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猪铜绿假单胞菌急性肺损伤中的血小板活化因子

Platelet-activating factor in porcine Pseudomonas acute lung injury.

作者信息

Byrne K, Sessler C N, Carey P D, Sielaff T D, Vasquez A, Tatum J L, Hirsch J I, Sugerman H J

机构信息

Department of Surgery, Medical College of Virginia, Virginia Commonwealth University, Richmond.

出版信息

J Surg Res. 1991 Feb;50(2):111-8. doi: 10.1016/0022-4804(91)90232-b.

DOI:10.1016/0022-4804(91)90232-b
PMID:1990214
Abstract

We investigated the role of platelet-activating factor (PAF) in acute septic lung injury by examining the effects of the selective PAF antagonist SRI 63-675 and by measuring PAF in lung tissue in the porcine model. Four groups of pigs (15-25 kg) were studied: saline control (C, n = 5); Pseudomonas (Ps, n = 9), given 5 x 10(8) CFU/ml at 0.3 ml/20 kg/min intravenously over 1 hr; SRI (n = 3), given SRI 63-675 in a 40 mg/kg bolus; and SRI + Ps (n = 5). Ps infusion produced a fulminant lung injury characterized by a threefold increase in pulmonary arterial pressure at 30 min and persistent pulmonary hypertension (P less than 0.05 vs C), a significant (P less than 0.05 vs C) decrease in arterial oxygen tension (PaO2) from 60 min, a significant (P less than 0.05 vs C) increase in extravascular lung water (EVLW) from 120 min, and a significant (P less than 0.05 vs C) increase in albumin flux determined scintigraphically as slope index at 150-180 min. Systemic arterial pressure and cardiac index (CI) decreased significantly (P less than 0.05) in the Ps group vs C at 60 and 180 min, respectively. Bolus injection of SRI 63-675 at the time of Ps infusion blocked the early pulmonary hypertension, attenuated the early and late fall in PaO2, ameliorated the increase in EVLW, and prevented the late (150-180 min) increase in albumin flux. SRI 63-675 had minimal effects on Ps-induced hypotension or alterations in CI.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们通过研究选择性血小板激活因子(PAF)拮抗剂SRI 63 - 675的作用以及测量猪模型肺组织中的PAF,来探究PAF在急性脓毒症肺损伤中的作用。研究了四组猪(体重15 - 25千克):生理盐水对照组(C组,n = 5);铜绿假单胞菌组(Ps组,n = 9),静脉注射5×10⁸CFU/ml,剂量为0.3 ml/20 kg/min,持续1小时;SRI组(n = 3),静脉推注40 mg/kg的SRI 63 - 675;SRI + Ps组(n = 5)。Ps输注导致暴发性肺损伤,表现为30分钟时肺动脉压增加三倍且持续肺动脉高压(与C组相比,P < 0.05),60分钟起动脉血氧张力(PaO₂)显著降低(与C组相比,P < 0.05),120分钟起血管外肺水(EVLW)显著增加(与C组相比,P < 0.05),150 - 180分钟时通过闪烁扫描测定的白蛋白通量斜率指数显著增加(与C组相比,P < 0.05)。Ps组在60分钟和180分钟时,全身动脉压和心脏指数(CI)分别较C组显著降低(P < 0.05)。在输注Ps时静脉推注SRI 63 - 675可阻断早期肺动脉高压,减轻PaO₂早期和晚期下降,改善EVLW增加,并防止晚期(150 - 180分钟)白蛋白通量增加。SRI 63 - 675对Ps诱导的低血压或CI改变影响极小。(摘要截短于250字)

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