S Thamaree, V Sitprija, S Leepipatpaiboon, S Witayalertpunya, N Thaworn
{"title":"Mediators and renal hemodynamics in Russell's viper envenomation.","authors":"S Thamaree, V Sitprija, S Leepipatpaiboon, S Witayalertpunya, N Thaworn","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The effects of Russell's viper venom on vasoactive mediators and renal hemodynamics were studied in five mongrel dogs. Intravenous administration of Russell's viper venom to the dogs caused a reduction of mean arterial pressure, renal blood flow, and glomerular filtration rate. The filtration fraction was decreased. This was accompanied by a rise in plasma norepinephrine, endothelin, 6-keto-PGF1 alpha, a stable metabolite of PGI2, and TXB2, a metabolite of TXA2. Plasma levels of epinephrine and dopamine showed no significant changes. The increase of plasma levels of both vasodilatator and vasoconstrictor were critical to systemic and renal hemodynamics. While vasodilatation predominated in the systemic circulation and resulted in hypotension, vasoconstriction played a major role in decreasing renal hemodynamics. Decreased renal blood flow and decreased glomerular filtration rate were the result of renal vasoconstriction and hypotension.</p>","PeriodicalId":16437,"journal":{"name":"Journal of natural toxins","volume":"9 1","pages":"43-8"},"PeriodicalIF":0.0000,"publicationDate":"2000-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of natural toxins","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 effects of Russell's viper venom on vasoactive mediators and renal hemodynamics were studied in five mongrel dogs. Intravenous administration of Russell's viper venom to the dogs caused a reduction of mean arterial pressure, renal blood flow, and glomerular filtration rate. The filtration fraction was decreased. This was accompanied by a rise in plasma norepinephrine, endothelin, 6-keto-PGF1 alpha, a stable metabolite of PGI2, and TXB2, a metabolite of TXA2. Plasma levels of epinephrine and dopamine showed no significant changes. The increase of plasma levels of both vasodilatator and vasoconstrictor were critical to systemic and renal hemodynamics. While vasodilatation predominated in the systemic circulation and resulted in hypotension, vasoconstriction played a major role in decreasing renal hemodynamics. Decreased renal blood flow and decreased glomerular filtration rate were the result of renal vasoconstriction and hypotension.