INHIBITION BY METHYLPREDNISOLONE OF LEUKOCYTE-INDUCED PULMONARY DAMAGE

被引:12
作者
CHIARA, O
GIOMARELLI, PP
BORRELLI, E
CASINI, A
SEGALA, M
GROSSI, A
机构
[1] UNIV SIENA, IST CHIRURG TORAC & CARDIOVASC, I-53100 SIENA, ITALY
[2] UNIV SIENA, IST PATOL GEN, I-53100 SIENA, ITALY
[3] UNIV MILAN, OSPED S RAFFAELE, I-20122 MILAN, ITALY
关键词
LEUKOCYTES; LIPID PEROXIDATION; METHYLPREDNISOLONE; LUNG MALONDIALDEHYDE; INTRAPERITONEAL ZYMOSAN; LUNG HOMOGENATES; HIGH-PRESSURE LIQUID CHROMATOGRAPHY; BLOOD GAS ANALYSIS; PULMONARY DISEASE; PULMONARY MICROCIRCULATION;
D O I
10.1097/00003246-199102000-00023
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Background and Methods: The purpose of this study was twofold: the development of a chronic model of leukocyte-mediated pulmonary injury and the evaluation of the protective effects of methylprednisolone. Rabbits were inoculated ip with zymosan. Blood gases and circulating leukocytes were evaluated. Survivors were killed on day 10 for microscopic studies and for the evaluation of lung lipid peroxidation through the by-product malondialdehyde. Results: Intraperitoneal zymosan resulted in a marked decrease of PaO2 and circulating leukocytes, and increased cellularity of alveolar septa, interstitial edema, and increased lung malondialdehyde. Pulmonary damage was partially prevented when methylprednisolone was administered before zymosan inoculation, but not when methylprednisolone was given 24 hr later. Conclusions: The authors conclude that a local nonseptic inflammatory stimulus may provoke remote changes to the lungs and that methylprednisolone may counteract the process only if it is administered before or very early after the onset of inflammation.
引用
收藏
页码:260 / 265
页数:6
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