Ibuprofen attenuates early lung injury in endotoxemic, neutropenic rats

被引：4

作者：

Daphtary, KM ^{[1
]}

Heidemann, DM ^{[1
]}

Glibetic, M ^{[1
]}

机构：

[1] Wayne State Univ, Childrens Hosp Michigan, Div Crit Care Med, Detroit, MI 48201 USA

来源：

PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS | 2001年 / 65卷 / 02期

关键词：

D O I：

10.1054/plef.2001.0289

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The objective of our study was to determine the role of ibuprofen in protecting neutropenic rats from cardiopulmonary injury due to endotoxemia. We hypothesized that ibuprofen would offer pulmonary protection by altering cytokine production. Neutropenic rats received E. coli lipopolysaccharide (LPS) alone or ibuprofen and LPS. After 4 h, arterial blood gases, heart rate and blood pressure were measured. Blood and bronchoalveolar lavage fluid (BALF) were collected for TNF-alpha and MIP-2 concentrations. Lung tissue for NOS mRNA and myeloperoxidase were obtained. The ibuprofen group had decreased heart rate and better oxygenation. Ibuprofen suppressed TNF-alpha and MIP-2 production in blood and MIP-2 concentrations in BALE Lung mRNA for NOS was higher in the ibuprofen group. Neutrophil infiltration in the lung was similar in both groups. Ibuprofen attenuated cardiopulmonary dysfunction by decreasing the early cytokine response. The balance of vasodilator to vasoconstrictor production in the lung may favor vasodilation as shown by increased NOS mRNA and suppression of thromboxane. (C) 2001 Harcourt Publishers Ltd.

引用

页码：59 / 65

页数：7

共 38 条

[1]

ABRAHAM E, 1989, CRIT CARE MED, V17, P590

[2] NONSTEROIDAL ANTIINFLAMMATORY DRUGS INHIBIT EXPRESSION OF THE INDUCIBLE NITRIC-OXIDE SYNTHASE GENE [J].

AEBERHARD, EE ;

HENDERSON, SA ;

ARABOLOS, NS ;

GRISCAVAGE, JM ;

CASTRO, FE ;

BARRETT, CT ;

IGNARRO, LJ .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1995, 208 (03) :1053-1059

[3]

[Anonymous], AM J PHYSL LUNG CELL

[4] EFFECTS OF IBUPROFEN ON NEUTROPHIL FUNCTION AND ACUTE LUNG INJURY IN CANINE ENDOTOXIN-SHOCK [J].

BALK, RA ;

JACOBS, RF ;

TRYKA, AF ;

TOWNSEND, JW ;

WALLS, RC ;

BONE, RC .

CRITICAL CARE MEDICINE, 1988, 16 (11) :1121-1127

[5] PASSIVE-IMMUNIZATION AGAINST CACHECTIN TUMOR NECROSIS FACTOR PROTECTS MICE FROM LETHAL EFFECT OF ENDOTOXIN [J].

BEUTLER, B ;

MILSARK, IW ;

CERAMI, AC .

SCIENCE, 1985, 229 (4716) :869-871

[6]

BRIGHAM KL, 1986, AM REV RESPIR DIS, V133, P913

[7] HIGH-LEVELS OF INTERLEUKIN-8 IN THE BLOOD AND ALVEOLAR SPACES OF PATIENTS WITH PNEUMONIA AND ADULT-RESPIRATORY-DISTRESS-SYNDROME [J].

CHOLLETMARTIN, S ;

MONTRAVERS, P ;

GIBERT, C ;

ELBIM, C ;

DESMONTS, JM ;

FAGON, JY ;

GOUGEROTPOCIDALO, MA .

INFECTION AND IMMUNITY, 1993, 61 (11) :4553-4559

[8] Nitric oxide and septic shock [J].

Cobb, JP ;

Danner, RL .

JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1996, 275 (15) :1192-1196

[9] Proinflammatory cytokines [J].

Dinarello, CA .

CHEST, 2000, 118 (02) :503-508

[10]

EVANS T, 1993, CIRC SHOCK, V41, P77

← 1 2 3 4 →