Nitric oxide attenuates and xanthine oxidase exaggerates lung damage-induced gut injury
Autor: | Eric C. Brooks, Zivotije Radisavljevic, Eugene D. Jacobson, Lance S. Terada, Nancy N. Mahr |
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Rok vydání: | 1997 |
Předmět: |
Lung Diseases
Male Pulmonary Circulation Xanthine Oxidase medicine.medical_specialty Arginine Physiology Neutrophile Allopurinol Nitric Oxide Nitric oxide Capillary Permeability Rats Sprague-Dawley chemistry.chemical_compound Physiology (medical) Internal medicine medicine Animals Enzyme Inhibitors Xanthine oxidase Lung Edetic Acid Intestinal permeability Hepatology Gastroenterology Antagonist medicine.disease Rats Trachea Intestinal Diseases NG-Nitroarginine Methyl Ester Endocrinology medicine.anatomical_structure chemistry Hydrochloric Acid medicine.drug |
Zdroj: | American Journal of Physiology-Gastrointestinal and Liver Physiology. 272:G845-G852 |
ISSN: | 1522-1547 0193-1857 |
Popis: | Aspirated gastric contents can evoke multiorgan failure. We hypothesized that secondary intestinal epithelial dysfunction after lung damage would be mediated by xanthine oxidase (XO) and antagonized by endogenous gut nitric oxide (NO). Isosmotic saline or HCl solutions were instilled intratracheally in anesthetized rats, and intestinal injury was assessed 190 min later by measuring the blood-to-lumen clearance of 51Cr-labeled EDTA (51Cr-EDTA clearance) and gut wall neutrophil population density. Intratracheal HCl increased 51Cr-EDTA clearance, and this transepithelial leak was attenuated by either systemic L-arginine or intraluminal NO and by chronic dietary pretreatment with allopurinol or sodium tungstate. Conversely, lung damage-induced gut leak was exaggerated by NO synthase inhibition or intravenous XO administration. Intratracheal HCl also increased intestinal wall neutrophil density and myeloperoxide activity. We conclude that two enzymatic systems involved in remote gut barrier dysfunction after endobronchial acidification are XO as mediator and NO synthase as antagonist. |
Databáze: | OpenAIRE |
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