge. By contrast, ketamine treatment significantly attenuated the decrease in MAP and LPS-induced TNF-alpha activity. Ketamine also significantly improved arterial oxygen tension (PaO2), metabolic acidosis and hypoglycemia, and attenuated endotoxin-induced hepatic injury in a dose-dependent fashion. In addition, ketamine treatment significantly improved LPS-induced lethality in CAR-sensitized mice.(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"44 3","pages":"160-8"},"PeriodicalIF":0.0,"publicationDate":"1994-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18605771","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

Accumulation of an endogenous inhibitor of nitric oxide synthase during graded hemorrhagic shock. 分级失血性休克期间一氧化氮合酶内源性抑制剂的积累。

Circulatory shock Pub Date : 1994-11-01

A Aneman, V Backman, J Snygg, C von Bothmer, L Fändriks, A Pettersson

{"title":"Accumulation of an endogenous inhibitor of nitric oxide synthase during graded hemorrhagic shock.","authors":"A Aneman, V Backman, J Snygg, C von Bothmer, L Fändriks, A Pettersson","doi":"","DOIUrl":"","url":null,"abstract":"Asymmetric dimethylarginine (ADMA) represents an endogenous inhibitor of nitric oxide (NO) production. The production of ADMA has been shown to increase during cellular stress, e.g., hypoxia. Furthermore, ADMA has recently been reported to accumulate in plasma during terminal renal failure as a consequence of diminished urinary excretion. Since tissue hypoxia and oliguria are both characteristics of severe hemorrhagic shock, this study was performed in order to establish whether plasma concentrations of ADMA increase during hemorrhagic shock. Six pigs were subjected to graded hemorrhage (20% and 40% of the calculated blood volume), resulting in significant (P < 0.05) reductions in blood pressure and cardiac output (from 98 +/- 4 to 36 +/- 5 mm Hg and from 3.0 +/- 0.2 to 1.4 +/- 0.2 L/min, respectively). Plasma ADMA concentrations as determined by high-performance liquid chromatography (HPLC) increased from a pre-hemorrhage value of 3.4 +/- 0.3 microM to 3.9 +/- 0.4 microM (ns) and 5.2 +/- 0.4 microM (P < 0.05), respectively. The present study demonstrates that plasma ADMA concentrations increase significantly during hemorrhagic shock. Thus, inhibition of the arginine-nitric oxide pathway as a result of ADMA accumulation, may represent an additional physiological mechanism to maintain systemic blood pressure in response to acute hypovolemia.","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"44 3","pages":"111-4"},"PeriodicalIF":0.0,"publicationDate":"1994-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18547033","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 E. coli-derived tissue factor pathway inhibitor reduces coagulopathic and lethal effects in the baboon gram-negative model of septic shock. 重组大肠杆菌来源的组织因子途径抑制剂在狒狒革兰氏阴性脓毒性休克模型中降低凝血病理和致死效应。

Circulatory shock Pub Date : 1994-11-01

C Carr, G S Bild, A C Chang, G T Peer, M O Palmier, R B Frazier, M E Gustafson, T C Wun, A A Creasey, L B Hinshaw

{"title":"Recombinant E. coli-derived tissue factor pathway inhibitor reduces coagulopathic and lethal effects in the baboon gram-negative model of septic shock.","authors":"C Carr, G S Bild, A C Chang, G T Peer, M O Palmier, R B Frazier, M E Gustafson, T C Wun, A A Creasey, L B Hinshaw","doi":"","DOIUrl":"","url":null,"abstract":"Excessive coagulation is a typical response to the vascular injury occurring in gram negative sepsis. This study evaluated the pharmacological effects of the use of a recombinant Escherichia coli derived form of tissue factor pathway inhibitor (ala-TFPI) in a baboon model of septic shock. Several doses of ala-TFPI were administered either 30 or 120 min after the initiation of a lethal intravenous infusion of E. coli into baboons. Treatment at 30 min with either 2.7 or 7.4 mg/kg of ala-TFPI resulted in the same survival rates and attenuation of both the coagulation response and cellular injury, as measured by clinical chemistry. When administration of ala-TFPI was delayed for 120 min, a dose of ala-TFPI protein continued to provide a benefit to survival. Ala-TFPI reduced the drop in mean systemic arterial pressure compared to control baboons in addition to partially attenuating the coagulopathic response. Baboons given ala-TFPI also maintained lower levels of plasma interleukin-6 (IL-6) and thrombin-antithrombin. These results suggest that the site of action of the protein may involve the later stage components of the coagulation and inflammatory pathways.","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"44 3","pages":"126-37"},"PeriodicalIF":0.0,"publicationDate":"1994-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18605129","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

Erythrocyte Ca2+ pump is defective during sepsis. 败血症时红细胞Ca2+泵有缺陷。

Circulatory shock Pub Date : 1994-11-01

Y T Lau, C C Hsieh, M S Liu, T L Hwang, M F Chen, H S Cheng

引用次数: 0

Effect of superoxide dismutase on hemorrhagic hypotension and retransfusion-evoked middle cerebral artery endothelial dysfunction. 超氧化物歧化酶对出血性低血压和再输血诱发的大脑中动脉内皮功能障碍的影响。

Circulatory shock Pub Date : 1994-11-01

C Szabó, C Csáki, Z Benyó, J Marczis, M Reivich, A G Kovách

{"title":"Effect of superoxide dismutase on hemorrhagic hypotension and retransfusion-evoked middle cerebral artery endothelial dysfunction.","authors":"C Szabó, C Csáki, Z Benyó, J Marczis, M Reivich, A G Kovách","doi":"","DOIUrl":"","url":null,"abstract":"Unlabelled: Middle cerebral artery rings (MCA) were prepared from control and hemorrhagic hypotension and retransfusion-subjected (HHR) cats, with or without superoxide dismutase (SOD) treatment. Two-mm-long MCA segments were suspended in organ chambers containing Krebs-Henseleit solution (37 degrees C, gassed with 95% O2-5% CO2) for isometric force measurements. HHR was produced by bleeding to 90, 70, and 50 mmHg MAP and maintained for 15 min at each level, followed by retransfusion. HHR resulted in a marked attenuation of the acetylcholine- and ATP-induced endothelium-dependent relaxations of the MCA in vitro. Relaxations induced by the nitric oxide (NO) donor SIN-1 remained unaltered. In vitro treatment of the vessels with SOD (150 U/ml), facilitated the acetylcholine-induced relaxations both in the control arteries and in the vessels after HHR. In the vessel rings from cats that received in vivo SOD (10 mg/kg initial bolus, followed by 0.1-mg/kg/min infusion) during HHR, cholinergic relaxations were more pronounced than in the HHR untreated cats. The ATP-induced relaxations, however, remained attenuated after SOD treatment, except for the highest dose (10(-5) M) that was applied.Conclusion: Superoxide release attenuates the endothelium-dependent relaxation by acetylcholine both in control arteries and after HHR in vitro. The protective effect of in vivo SOD treatment on cerebrovascular endothelium-dependent reactivity in cats suggests that superoxide free radicals contribute to the development of the endothelium dysfunction in MCA rings after HHR.","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"44 3","pages":"104-10"},"PeriodicalIF":0.0,"publicationDate":"1994-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18605126","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

Molecular mechanisms of natural resistance to mycobacterial infections. 自然抵抗分枝杆菌感染的分子机制。

Circulatory shock Pub Date : 1994-11-01

D Radzioch, I Kramnik, E Skamene

{"title":"Molecular mechanisms of natural resistance to mycobacterial infections.","authors":"D Radzioch, I Kramnik, E Skamene","doi":"","DOIUrl":"","url":null,"abstract":"Natural resistance to infection with intracellular parasites is controlled by a dominant gene on mouse chromosome 1, called Bcg. Bcg affects the capacity of macrophages to destroy ingested intracellular parasites early during infection. Reactive nitrogen intermediates (RNI) have been implicated in the interferon-gamma (IFN-gamma)-induced antimicrobial action of macrophages against a wide variety of pathogens. To determine whether Bcg (Nramp) is involved in the production of RNI, these studies have taken advantage of the recent cloning of the Bcg candidate gene, designated Nramp. The expression of Bcg has been down-regulated in the B10R (Bcgr) macrophage cell line using a ribozyme hybrid to site-specifically cleave the Nramp mRNA. Following activation with IFN-gamma, the secretory activity [nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha)] and surface marker expression (la antigen) of these Bcg(Nramp) ribozyme-transfected macrophages were markedly lower than in activated control mock-transfected macrophages (B10R-CTL). However, there was no difference in NO production of B10R-Bcg(Nramp)Rb and B10R-CTL macrophages if the treatment with IFN-gamma occurred in the presence of lipopolysaccharide (LPS). These studies support the hypothesis that the Bcg(Nramp) gene is involved in the regulation of early signaling that occurs in macrophages activated with IFN-gamma. Furthermore, it seems that IFN-gamma, but not LPS-induced activation is affected by the inhibition of Bcg(Nramp) gene expression. Definitive evidence will be provided by transfection experiments that will show whether the Bcgr allele of Bcg(Nramp) can restore NO production of the Bcgs macrophage.","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"44 3","pages":"115-20"},"PeriodicalIF":0.0,"publicationDate":"1994-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18605127","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

Modulation of lung injury by platelet-activating factor antagonism in nonhypotensive porcine endotoxemia. 非低血压猪内毒素血症中血小板活化因子拮抗对肺损伤的调节作用。

Circulatory shock Pub Date : 1994-11-01

F M Abu-Zidan, S Walther, S Lennquist

引用次数: 0