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Biomedical subjects

R F Villa

Publications and source records attributed to R F Villa.

At least 91 records · Page 5Linked to original sources
PubMed1980

Acetylcholine esterase sensitivity to chronic administration of diphenylhydantoin and effects on cerebral enzymatic activities related to energy metabolism.

The effect of chronic treatment (8 months) with diphenylhydantoin (DPH) on rat brain was studied. The activity of some enzymes related to energy transduction (lactate dehydrogenase, citrate synthase, and malate dehydrogenase; NADH-cytochrome c reductase and cytochrome oxidase) and neurotransmission (acetylcholine esterase) was evaluated both in the whole brain homogenate and/or in the crude mitochondrial fraction. A clear-cut decrease of acetylcholine esterase activity was observed, the decrease continuing even after treatment was discontinued. Effects on energy metabolism and on lactate dehydrogenase, malate dehydrogenase, and cytochrome oxidase are discussed.

Acetylcholinesterase↗
PubMed1980

Drug interference on some biochemical parameters of rat cerebral cortex during post-ischemic recovery.

Glycolytic substrates and metabolites (glycogen, glucose, glucose-6-phosphate, pyruvate, lactate), tricarboxylic acid cycle intermediates (citrate, alpha-ketoglutarate, succinate, fumarate, malate), related amino acids (glutamate, glutamine, alanine, gamma-aminobutyrate) and energy mediators (ATP, ADP, AMP, creatine phosphate) were evaluated in the cerebral cortex of rats after 5 min of complete compression ischemia as well as after 3, 15 or 30 min of recirculation following 5 min ischemia. The post-ischemic recovery was studied in control animals or in animals treated (30 min before ischemia and during discovery) by intravenous perfusion of vincamine, theophylline, dihydroergocristine and alanine. Interrelated changes of intermediates of the carbohydrate and the amino acid metabolism have been observed. It is concluded that alanine perfusion induced a partial detour of the lactacid anaerobic process towards the succinate-related alactacid cycle, leading to an increase in the cortical gamma-aminobutyrate content. Vincamine and dihydroergocristine acted in the opposite direction.

Alanine↗
PubMed1980

Effect of alphaxalone-alphadolone on some enzymatic activities from rat brain.

The changes induced by alphaxalone-alphadolone (3:1) in the cerebral enzymatic activities of the Kreb's cycle (citrate synthase, malate dehydrogenase) and electron transfer chain (total NADH-cytochrome c reductase and cytochrome oxidase) were studied. In addition, the activation of lactate dehydrogenase (for the glycolytic pathway) and of acetylcholine esterase (as indicative of transmission) were investigated. These enzymatic activities were evaluated in the homogenate in toto and/or in the crude mitochondrial fraction of rat brain, since these enzymes are variously located in the cytoplasm. Two relationships were studied: a) dose/action (0.5, 1. 2, 4, 8, 16 and 32 mg . kg-1) by measurements carried out 60 min after i.p. administration; b) time/action (16 mg . kg-1 i.p.; measurements 15, 30, 60, 120 and 240 min after administration). The results show that in both kinds of trials alphaxalone-adphadolone reduced only the activity of the enzyme cytochrome oxidase evaluated on the brain homogenate in toto. More specifically, with regard to the dose/action relationship, the effect occurred starting with the dose of 2 mg . kg-1 and did not take place linearly with the higher ones. As to the time/action relationship, the effect began 60 min after administration, the changes being observed also at the subsequent times. The data obtained are discussed with regard to the interactions between alphaxalone -alphadolone and mitochondrial enzymatic systems, and compared with the effects of phenobarbital on the same systems.

Alfaxalone Alfadolone Mixture↗
PubMed1979

[Cerebral enzymatic activities related to energy transduction processes. A model for the evaluation of pharmacological changes in the brain of the adult rat].

A test model of studying the effects of chronic pharmacological treatment on cerebral metabolism related to energy transduction was developed. The most useful biochemical parameters were the cerebral enzymatic activities related to the glycolytic pathway (lactate dehydrogenase), the Krebs' cycle (citrate synthetase and malate dehydrogenase) and the electron transfer chain (total NADH-cytochrome c reductase and cytochrome oxidase). The model is based on the natural growth-dependent changes occurring in the rat during aging (from 10 to 60 weeks of life). As test drug, 10-methoxy-1,6-dimethyl-ergoline-8 beta-methanol-(5-bromonicotinate) (nicergoline, Sermion) was administered daily for three periods of 16 weeks each (10-26, or 28-44, or 44-60 weeks of life) by two different administration routes (oral and i.p.), and at two different dose levels: oral 1 or 4, i.p. 0.25 or 1 mg/kg. Biochemical data were obtained blindly after 4, 8, 12 and 16 weeks of treatment. The drug tested exerted different effects which were dependent on the various administration periods and the administration routes. No dose-effect relationship was established.

Animals↗
PubMed1978

Effect of (-)eburnamonine, papaverine and UDP-glucose on cerebral energy state during and after experimental hypoxia and ischaemia in beagle dog.

The effect of (-)eburnamonine, papaverine and UDP-glucose intracarotid perfusion has been evaluated in the brain of beagle dogs during various conditions of cerebral damage (hypoxia, hypoxia plus incomplete ischaemia, hypoxia plus complete ischaemia), and after 3, 15 or 30 min of the post-hypoxic recovery and recirculation. The behaviour of fuels (glycogen, glucose), of glycolytic pathway intermediates (glucose-6-phosphate, pyruvate) and end-product (lactate), of the pool of labile phosphates (ATP, ADP, AMP, creatine phosphate) and the energy charge potential of the brain were evaluated in the motor area of the cerebral cortex. The different pharmacological effects of (-)eburnamonine, papaverine and UDP-glucose are discussed with regard to the biochemical changes taking place during the physiopathological conditions tested.

Adenosine Diphosphate↗
PubMed1978

Drug action on cerebral energy state during and after various hypoxic conditions.

The behaviour of fuels (glycogen, glucose), of glycolytic pathway intermediates (glucose-6-phosphate, pyruvate) and end-product (lactate), as well as the pool of labile phosphates (ATP, ADP, AMP, creatine phosphate) and the energy charge of the brain were studied in the motor area of the cerebral cortex of beagle dogs. These parameters were evaluated both after various hypoxic conditions (hypoxic hypoxia, hypoxia plus complete or incomplete ischemia) and after 3, 15 or 30 min of post-hypoxic recovery and recirculation. The effect of some drugs (papaverine, UDP-glucose, (-)eburnamonine, suloctidil) following intracarotid perfusion has been evaluated in the various quoted experimental conditions. The tested drugs proved unable to improve the deranged brain metabolism under all the hypoxic conditions. On the contrary, an activating effect of suloctidil and (-)eburnamonine could be observed during the recovery after both hypoxia and hypoxia plus complete ischemia, papaverine being ineffective and UDP-glucose increasing the glycogen synthesis. The drugs proved unable to induce a restitution of the altered brain metabolism after hypoxia plus incomplete ischemia.

Adenosine Triphosphate↗