Reduction of shock-induced gastric damage by a nitric oxide-releasing aspirin derivative: role of neutrophils

The American Journal of Physiology
John L WallaceG Cirino

Abstract

The gastric damage associated with hemorrhagic shock appears to occur, at least in part, through neutrophil-dependent mechanisms. Nitric oxide (NO)-releasing derivatives of aspirin have been shown to spare the gastrointestinal tract of injury. As NO can inhibit neutrophil adherence, it is possible that such a derivative of aspirin (NCX-4016) would exert inhibitory effects on neutrophil adherence and therefore be capable of protecting the stomach against shock-induced gastric damage. This hypothesis was tested in this study. Oral administration of NCX-4016 or glyceryl trinitrate or depletion of circulating neutrophils with antineutrophil serum significantly reduced the extent of gastric damage induced by hemorrhagic shock, whereas aspirin had no effect. NCX-4016 and antineutrophil serum pretreatment resulted in significant preservation of gastric blood flow during the shock period. Moreover, NCX-4016, but not aspirin, was capable of inhibiting N-formyl-Met-Leu-Phe-induced leukocyte adherence to postcapillary mesenteric venules. These results suggest that an NO-releasing aspirin derivative reduces the susceptibility of the stomach to shock-induced damage through inhibitory effects on neutrophil adherence to the vascular endothelium.

References

Jun 1, 1991·Proceedings of the National Academy of Sciences of the United States of America·P KubesD N Granger
Apr 1, 1990·Proceedings of the National Academy of Sciences of the United States of America·N B VedderJ M Harlan
Jun 23, 1995·European Journal of Pharmacology·J L WallaceS N Elliott
May 23, 1994·European Journal of Pharmacology·J L WallaceG Cirino
Feb 1, 1994·Digestive Diseases and Sciences·F J AndrewsP E O'Brien
Jan 1, 1993·British Journal of Pharmacology·J Lopez-BelmonteS Moncada
Jan 1, 1993·Canadian Journal of Physiology and Pharmacology·J L Wallace
Dec 1, 1995·The Journal of Clinical Investigation·J L WallaceG Cirino
Feb 1, 1997·Alimentary Pharmacology & Therapeutics·N M DaviesJ L Wallace

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Citations

May 10, 2006·Digestive Diseases and Sciences·Laura Iris Cosen-BinkerOsvaldo Tiscornia
Oct 16, 2007·American Journal of Physiology. Heart and Circulatory Physiology·Anitaben TailorD Neil Granger
Jan 21, 2016·Evidence-based Complementary and Alternative Medicine : ECAM·Nylane Maria Nunes de AlencarMarcio Viana Ramos
Jul 21, 2020·Microcirculation : the Official Journal of the Microcirculatory Society, Inc·Anoek L I van LeeuwenCharissa E van den Brom
Oct 18, 2003·American Journal of Physiology. Gastrointestinal and Liver Physiology·Silvia BertugliaPiero Del Soldato
Jan 24, 2003·Annual Review of Pharmacology and Toxicology·Claudio Napoli, Louis J Ignarro
Jan 23, 2015·Evidence-based Complementary and Alternative Medicine : ECAM·Jung-Woo KangSun-Mee Lee
Dec 11, 2003·American Journal of Physiology. Gastrointestinal and Liver Physiology·John L WallaceStefano Fiorucci
Mar 25, 2016·Chemical & Pharmaceutical Bulletin·Wei PengDeng-Gao Zhao
Mar 10, 2001·Nihon yakurigaku zasshi. Folia pharmacologica Japonica·K Takeuchi, A Tanaka
Jul 24, 2015·Journal of Medicinal Chemistry·Yingdong ZhuShengmin Sang

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