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Effects of early administration of a novel anticholinergic drug on acute respiratory distress syndrome induced by sepsis.

Authors: Li, H  Qian, Z  Li, J  Han, X  Liu, M 
Citation: Li H, etal., Med Sci Monit. 2011 Nov;17(11):BR319-325.
Pubmed: (View Article at PubMed) PMID:22037734

BACKGROUND: Acute respiratory distress syndrome (ARDS) is the inflammatory disorder of the lung most commonly caused by sepsis. It was hypothesized that treating the lung with penehyclidine hydrochloride (PHC), a new type of hyoscyamus drug, early in the development of sepsis could diminish the lung dysfunction. MATERIAL/METHODS: Sprague-Dawley rats were divided into 4 groups: 1) a control group; 2) a sham-operated group; 3) a cecal ligation and puncture (CLP) group; 4) a PHC-treated group. One hour after CLP surgery, rats were either untreated or treated with PHC via intraperitoneal injection. Lung wet/dry weight ratio, bronchoalveolar lavage fluid (BALF), serum tumor necrosis factor (TNF-alpha), interleukin 6 (IL-6), interleukin 10 (IL-10), total nitrite/nitrate (NOx), superoxide dismutase (SOD), malondialdehyde (MDA) in lung tissues, and pulmonary functions were examined 24 hour after surgery. Another 60 rats were randomly assigned to 4 equal groups to observe survival status 96 hours after surgery. RESULTS: Treatment of PHC markedly decreased TNF-alpha, IL-6, NOx, SOD, MDA content, protein concentration in BALF, and lung wet/dry weight ratio and enhanced SOD activity (p<0.05), which are indicative of PHC-induced suppression in the pathogenesis of ARDS caused by sepsis. In comparison to group CLP/saline, plasma IL-10 level markedly increased in group CLP/PHC. In PHC-treated groups, the administered PHC had a significant protective effect on the lung dysfunction induced by sepsis. CONCLUSIONS: We conclude that administration of PHC at the time of a systemic insult can protect the lung from the damaging effects of sepsis.

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RGD ID: 11049486
Created: 2016-04-06
Species: All species
Last Modified: 2016-04-06
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.