RESUMEN
The small intestine is highly sensitive to oxygen free radical-induced injury. Post-ischemic intestinal tissue damage appears to be due to the formation of oxygen radicals. Free radical initiated lipid peroxidation (LP) following intestinal ischemia/reperfusion (I/R) may disrupt mucosal integrity. Indirectly, the radicals trigger the accumulation of neutrophils within the affected tissue, initiating inflammatory processes that lead to severe mucosal lesions. In the present study we investigated the effect of pentoxifylline (PTX), a potent inhibitor of tumour necrosis factor production, on I/R induced intestinal injury. Wistar albino rats were divided into four groups: (1) Sham operation (S); (2) Sham operation + PTX (50 mg/kg i.v.) (S + PTX); (3) 1 h ischemia + 2 h reperfusion (I/R); and (4) I/R + PTX. Animals were sacrificed at the end of the reperfusion period and ileum samples were obtained. Malondialdehyde (MDA) levels, an end product of LP, glutathione (GSH) levels, a key antioxidant, and myeloperoxidase (MPO) activity (an index of polymorphonuclear neutrophils) stimulation, were determined in ileum homogenates. The results of the present study indicate that ischemia/reperfusion results in a significant increase in MDA content and MPO activity with a significant decrease in GSH content. Treatment with PTX returns these biomarkers to control values. A mechanism of this protective effect may involve inhibition of neutrophil oxidative burst.
Asunto(s)
Depuradores de Radicales Libres/farmacología , Intestino Delgado/efectos de los fármacos , Pentoxifilina/farmacología , Daño por Reperfusión/prevención & control , Animales , Biomarcadores , Radicales Libres/efectos adversos , Glutatión/metabolismo , Íleon/irrigación sanguínea , Íleon/efectos de los fármacos , Íleon/patología , Mucosa Intestinal/irrigación sanguínea , Mucosa Intestinal/efectos de los fármacos , Mucosa Intestinal/patología , Intestino Delgado/irrigación sanguínea , Intestino Delgado/patología , Peroxidación de Lípido/efectos de los fármacos , Malondialdehído/metabolismo , Neutrófilos/efectos de los fármacos , Neutrófilos/patología , Peroxidasa/metabolismo , Ratas , Ratas Wistar , Estallido RespiratorioRESUMEN
Rat liver and brain lipid peroxide and glutathione levels were determined after chronic ethanol treatment. Although hepatic lipid peroxidation was significantly stimulated, we have failed to observe any change in brain lipid peroxide and glutathione levels of rats chronically treated with ethanol.
Asunto(s)
Encéfalo/metabolismo , Etanol/farmacología , Glutatión/metabolismo , Peróxidos Lipídicos/metabolismo , Hígado/metabolismo , Animales , Masculino , Ratas , Ratas EndogámicasRESUMEN
The effects of acute i.p. administration of lithium (2 mmol/kg), diazepam (10 mg/kg) and dl-propranolol (2 mg/kg) on brain Na+-K+-ATPase activity in mice exposed to two stressful stimuli (cold and immobilization) were examined. In unstressed mice, lithium and propranolol did not affect the enzyme activity, while diazepam increased it. Interestingly, all the three drugs reversed the stress-induced increase in the brain Na+-K+-ATPase activity. The specificity of this action remains to be clarified.
Asunto(s)
Encéfalo/enzimología , Diazepam/farmacología , Litio/farmacología , Propranolol/farmacología , ATPasa Intercambiadora de Sodio-Potasio/metabolismo , Estrés Fisiológico/enzimología , Adenosina Trifosfatasas/metabolismo , Animales , Encéfalo/efectos de los fármacos , ATPasa de Ca(2+) y Mg(2+) , Masculino , Ratones , Ratones Endogámicos BALB CAsunto(s)
Aminoácidos/metabolismo , Apomorfina/farmacología , Aminas Biogénicas/metabolismo , Encéfalo/metabolismo , Clorpromazina/farmacología , Glicina/farmacología , Animales , Unión Competitiva , Encéfalo/efectos de los fármacos , Dopamina/metabolismo , Levodopa/farmacología , Ratas , Ratas Endogámicas , Factores de TiempoRESUMEN
Morphine and aspartic acid were administered separately and in combination to 80 rats divided into 8 groups. Ten and 20 min following the injections, brain, liver and kidney L-asparaginase activity was determined. Morphine decreased brain and liver L-asparaginase activity and increased that of kidney. Aspartic acid completely antagonized the effect of morphine. Additionally 500 IU/kg L-asparaginase and 5 or 10 mg/kg morphine were i.v. injected into 56 rats divided into 5 groups. L-Asparaginase, which, in turn, increased motor activity, antagonized the morphine-induced hypoactivity and analgesia. These results support our previous findings.
