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1
Mediation systems in bacterial lipopolysaccharide-induced hypotension and disseminated intravascular coagulation. I. The role of complement.细菌脂多糖诱导的低血压和弥散性血管内凝血中的介导系统。I. 补体的作用。
J Exp Med. 1975 Dec 1;142(6):1570-90. doi: 10.1084/jem.142.6.1570.
2
Role of complement in lethal bacterial lipopolysaccharide-induced hypotensive and coagulative changes.补体在致死性细菌脂多糖诱导的低血压和凝血变化中的作用。
Infect Immun. 1978 Jan;19(1):204-11. doi: 10.1128/iai.19.1.204-211.1978.
3
Complement-dependent hemodynamic and hematologic changes in the rabbit.兔体内补体依赖的血流动力学和血液学变化。
Inflammation. 1977 Sep;2(3):199-216. doi: 10.1007/BF00917596.
4
The distribution of lipopolysaccharide in normocomplementemic and C3-depleted rabbits and rhesus monkeys.脂多糖在补体正常和C3缺失的兔及恒河猴体内的分布
Am J Pathol. 1980 Nov;101(2):245-64.
5
Complement independent lipopolysaccharide (LPS) induced hypotension and disseminated intravascular coagulation: a correlation of LPS structure with in vivo and in vitro biological activities.补体非依赖性脂多糖(LPS)诱导的低血压和弥散性血管内凝血:LPS结构与体内外生物学活性的相关性
Adv Exp Med Biol. 1976;73 PT-A:339-49. doi: 10.1007/978-1-4684-3297-8_28.
6
The effect of complement depletion on bacterial lipopolysaccharide (LPS)-induced hemodynamic and hematologic changes in the Rhesus monkey.补体耗竭对恒河猴体内细菌脂多糖(LPS)诱导的血流动力学和血液学变化的影响。
Am J Pathol. 1978 Jul;92(1):227-40.
7
Contribution of complement activation to the rise in blood levels of 6-oxo-prostaglandin F1 alpha during endotoxin-induced hypotension in rabbits.补体激活对兔内毒素诱导低血压期间6-氧代前列腺素F1α血水平升高的作用。
Eur J Pharmacol. 1982 Apr 8;79(1-2):91-9. doi: 10.1016/0014-2999(82)90578-7.
8
Participation of tumor necrosis factor in the mediation of gram negative bacterial lipopolysaccharide-induced injury in rabbits.肿瘤坏死因子参与革兰氏阴性菌脂多糖诱导的家兔损伤的介导过程。
J Clin Invest. 1988 Jun;81(6):1925-37. doi: 10.1172/JCI113540.
9
Interactions of the classical and alternate complement pathway with endotoxin lipopolysaccharide. Effect on platelets and blood coagulation.经典补体途径和替代补体途径与内毒素脂多糖的相互作用。对血小板和血液凝固的影响。
J Clin Invest. 1973 Feb;52(2):370-6. doi: 10.1172/JCI107193.
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Expression of tissue factor and interleukin-1 beta in a novel rabbit model of disseminated intravascular coagulation induced by carrageenan and lipopolysaccharide.角叉菜胶和脂多糖诱导的新型兔弥散性血管内凝血模型中组织因子和白细胞介素-1β的表达
Pathobiology. 1995;63(6):328-40. doi: 10.1159/000163969.

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1
Therapy with antibody to tumor necrosis factor against endotoxin shock in rabbits.抗内毒素休克兔肿瘤坏死因子抗体治疗。
J Anesth. 1994 Sep;8(3):305-10. doi: 10.1007/BF02514656.
2
TLR4 signaling is coupled to SRC family kinase activation, tyrosine phosphorylation of zonula adherens proteins, and opening of the paracellular pathway in human lung microvascular endothelia.Toll样受体4(TLR4)信号传导与SRC家族激酶激活、紧密连接蛋白的酪氨酸磷酸化以及人肺微血管内皮细胞旁细胞途径的开放相关联。
J Biol Chem. 2008 May 9;283(19):13437-49. doi: 10.1074/jbc.M707986200. Epub 2008 Mar 7.
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Infect Immun. 2002 May;70(5):2519-25. doi: 10.1128/IAI.70.5.2519-2525.2002.
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Clindamycin suppresses endotoxin released by ceftazidime-treated Escherichia coli O55:B5 and subsequent production of tumor necrosis factor alpha and interleukin-1 beta.克林霉素可抑制头孢他啶处理的大肠杆菌O55:B5释放内毒素以及随后肿瘤坏死因子α和白细胞介素-1β的产生。
Antimicrob Agents Chemother. 1999 Mar;43(3):616-22. doi: 10.1128/AAC.43.3.616.
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The third component of complement protects against Escherichia coli endotoxin-induced shock and multiple organ failure.补体的第三成分可抵御大肠杆菌内毒素诱导的休克和多器官衰竭。
J Exp Med. 1994 Feb 1;179(2):569-78. doi: 10.1084/jem.179.2.569.
6
The distribution of lipopolysaccharide in normocomplementemic and C3-depleted rabbits and rhesus monkeys.脂多糖在补体正常和C3缺失的兔及恒河猴体内的分布
Am J Pathol. 1980 Nov;101(2):245-64.
7
Role of complement activation in a model of adult respiratory distress syndrome.补体激活在成人呼吸窘迫综合征模型中的作用。
J Clin Invest. 1980 Aug;66(2):375-82. doi: 10.1172/JCI109866.
8
In vivo clearance and tissue distribution of C5a and C5a des arginine complement fragments in rabbits.兔体内C5a和C5a去精氨酸补体片段的清除率及组织分布
J Clin Invest. 1982 Dec;70(6):1177-83. doi: 10.1172/jci110716.
9
Alternative complement pathway activation increases mortality in a model of burn injury in mice.替代补体途径激活增加小鼠烧伤模型的死亡率。
J Clin Invest. 1982 Dec;70(6):1170-6. doi: 10.1172/jci110715.
10
Intravascular coagulation in mice by the compact-colony-forming active substance (CCFAS) extracted from a strain of Staphylococcus aureus.用从一株金黄色葡萄球菌中提取的致密菌落形成活性物质(CCFAS)诱导小鼠血管内凝血。
Br J Exp Pathol. 1981 Dec;62(6):583-90.

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Complement in endotoxin shock: effect of complement depletion on the early hypotensive phase.补体在内毒素休克中的作用:补体耗竭对内毒素休克早期低血压期的影响。
Infect Immun. 1970 Jul;2(1):38-41. doi: 10.1128/iai.2.1.38-41.1970.
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PATHOGENIC FACTORS IN VASULAR LESIONS OF EXPERIMENTAL SERUM SICKNESS.实验性血清病血管病变中的致病因素
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PLATELET SEQUESTRATION IN MAN. I. METHODS.人体中的血小板隔离。一、方法。
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Reduction of serum complement in rabbits after injection of endotoxin.注射内毒素后家兔血清补体的降低。
J Exp Med. 1962 Oct 1;116(4):477-90. doi: 10.1084/jem.116.4.477.
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Mechanisms of the hemodynamic effects of endotoxin.内毒素血流动力学效应的机制。
Physiol Rev. 1960 Apr;40:245-79. doi: 10.1152/physrev.1960.40.2.245.
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A new method for the extraction of R lipopolysaccharides.一种提取R脂多糖的新方法。
Eur J Biochem. 1969 Jun;9(2):245-9. doi: 10.1111/j.1432-1033.1969.tb00601.x.
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The interaction of leukocytes and the kinin system.白细胞与激肽系统的相互作用。
Biochem Pharmacol. 1968 Mar:Suppl:271-81. doi: 10.1016/0006-2952(68)90313-4.
8
Protective function of C6 in rabbits treated with bacterial endotoxin.C6在接受细菌内毒素治疗的兔子中的保护作用。
J Immunol. 1971 Apr;106(4):1125-7.
9
An ultrastructural study of endotoxin induced damage in rabbit mesenteric arteries.内毒素诱导兔肠系膜动脉损伤的超微结构研究。
Br J Exp Pathol. 1971 Feb;52(1):75-80.
10
The role of endotoxin in disseminated intravascular coagulation.内毒素在弥散性血管内凝血中的作用。
Thromb Diath Haemorrh Suppl. 1969;36:125-49.

细菌脂多糖诱导的低血压和弥散性血管内凝血中的介导系统。I. 补体的作用。

Mediation systems in bacterial lipopolysaccharide-induced hypotension and disseminated intravascular coagulation. I. The role of complement.

作者信息

Ulevitch R J, Cochrane C G, Henson P M, Morrison D C, Doe W F

出版信息

J Exp Med. 1975 Dec 1;142(6):1570-90. doi: 10.1084/jem.142.6.1570.

DOI:10.1084/jem.142.6.1570
PMID:1104750
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2190070/
Abstract

We have studied the role of complement in lipopolysaccharide (LPS)-induced hypotension and disseminated intravascular coagulation (DIC) by comparing the effects of injection of three preparations of LPS from E. Coli 0111:B4, S. minnesota Re595, and S. marcescens. Injections of nonlethal doses of these LPS preparations into normal rabbits produced decreases in mean arterial blood pressure during a 5-h period. When rabbits treated with cobra venom factor (CoF) to deplete C3 were injected with the various LPS preparations, mean arterial pressures fell at a rate and extent essentially identical to that observed in normal rabbits. Rabbits genetically deficient in C6 also demonstrated LPS-induced hypotensive changes. Only minimal, or no changes in plasma C3 levels or serum CH50 values were detected in normal rabbits after LPS injection. Hypotensive changes were also induced in rabbits when complement was rapidly activated by intravenous injection of CoF. In contrast to the hypotension induced by LPS, the fall in arterial pressure associated with the consumption of complement was short lived and required the rapid consumption of considerable amounts of C3. The occurrence of DIC noted in normal rabbits injected with each preparation of LPS was not inhibited in either rabbits treated with cobra factor or in C6-deficient rabbits. The DIC was most pronounced after injection of Re595 and S. marcescens LPS. Injection of the various LPS preparations produced a rapid disappearance of circulating neutrophils and mononuclear cells, which occurred with the same kinetics and to the same extent in normal, CoF-treated, and C6-deficient rabbits. Injection of either Re595 LPS or S. marcescens LPS produced a biphasic disappearance of circulating 51Cr-platelets. In contrast, injection of 0111:B4 LPS affected only slightly the rate of disappearance of 51Cr-platelets. Depletion of C3 by cobra factor treatment had no effect on the disappearance of platelets in animals injected with 0111:B4. In marked contrast cobra factor treatment greatly reduced the initial rapid disappearance of platelets in rabbits injected with either Re595 or S. marcescens LPS, but had no effect in the secondary disappearance phase.

摘要

我们通过比较注射三种来自大肠杆菌0111:B4、明尼苏达沙门氏菌Re595和粘质沙雷氏菌的脂多糖(LPS)制剂的效果,研究了补体在LPS诱导的低血压和弥散性血管内凝血(DIC)中的作用。将这些LPS制剂的非致死剂量注射到正常兔体内,在5小时内平均动脉血压下降。当用眼镜蛇毒因子(CoF)处理以耗尽C3的兔注射各种LPS制剂时,平均动脉压下降的速率和程度与正常兔中观察到的基本相同。C6基因缺陷的兔也表现出LPS诱导的低血压变化。LPS注射后,正常兔的血浆C3水平或血清CH50值仅检测到最小变化或无变化。当通过静脉注射CoF快速激活补体时,兔也会出现低血压变化。与LPS诱导的低血压相反,与补体消耗相关的动脉压下降是短暂的,并且需要大量C3的快速消耗。在注射每种LPS制剂的正常兔中观察到的DIC的发生,在用眼镜蛇因子处理的兔或C6缺陷兔中均未受到抑制。注射Re595和粘质沙雷氏菌LPS后DIC最为明显。注射各种LPS制剂导致循环中的中性粒细胞和单核细胞迅速消失,在正常、CoF处理和C6缺陷的兔中以相同的动力学和相同的程度发生。注射Re595 LPS或粘质沙雷氏菌LPS会导致循环中的51Cr标记血小板出现双相消失。相比之下,注射0111:B4 LPS对51Cr标记血小板的消失速率影响很小。用眼镜蛇因子处理耗尽C3对注射0111:B4的动物中血小板的消失没有影响。与之形成鲜明对比的是,眼镜蛇因子处理大大减少了注射Re595或粘质沙雷氏菌LPS的兔中血小板最初的快速消失,但对二次消失阶段没有影响。