Nitric oxide and malondialdehyde in gastric contents and blood in an equine model of gastric ulcer induced by phenylbutazone

Abstract

Concentración de óxido nítrico y malonaldehído en contenido gástrico y en sangre en un modelo de úlcera gástrica equina inducida por fenilbutazona Concentração de óxido nítrico e malondialdeído no conteúdo gástrico e no sangue em modelo equino de úlcera gástrica Summary Background: mechanisms of gastric mucosal injury include cellular damage by oxygen free radicals, which can be indirectly measured through malondialdehyde (MDA). Production of nitric oxide (NO) maintains gastric tissue perfusion through vasodilatation. Objective: to demonstrate oxidative stress and impaired gastric perfusion measuring NO and MDA in gastric contents and blood of equines subjected to a gastrointestinal ulceration induction protocol. Methods: a gastrointestinal ulceration induction protocol involving fasting and oral administration of phenylbutazone was performed on five horses. NO and MDA were measured before and after protocol induction and presence of fecal occult blood (FOB) was evaluated. Animals underwent gastroscopy at the beginning and end of the protocol. Results: horses presented variability in hematological and FOB exams. Azotemia, hyperphosphatemia, and hypocalcemia were found in all animals. No significant changes were found in enzymatic activity. At the end of the protocol, 40% of the horses showed varying degrees of gastric ulceration. NO production in the stomach decreased by 60%, whereas MDA production increased by 55% after the protocol. Plasma concentration of MDA average increased 96 hours after starting the protocol. There were no significant differences in mean plasma NO during the protocol. Conclusion: the

Therapeutic effect of low molecular weight chitosan containing sepia ink on ethanol-induced gastric ulcer in rats

“…Hence, determination of MDA levels can be used to access lipid peroxidation 25 . Present study showed that MDA was sharply There is increasing evidence that major source of ROS in gastric mucosal injury is the activated neutrophlis 28 , which play an vital role in the development of gastric damage by their aggregation and release of tissue-disrupting substance, such as oxygen free radicals and proteases 29 .…”

Equine Gastric Ulcer Syndrome: An Update on Current Knowledge

“…Furthermore, several population-based studies have failed to find NSAID use associated with increased risk of EGGD [ 28 , 30 , 90 ]. At an experimental level, multiple studies have shown the ulcerogenic capacity of NSAIDs at high doses in horses [ 50 , 91 , 92 , 93 , 94 , 95 , 96 , 97 ]. Most of these studies, however, use NSAID doses in excess of what is typically recommended for clinical use [ 98 ].…”

“…Most of these studies, however, use NSAID doses in excess of what is typically recommended for clinical use [ 98 ]. The ability for fed-fasted NSAID models to cause both ESGD and EGGD at normal therapeutic doses has also been demonstrated [ 92 , 97 ]. These models are worth considering when assessing the risk of EGUS in hospitalized horses that often undergo periods of fasting with concurrent NSAID administration.…”

Manifestation of gastric ulcers in horses used in public safety

“…This is an easy procedure to perform and is minimally invasive, allowing the assessment of nonglandular and glandular region (Jorge Nieto, 2012). Such examination is performed with the horse under a sedation state and 12 to 14 hours solids fasting (Zuluaga et al, 2016).…”