{"title":"In vivo effect of methylprednisolone on lipopolysaccharide-induced superoxide production by pulmonary and circulating blood neutrophils in rats.","authors":"C Tsuji, S Shioya","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The effect of methylprednisolone on superoxide production by pulmonary and circulating blood neutrophils was investigated in rats after the intravenous injection of lipopolysaccharide. Superoxide production by both types of neutrophils was increased by lipopolysaccharide injection, and pretreatment with methylprednisolone inhibited this increase. The inhibitory effect of methylprednisolone on pulmonary neutrophils was greater than that on circulating blood neutrophils. Methylprednisolone also prevented the increase in pulmonary vascular permeability induced by lipopolysaccharide, but failed to inhibit intrapulmonary neutrophil accumulation. These results suggest that the suppression of superoxide production may be one mechanism by which methylprednisolone prevents endotoxin-induced lung damage.</p>","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"42 3","pages":"128-34"},"PeriodicalIF":0.0000,"publicationDate":"1994-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Circulatory shock","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
The effect of methylprednisolone on superoxide production by pulmonary and circulating blood neutrophils was investigated in rats after the intravenous injection of lipopolysaccharide. Superoxide production by both types of neutrophils was increased by lipopolysaccharide injection, and pretreatment with methylprednisolone inhibited this increase. The inhibitory effect of methylprednisolone on pulmonary neutrophils was greater than that on circulating blood neutrophils. Methylprednisolone also prevented the increase in pulmonary vascular permeability induced by lipopolysaccharide, but failed to inhibit intrapulmonary neutrophil accumulation. These results suggest that the suppression of superoxide production may be one mechanism by which methylprednisolone prevents endotoxin-induced lung damage.