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抗炎剂可抑制白三烯及受刺激的人中性粒细胞诱导的微血管通透性。

Antiinflammatory agents inhibit microvascular permeability induced by leukotrienes and by stimulated human neutrophils.

作者信息

Dunham B M, Hechtman H B, Valeri C R, Shepro D

出版信息

Microcirc Endothelium Lymphatics. 1984 Aug;1(4):465-89.

PMID:6100791
Abstract

One pathologic change common to the inflammatory process is loss of microvessel membrane integrity which results in edema. Polymorphonuclear leukocytes (PMN) are primary contributors to the development of edema because they cause tissue injury which alters vascular permeability and hemodynamics. The aim of this study was to assess the influence of arachidonic acid metabolites generated by activation of human PMN on the in vivo microvascular preparation of the hamster cheek pouch. Fluorescein-labeled dextran MW: 150,000 was used to assess microvascular permeability. Human PMN were activated with arachidonic acid (AA) and the calcium ionophore A23187, and the supernatant retained for testing. Topical application of the PMN supernatant, purified LTD4 or LTB4 resulted in marked extravasation of macromolecules from post-capillary venules of control hamsters. The extravasation was reduced when hamsters were pretreated with indomethacin (5 mg/kg), imidazole (25 mg/kg), ketoconazole (10 mg/kg), 13-azaprostanoic acid (30 mg/kg), FPL 55712 (1 mg/kg) and dimethylthiourea (500 mg/kg). The interpretation of the results suggests that the increased vascular permeability induced by PMN secretions may be mediated in part by the thromboxane pathway.

摘要

炎症过程中常见的一种病理变化是微血管膜完整性丧失,这会导致水肿。多形核白细胞(PMN)是水肿形成的主要促成因素,因为它们会造成组织损伤,进而改变血管通透性和血流动力学。本研究的目的是评估人PMN激活后产生的花生四烯酸代谢产物对仓鼠颊囊体内微血管制剂的影响。使用荧光素标记的葡聚糖(分子量:150,000)来评估微血管通透性。用人花生四烯酸(AA)和钙离子载体A23187激活人PMN,并保留上清液用于测试。局部应用PMN上清液、纯化的白三烯D4(LTD4)或白三烯B4(LTB4)会导致对照仓鼠毛细血管后微静脉出现明显的大分子外渗。当仓鼠用吲哚美辛(5毫克/千克)、咪唑(25毫克/千克)、酮康唑(10毫克/千克)、13-氮杂前列腺酸(30毫克/千克)、FPL 55712(1毫克/千克)和二甲基硫脲(500毫克/千克)预处理时,外渗减少。结果解释表明,PMN分泌物诱导的血管通透性增加可能部分由血栓素途径介导。

相似文献

1
Antiinflammatory agents inhibit microvascular permeability induced by leukotrienes and by stimulated human neutrophils.抗炎剂可抑制白三烯及受刺激的人中性粒细胞诱导的微血管通透性。
Microcirc Endothelium Lymphatics. 1984 Aug;1(4):465-89.
2
Oxygen free radicals and leukotriene B4 induced increase in vascular leakage is mediated by polymorphonuclear leukocytes.氧自由基和白三烯B4诱导的血管通透性增加是由多形核白细胞介导的。
Agents Actions Suppl. 1982;11:63-72.
3
Oxygen radicals are not a prerequisite for neutrophil-mediated increased vascular permeability.氧自由基并非中性粒细胞介导的血管通透性增加的必要条件。
Lab Invest. 1988 May;58(5):559-64.
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Topical citrate inhibits the adherence of neutrophils to postcapillary venules.
Cornea. 1990 Jul;9(3):238-45.
5
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Diapedesis and the permeability of venous microvessels to protein macromolecules: the impact of leukotriene B4 (LTB4).白细胞渗出及静脉微血管对蛋白质大分子的通透性:白三烯B4(LTB4)的影响。
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Leukotriene B4-induced permeability increase in postcapillary venules and its inhibition by three different antiinflammatory drugs.白三烯B4诱导毛细血管后微静脉通透性增加及其被三种不同抗炎药物的抑制作用。
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8
[Pharmacology of the leukotrienes].[白三烯的药理学]
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Leukocyte inhibitory factor (LIF) potentiates human macrophage aggregation and activation responses to calcium ionophore A23187 and directly induces leukotriene B4 and thromboxane A2 release.白细胞抑制因子(LIF)可增强人巨噬细胞对钙离子载体A23187的聚集和激活反应,并直接诱导白三烯B4和血栓素A2的释放。
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The influence of acetylshikonin, a natural naphthoquinone, on the production of leukotriene B4 and thromboxane A2 in rat neutrophils.天然萘醌乙酰紫草素对大鼠中性粒细胞中白三烯B4和血栓素A2生成的影响。
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引用本文的文献

1
Leukotriene inhibition in hamster periodontitis. A histochemical and morphometric study.白三烯抑制在仓鼠牙周炎中的作用。组织化学和形态计量学研究。
Mediators Inflamm. 1992;1(5):335-9. doi: 10.1155/S0962935192000504.
2
The preventive effect of ketoconazole on experimental metastasis from a human pancreatic carcinoma may be related to its effect on prostaglandin synthesis.酮康唑对人胰腺癌实验性转移的预防作用可能与其对前列腺素合成的影响有关。
Int J Gastrointest Cancer. 2002;32(1):23-30. doi: 10.1385/IJGC:32:1:23.
3
Leukotriene induction of TxB2 in cultured bovine aortic endothelial cells.
白三烯在培养的牛主动脉内皮细胞中诱导血栓素B2的产生。
Inflammation. 1984 Sep;8(3):313-21. doi: 10.1007/BF00916419.
4
Thromboxane A2 moderates permeability after limb ischemia.血栓素A2可减轻肢体缺血后的通透性。
Ann Surg. 1985 Nov;202(5):642-6. doi: 10.1097/00000658-198511000-00017.
5
Limb ischemia-induced increase in permeability is mediated by leukocytes and leukotrienes.肢体缺血诱导的通透性增加是由白细胞和白三烯介导的。
Ann Surg. 1988 Dec;208(6):755-60. doi: 10.1097/00000658-198812000-00014.
6
Eicosanoid modulation of stress fibers in cultured bovine aortic endothelial cells.二十碳类化合物对培养的牛主动脉内皮细胞中应力纤维的调节作用。
Inflammation. 1985 Dec;9(4):439-50. doi: 10.1007/BF00916343.
7
Leukotriene B4-induced permeability increase in postcapillary venules and its inhibition by three different antiinflammatory drugs.白三烯B4诱导毛细血管后微静脉通透性增加及其被三种不同抗炎药物的抑制作用。
Inflammation. 1989 Dec;13(6):693-705. doi: 10.1007/BF00914313.
8
Evidence that prolonged histamine suffusions produce transient increases in vascular permeability subsequent to the formation of venular macromolecular leakage sites. Proof of the Majno-Palade hypothesis.有证据表明,在小静脉大分子渗漏部位形成后,长时间组胺灌注会导致血管通透性短暂增加。这证明了马伊诺-帕拉德假说。
Am J Pathol. 1986 Jun;123(3):570-6.