Browsing by Author "VARGAS, L"
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- ItemINDUCTION OF PEROXISOMAL FATTY ACYL-COENZYME A-OXIDASE AND TOTAL CARNITINE ACETYL-COENZYME A-TRANSFERASE IN PRIMARY CULTURES OF RAT HEPATOCYTES BY GARLIC EXTRACTS(1992) ORELLANA, A; KAWADA, ME; MORALES, MN; VARGAS, L; BRONFMAN, MGarlic has been proposed as a natural hypolipidemic substance. Most hypolipidemic compounds induce peroxisomal proliferation and increase enzyme activities associated with peroxisomal beta-oxidation in rat liver. Here we report that garlic methanol-extracts behave as hypolipidemic drugs, increasing the activity of peroxisomal fatty acyl-coenzyme A oxidase and of total carnitine acetyl-coenzyme A transferase in primary cultures of rat hepatocytes. Both enzymes are considered markers associated with increased peroxisomal beta-oxidation. As in the case of hypolipidemic peroxisome proliferators, garlic extracts partially prevented the decrease in fatty acyl-coenzyme A oxidase as the culture aged. No changes were observed in the activity of microsomal NADPH cytochrome c reductase or of mitochondrial glutamate dehydrogenase.
- ItemINHIBITION OF STRESS-INDUCED HYPERGLYCEMIA BY TAIL PINCHING OR INTRAVENTRICULAR ENKEPHALIN ADMINISTRATION IN THE RAT(1988) SANCHEZ, R; VARGAS, LThe tail pinch (t-p) method added to a basal restraint stress produced inhibition of the stress-induced hyperglycemia, an effect that was neutralized with intrathecal anesthesia but not with intracerebroventricular (i.c.v.) naloxone (50, 100, 1000 ng/100 g) or with intraperitoneal naloxone injections (0.1-0.3 mg/100 g). A similar negative result was obtained with i.c.v. administration of 500 and 1000 ng/100 g of .beta.-endorphin. In contrast, a single i.c.v. injection of 1000 ng/100 g of Met-enkephalin reproduced the t-p inhibitory effect. The latter was not elicited by i.c.v. FK 33824, an enkephalin analogue, a result that supports the specific participation of the .delta.-opioid receptors. The results obtained with central .alpha.-adrenoceptor antagonists and central noradrenergic chemical destruction, or central .alpha.-adrenoceptor agonists, support the production of a reinforcement of the .alpha.-adrenoceptor stress stimulation by the t-p procedure, probably through noradrenaline and enkephalin mediation.
- ItemSTRESS HYPERGLYCEMIC RESPONSE AFTER CENTRAL AND PERIPHERAL MONO-AMINERGIC NEURONS DESTRUCTION, OR ADRENAL CATECHOLAMINES DEPRIVATION(1982) ROMERO, G; VALDES, EM; YANEZ, MT; KAWADA, ME; VARGAS, LRestraint stress of 60 min in unfasted non-diabetic 80%-pancreatectomized rats produced a stress diabetic response with significant glycosuria and hyperglycemia. This model was used to investigate the influence of central noradrenergic, dopaminergic, serotoninergic and peripheral noradrenergic neurons, by means of selective chemical lesion. 6-Hydroxydopamine (6-OH-DA) was used to damage noradrenergic and dopaminergic neurons and 5,6-dihydroxytryptamine for serotoninergic neurons. The sympatho-adrenal system was also studied by adrenal demedullation. Results showed that intracerebro-ventricular administration of 6-OH-DA alone, or followed by 5,6-dihydroxytryptamine, had no influence on the stress hyperglycemic response. Central and peripheral 6-OH-DA administration to intact new born rats did not modify the stress response at the adult age. The hypothalamic monoaminergic and neighboring neurons appear to have no influence in the mechanism of stress hyperglycemia. The pseudo-aggressive behavior which arose after central noradrenergic and dopaminergic lesion, returned to normal after serotoninergic neuron destruction. Bilateral adrenal-medullectomy abolished the stress hyperglycemia. Adrenal catecholamines were necessary for the production of restraint stress hyperglycemia. Among these catecholamines, adrenaline [epinephrine] is proposed as the trigger factor.
- ItemSYMPATHETIC NERVOUS-SYSTEM MEDIATES URINARY KALLIKREIN EXCRETION IN CONSCIOUS RATS(1987) ALBERTINI, R; VARGAS, L; OLIVERI, P; PARDO, F; PAREDES, MC