Nitric oxide decreases lung injury after intestinal ischemia
| Autor: | Nancy N. Mahr, Eugene D. Jacobson, Lance S. Terada |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Male
medicine.medical_specialty Pathology Physiology Neutrophils Neutrophile Ischemia Inflammation Lung injury Nitric Oxide Nitric oxide Rats Sprague-Dawley chemistry.chemical_compound Physiology (medical) Internal medicine medicine Animals Xanthine oxidase Lung business.industry Intestinal ischemia Respiratory disease Lung Injury medicine.disease Rats Intestinal Diseases Endocrinology NG-Nitroarginine Methyl Ester chemistry medicine.symptom business |
| Zdroj: | Journal of applied physiology (Bethesda, Md. : 1985). 81(6) |
| ISSN: | 8750-7587 |
| Popis: | Terada, Lance S., Nancy N. Mahr, and Eugene D. Jacobson.Nitric oxide decreases lung injury after intestinal ischemia. J. Appl. Physiol. 81(6): 2456–2460, 1996.—After injury to a primary organ, mediators are released into the circulation and may initiate inflammation of remote organs. We hypothesized that the local production of nitric oxide (NO) may act to limit the spread of inflammation to secondarily targeted organs. In anesthetized rats, 30 min of intestinal ischemia followed by 2 h of reperfusion (I/R) did not increase lung albumin leak. However, after treatment with N G-nitro-l-arginine methyl ester (l-NAME), intestinal I/R led to increased lung leak, suggesting a protective effect of endogenous NO. The site of action of NO appeared to be the lung and not the gut because 1) after treatment withl-NAME, local delivery of NO to the lung by inhalation abolished the increase in intestinal I/R-induced lung leak; 2)l-NAME had no effect on epithelial permeability (51Cr-labeled EDTA clearance) of reperfused small bowel; and 3) after treatment with l-NAME, local delivery of NO to the gut by luminal perfusion did not improve epithelial permeability of reperfused intestines. Furthermore,l-NAME increased, and inhaled NO de- creased, the density of lung neutrophils in rats subjected to intestinal I/R, and treatment with the selectin antagonist fucoidan abolished l-NAME-induced lung leak in rats subjected to intestinal I/R. We conclude that endogenous lung NO limits secondary lung injury after intestinal I/R by decreasing pulmonary neutrophil retention. |
| Databáze: | OpenAIRE |
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