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血小板活化因子拮抗剂对眼血管通透性的非前列腺素依赖性抑制作用。

Prostaglandin-independent inhibition of ocular vascular permeability by a platelet-activating factor antagonist.

作者信息

Rubin R M, Samples J R, Rosenbaum J T

机构信息

Oregon Health Sciences University, Portland 97201.

出版信息

Arch Ophthalmol. 1988 Aug;106(8):1116-20. doi: 10.1001/archopht.1988.01060140272040.

DOI:10.1001/archopht.1988.01060140272040
PMID:3261165
Abstract

Platelet-activating factor (PAF), a lipid mediator of inflammation, may markedly increase vascular permeability. We assessed the ability of the PAF antagonist SRI 63-441 to inhibit ocular vascular permeability induced by the intravenous injection of endotoxin or anterior chamber paracentesis. The PAF antagonist SRI 63-441 significantly blocked ocular vascular permeability following either intravenous endotoxin or anterior chamber paracentesis as determined by the reduction in accumulation of 70,000-molecular-weight fluorescein isothiocyanate-conjugated dextran or serum proteins into the anterior chamber. SRI 63-441 did not reduce increases in aqueous humor prostaglandin E2 levels. The efficacy of the PAF antagonist was additive in combination with either topical indomethacin or topical corticosteroid. Combined therapy almost completely prevented increases in ocular vascular permeability. These data support the conclusion that multiple mediators contribute to ocular vascular permeability and that combinations of pharmacologic agents may be superior to a single drug.

摘要

血小板活化因子(PAF)是一种炎症脂质介质,可显著增加血管通透性。我们评估了PAF拮抗剂SRI 63 - 441抑制静脉注射内毒素或前房穿刺诱导的眼血管通透性的能力。通过70000分子量异硫氰酸荧光素偶联葡聚糖或血清蛋白在前房积聚的减少来确定,PAF拮抗剂SRI 63 - 441在静脉注射内毒素或前房穿刺后均能显著阻断眼血管通透性。SRI 63 - 441并未降低房水前列腺素E2水平的升高。PAF拮抗剂与局部吲哚美辛或局部皮质类固醇联合使用时具有相加疗效。联合治疗几乎完全防止了眼血管通透性的增加。这些数据支持以下结论:多种介质促成眼血管通透性,并且药物组合可能优于单一药物。

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Mediators of the ocular inflammatory response to interleukin-1 beta plus tumor necrosis factor-alpha.
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