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相似文献

1
The role of the platelet in the generalized Shwartzman reaction.血小板在全身性施瓦茨曼反应中的作用。
J Exp Med. 1969 Mar 1;129(3):585-90. doi: 10.1084/jem.129.3.585.
2
PLATELETS AND THE SHWARTZMAN PHENOMENON.血小板与施瓦茨曼现象
J Exp Med. 1965 Feb 1;121(2):235-46. doi: 10.1084/jem.121.2.235.
3
Effect of platelet antiserum on the precipitation of soluble fibrin by endotoxin.血小板抗血清对内毒素诱导可溶性纤维蛋白沉淀的影响。
Thromb Haemost. 1976 Feb 29;35(1):237-48.
4
Effect of platelet antiserum on the activation of intravascular coagulation by endotoxin.血小板抗血清对内毒素激活血管内凝血的作用。
Thromb Res. 1977 Jan;10(1):47-70. doi: 10.1016/0049-3848(77)90080-9.
5
The role of the platelet and leukocyte in disseminated intravascular coagulation caused by bacterial endotoxin.血小板和白细胞在细菌内毒素所致弥散性血管内凝血中的作用。
Thromb Diath Haemorrh Suppl. 1969;36:151-7.
6
The effect of leukocyte and platelet transfusion on the activation of intravascular coagulation by endotoxin in granulocytopenic and thrombocytopenic rabbits.白细胞和血小板输注对粒细胞减少和血小板减少兔体内内毒素激活血管内凝血的影响。
Am J Pathol. 1976 Aug;84(2):239-58.
7
The effects of indomethacin on the generalized shwartzman reaction.消炎痛对全身性施瓦茨曼反应的影响。
Am J Pathol. 1978 Jan;90(1):7-22.
8
Vascular lesions: possible pathogenetic basis of the generalized Shwartzman reaction.血管病变:全身性施瓦茨曼反应的可能发病机制基础。
Science. 1970 Nov 27;170(3961):986-8. doi: 10.1126/science.170.3961.986.
9
Failure of cobra venom factor to prevent the generalized Shwartzman reaction and loss of renal cortical fibrinolytic activity.眼镜蛇毒因子未能预防全身性施瓦茨曼反应及肾皮质纤溶活性丧失。
Am J Pathol. 1974 Jan;74(1):19-31.
10
Induction of generalized shwartzman reaction(GSR) in irradiated rabbits by a single injection of endotoxin.单次注射内毒素在受辐照兔中诱导全身性施瓦茨曼反应(GSR)。
Thromb Res. 1976 Apr;8(4):501-12. doi: 10.1016/0049-3848(76)90228-0.

引用本文的文献

1
Vasomotor factors in the Shwartzman phenomenon.施瓦茨曼现象中的血管舒缩因素。
Am J Pathol. 1969 Dec;57(3):559-80.
2
Heterophile antibodies and tissue injury. 3. A role for platelets in the development of lethal vascular injury during Forssman shock in guinea pigs.嗜异性抗体与组织损伤。3. 血小板在豚鼠福斯曼休克致死性血管损伤发展中的作用。
Am J Pathol. 1973 Aug;72(2):179-200.
3
Activation of the alternate complement pathway by autologous red cell stroma.自体红细胞基质激活替代补体途径。
J Exp Med. 1973 Sep 1;138(3):715-22. doi: 10.1084/jem.138.3.715.
4
The participation of the platelet in the vascular response to endotoxemia in the rabbit eye.血小板在兔眼对内毒素血症的血管反应中的参与情况。
Am J Pathol. 1973 Jan;70(1):25-44.
5
Heterophile antibodies and tissue injury. 1. Ultrastructure of pulmonary vascular lesions produced by Forssman antiserum in guinea-pigs.嗜异性抗体与组织损伤。1. 福斯曼抗血清在豚鼠中引起的肺血管病变的超微结构
Immunology. 1972 Jan;22(1):93-102.
6
The requirement for platelets in the active Arthus reaction.主动Arthus反应中对血小板的需求。
Am J Pathol. 1971 Aug;64(2):257-70.
7
Platelets mediate neutrophil-dependent immune complex nephritis in the rat.血小板介导大鼠中性粒细胞依赖性免疫复合物肾炎。
J Clin Invest. 1988 Oct;82(4):1225-35. doi: 10.1172/JCI113720.
8
Effects of intravascular clotting on the activation of the complement system: The role of the platelet.血管内凝血对补体系统激活的影响:血小板的作用。
Am J Pathol. 1975 Mar;78(3):525-36.
9
The effect of leukocyte and platelet transfusion on the activation of intravascular coagulation by endotoxin in granulocytopenic and thrombocytopenic rabbits.白细胞和血小板输注对粒细胞减少和血小板减少兔体内内毒素激活血管内凝血的影响。
Am J Pathol. 1976 Aug;84(2):239-58.
10
Accumulation of platelets at acute inflammatory sites [proceedings].急性炎症部位血小板的聚集[会议记录]
Br J Pharmacol. 1977 Sep;61(1):158P-159P.

本文引用的文献

1
Morphology and enumeration of human blood platelets.人体血小板的形态学与计数
J Appl Physiol. 1950 Dec;3(6):365-77. doi: 10.1152/jappl.1950.3.6.365.
2
PLATELETS AND THE SHWARTZMAN PHENOMENON.血小板与施瓦茨曼现象
J Exp Med. 1965 Feb 1;121(2):235-46. doi: 10.1084/jem.121.2.235.
3
Effects of bacterial endotoxin on rabbit platelets. II. Enhancement of platelet factor 3 activity in vitro and in vivo.细菌内毒素对兔血小板的作用。II. 体内外血小板第3因子活性的增强。
J Exp Med. 1962 Nov 1;116(5):619-33. doi: 10.1084/jem.116.5.619.
4
Antigen-antibody reaction in the pathogenesis of bilateral renal cortical necrosis.双侧肾皮质坏死发病机制中的抗原抗体反应。
J Exp Med. 1963 Mar 1;117(3):365-76. doi: 10.1084/jem.117.3.365.
5
Alterations in the blood coagulation system induced by bacterial endotoxin. I. In vivo (generalized Shwartzman reaction).细菌内毒素引起的血液凝固系统改变。I. 体内(全身性施瓦茨曼反应)
J Exp Med. 1958 Mar 1;107(3):353-67. doi: 10.1084/jem.107.3.353.
6
Studies on the generalized Shwartzman reaction. IV. Prevention of the local and generalized Shwartzman reactions with heparin.全身性施瓦茨曼反应的研究。IV. 用肝素预防局部和全身性施瓦茨曼反应
J Exp Med. 1953 Jun;97(6):871-88. doi: 10.1084/jem.97.6.871.
7
Studies on the generalized Shwartzman reaction: I. General observations concerning the phenomenon.关于全身性施瓦茨曼反应的研究:I. 关于该现象的一般观察
J Exp Med. 1952 Dec;96(6):605-24. doi: 10.1084/jem.96.6.605.
8
Intravascular activation of the clotting system with phospholipids. Production of the generalized Shwartzman reaction with platelet factor 3.凝血系统与磷脂的血管内激活。利用血小板第3因子产生全身性施瓦茨曼反应。
Blood. 1965 Nov;26(5):541-53.
9
Platelet factor 3 and the generalized Shwartzman reaction.血小板第3因子与全身性施瓦茨曼反应
Thromb Diath Haemorrh. 1967 Dec 31;18(3-4):726-35.

血小板在全身性施瓦茨曼反应中的作用。

The role of the platelet in the generalized Shwartzman reaction.

作者信息

Margaretten W, McKay D G

出版信息

J Exp Med. 1969 Mar 1;129(3):585-90. doi: 10.1084/jem.129.3.585.

DOI:10.1084/jem.129.3.585
PMID:4886043
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2138615/
Abstract

Rabbits were injected with an antiplatelet serum to produce selective thrombocytopenia without inducing a significant alteration of their leukocyte counts. Thrombocytopenic levels persisted for 8 hr after the injection of platelet antiserum. During this time, the generalized Shwartzman reaction could not be provoked with the second injection of endotoxin. Since platelet phospholipid is required for the formation of plasma thromboplastin, the results indicate that platelets are essential to the evolution of the generalized Shwartzman reaction and endotoxin triggers the intrinsic rather than the extrinsic clotting system to elicit the lesions.

摘要

给兔子注射抗血小板血清以产生选择性血小板减少症,而不引起其白细胞计数的显著改变。注射血小板抗血清后,血小板减少水平持续8小时。在此期间,第二次注射内毒素不能引发全身性施瓦茨曼反应。由于血浆凝血活酶的形成需要血小板磷脂,结果表明血小板对于全身性施瓦茨曼反应的发展至关重要,并且内毒素触发内源性而非外源性凝血系统以引发病变。