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Biomedical subjects

G Benzi

Publications and source records attributed to G Benzi.

At least 145 records · Page 8Linked to original sources
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

Acute model for the estimation of the cerebral energy state during or after hypoxia and complete or incomplete ischaemia.

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 in hypovolaemic hypotension. These parameters were evaluated after acute hypoxia (obtained by altering the composition of the inhalation mixture), after acute hypoxia plus incomplete ischaemia, after acute hypoxia plus complete ischaemia, during post-hypoxic recovery (3, 15 or 30 min after the restoration of normal ventilation), during post-hypoxic recovery and recirculation. A comparative examination of the different conditions showed that the most dramatic fall in the cerebral energy state took place in hypoxia plus complete ischaemia followed, in the order, by hypoxia plus incomplete ischaemia and simple hypoxia. However, reversal was most difficult in hypoxia plus incomplete ischaemia. The different situations are discussed in this paper with regard to the changes taking place in cerebral biochemical events.

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↗
PubMed1976

Adenyl cyclase system and cerebral energy state.

The energy charge potential of the cerebral adenylate system, the cerebral lactate: pyruvate system, and the cerebral glycogen level were used to characterize the cerebral energy state of the brain. Cerebral adenyl cyclase activity and cyclic AMP concentrations were investigated to evaluate their possible influence on the regulatory processes in brain metabolism. These biochemical parameters were evaluated on the cortical motor area of the brain of the beagle dog in hypovolaemic hypotension during acute hypoxia (obtained by altering the composition of the inhalation mixture) and during the post-hypoxic recovery (three minutes after the restoration of normal ventilation). This experimental model of acute hypoxia was also used for investigating the action of some substances acting at beta-adrenergic receptor level or at vascular level. The substances were perfused into the carotid artery at the rate of 0.5 ml/min for three to six minutes. During the first stage of hypoxia, the adenyl cyclase system is probably an important biochemical regulatory factor. This system becomes less important when a critical threshold is crossed (oxygen arterial partial pressure less than 25-20 mmHg) below which other factors become rate-limiting. A beta-receptor stimulating agent enhanced the mechanisms of physiological post-hypoxic recovery; inhibition of this action was obtained with a beta-receptor blocking agent. Under these experimental conditions, no correlation existed between the vascular effects of the agents and brain metabolism.

Adenosine Diphosphate↗
PubMed1976

Drugs and brain mitochondrial enzymatic activities during post-natal development in rat.

The enzymatic activities of two mitochondrial enzymes, i.e. succinate dehydrogenase and NADH-cytochrome c reductase were investigated in the brain of rats at different stages of post-natal development. In addition, the effect of the pharmacological treatment with two drugs, nicergoline and bamethan, able to interact with the alpha or the beta receptors respectively, was evaluated. The results show that both the enzymatic activities rapidly increase in the first days of extra-uterine life, thus indicating an adaptation of mitochondrial oxidative processes to post-natal environmental conditions. The pharmacological treatment with the two drugs does not induce any changes in the enzymatic activities tested.

Animals↗
PubMed1976

Muscle metabolism investigated at rest and during exercise and/or pharmacological treatment by vasodilators.

The Ruderman's preparation was utilized to investigate in situ some aspects of the muscular metabolism both at rest and during submaximal exercise upon bilateral sciatic nerve stimulation, and/or during perfusion with some vasodilators: papaverine, caffeine, nicergoline, bamethan. O2 and glucose uptake, the production of lactate and the glycogen level of the muscle were studied. The availability of acetoacetate modifies the muscular metabolism; other fuels (e.g. the ketone body itself) are probably used for energetic purposes both under basal conditions and during exercise, even in the presence of high glycogen concentrations in the tissues. Some vasodilators increase the utilization of other fuels in replacement of glycogen (e.g. nicergoline), some others increase the ulilization of glycogen itself (e.g. bamethan and caffeine), whereas others (e.g. papaverine) do not effect the biochemical parameters studied. The present data confirm the importance both of the substrate availability and of the power of drugs to interfere with some enzymatic systems which modulate the utilization of available substrates, especially during exercise.

Animals↗
PubMed1975

Mitochondrial enzymatic adaptation of skeletal muscle to endurance training.

Some mitochondrial enzymatic activities (succinate dehydrogenase, NADH cytochrome reductase, cytochrome oxidase) were studied in the gastrocnemius and soleus muscle of the rat. The modifications of the enzyme activity, induced by endurance training, were found to be functions of 1) daily work load and 2) total training time. The treatment with an effective dose of vasodilating substances (papaverine, nicergoline, dipyridamole, and bamethan) showed that 1) nicergoline, bamethan, and dipyridamole were differently able to shorten the time of appearance of the increase in the enzymatic activities; 2) however, long-term treatments with these drugs did not prove able to modify the plateau level of the enzymatic activity increase, for a given amount of endurance training; 3) the pharmacodynamic effect on enzymatic activities was in no way related to the vasodilating effect of these drugs, since the effect was not observed with papaverine. The transition from a given level of endurance training to a lower one led to a proportional decrease of the mitochondrial enzymatic activities, thus pointing out the relation between amount of training and enzymatic activity. The drugs studied were unable to modify the decrease of enzymatic activity induced by lower work load.

Adaptation, Physiological↗