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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 protocol used to induce gastric ulcers produces diminished cytoprotection (by NO) and induces oxidative stress in the gastric mucosa. Keywords: anti-inflammatory, antioxidant, NSAID, oxidative stress, stomach. Resumen Antecedentes: los mecanismos de lesion de la mucosa gastrica incluyen dano celular por radicales libres de oxigeno que puede ser medido a traves del malonaldehido (MDA). La produccion de oxido nitrico (NO) sostiene la perfusion del tejido gastrico mediante vasodilatacion. Objetivo: demostrar el estres oxidativo y alteracion de la perfusion gastrica mediante la medicion de NO y MDA en contenido gastrico y sangre de equinos sometidos a un protocolo de induccion de ulceracion gastrointestinal. Metodos: el protocolo de ulceracion se hizo en 5 caballos con fenilbutazona y periodos de ayuno. Antes y despues de aplicar el protocolo fueron medidos NO y MDA y se evaluo la presencia de sangre oculta en heces (FOB). Los animales fueron sometidos a gastroscopia al inicio y final del protocolo. Resultados: los equinos presentaron variabilidad en los examenes hematologicos y FOB. Se encontro Azotemia, hiperfosfatemia e hipocalcemia en todos los animales. No fueron encontradas alteraciones significativas en la actividad enzimatica. Al final del protocolo, el 40% de los equinos presento ulceracion gastrica en grado variable. La produccion de NO en estomago disminuyo 60%, mientras que la produccion de MDA aumento 55% despues del protocolo. El promedio de la concentracion plasmatica de MDA aumento despues de 96 horas de iniciar el protocolo. No hubo diferencias significativas en el promedio de NO plasmatico durante el protocolo. Conclusion: el protocolo utilizado para inducir ulceras gastricas produce disminucion en la citoproteccion derivada del NO e induce estres oxidativo en la mucosa gastrica. Palabras clave: AINE, anti-inflamatorio, antioxidante, estomago, estres oxidativo. Resumo Antecedentes: mecanismos de lesao da mucosa gastrica incluem o dano celular pela acao dos radicais livres de oxigenio que pode ser medido a traves do malonaldehido (MDA). A producao de oxido nitrico (NO) mante a perfusao do tecido gastrico a traves da vasodilatacao. Objetivo: demostrar estrese oxidativo e alteracao da perfusao gastrica pela quantificacao de NO e MDA a partir do conteudo gastrico e sangue de equinos que foram submetidos a um protocolo de inducao de ulceracao gastrointestinal. Metodos: realizou-se um protocolo a base de fenilbutazona e periodos de jejum em 5 cavalos. Antes e depois do protocolo foram dosados NO e MDA e se avaliou a presencia de sangue oculta em fezes (FOB). No inicio e no final do protocolo, os animais foram avaliados pela gastroscopia. Resultados: os equinos apresentaram variabilidade nos exames hematologicos e FOB. Encontrou-se azotemia, hiperfosfatemia e hipocalcemia em todos os animais. Nao foram achadas alteracoes significativas na atividade enzimatica. Ao final do protocolo, o 40% dos equinos apresentou grado variavel de ulceracao gastrica. A producao de NO no estomago diminuiu 60%, entretanto a producao de MDA aumentou 55% apos do protocolo. A concentracao media plasmatica de MDA aumentou depois de 96 horas de comecar o protocolo. Nao houve diferencias significativas na media de NO plasmatico durante o protocolo. Conclusao: o protocolo utilizado para induzir ulceras gastricas produz diminuicao na citoprotecao derivada do NO e induz estresse oxidativo na mucosa gastrica. Palavras chave: AINE, anti-inflamatorio, antioxidante, estomago, estresse oxidativo.

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