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E Vincenti

Publications and source records attributed to E Vincenti.

At least 37 records · Page 2Linked to original sources
PubMed1991

Influence of the anesthetic 2,6-diisopropylphenol on the oxidative phosphorylation of isolated rat liver mitochondria.

Isolated rat liver mitochondria have been incubated in the presence of the general anesthetic 2,6-diisopropylphenol (0-100 microM) and the efficiency of oxidative phosphorylation has been evaluated by measuring the respiratory rates, the rates of ATP synthesis or hydrolysis and the magnitude of the transmembrane electrical potential. The results obtained indicate that: (a) in mitochondria energized either by succinate or by ATP, 2,6-diisopropylphenol decreased the transmembrane electrical potential and increased the rates of either electron transfer or ATP hydrolysis; (b) in succinate-energized mitochondria 2,6-diisopropylphenol, at concentrations causing substantial depression of the transmembrane electrical potential, did not modify either the rate of phosphorylation of added ADP or the rate of ADP-stimulated respiration: (c) in succinate-energized mitochondria 2,6-diisopropylphenol caused a concentration-dependent inhibition of the uncoupler-stimulated rate of succinate oxidation. These findings suggest that under the experimental conditions reported 2,6-diisopropylphenol affected the generation and/or maintenance of the transmembrane electrical potential while leaving unchanged the coupling between the electron flow in the respiratory chain and the synthesis of ATP.

Adenosine Triphosphate↗
PubMed1991

Effects of acute systemic hyperinsulinemia on forearm muscle proteolysis in healthy man.

To investigate the mechanism(s) of insulin-induced suppression of plasma amino acid concentration and release, we studied forearm as well as whole-body leucine and phenylalanine uptake and release during a peripheral insulin infusion in postabsorptive normal subjects using isotope-dilution methods. Before insulin, leucine and phenylalanine release exceeded uptake (P less than 0.01 and P less than 0.07, respectively). A net output of alpha-ketoisocaproate (KIC) was also observed. During insulin, arterial plasma leucine, KIC and phenylalanine concentrations decreased (P less than 0.05 or less vs. basal), despite ongoing net output of these substrates by the forearm, that persisted after correction for the mean transit time spent through the extracellular muscular space. By the end of insulin, whole-body leucine and phenylalanine concentrations and rate of appearance were decreased (P less than 0.01 vs. basal). However, release and uptake of both amino acids by the forearm were not significantly decreased vs. the preinsulin values. These data indicate that systemic hyperinsulinemia acutely decreases plasma amino acid concentrations by acting primarily at sites other than skeletal muscle.

Adult↗
PubMed1989

Energetic behaviour of mitochondria isolated from rat livers perfused with a perfluorodecalin + N,N-perfluorodiethylcyclohexylamine emulsion.

Rat livers have been perfused with a saline control medium or with a perfluorocarbon emulsion containing perfluorodecalin and N,N-perfluorodiethylcyclohexylamine, and the respiratory rates and transmembrane electrical potentials of mitochondria isolated following perfusion have been evaluated. The results indicate that the perfluorocarbon emulsion used, by providing a good oxygen supply to the perfused liver, allowed to preserve the efficiency of mitochondrial oxidative phosphorylation.

Adenosine Triphosphate↗
PubMed1989

General anesthetics: interferences with some mitochondrial energy-dependent mechanisms.

The anesthetics halothane, enflurane, isoflurane and 2,6-diisopropylphenol negatively affect several energy-linked processes in isolated rat liver mitochondria, decreasing their efficiency. The adverse effects observed in the presence of halothane, enflurane and 2,6-diisopropylphenol are similar for many aspects although, being caused by anesthetics having different molecular structures, they differ significantly from the quantitative point of view. A relevant role in the anesthetic-induced mitochondrial injuries appears to be played by long-chain acylCoA, whose level is markedly increased in mitochondria incubated in the presence of halogenated anesthetics. In addition, the amount of intramitochondrial calcium may also influence the severity of these injuries.

Anesthetics↗
PubMed1988

The inhibition of calcium efflux from rat liver mitochondria by halogenated anesthetics.

The halogenated anesthetics halothane, enflurane and isoflurane inhibit the calcium efflux induced by Ruthenium Red in isolated rat liver mitochondria. The extent of the inhibition is higher for enflurane (approximately 50%) than for either isoflurane (approximately 35%) or halothane (approximately 15%), and does not increase significantly between 0.1 and 0.6-1.0 mM anesthetic. Both the mitochondrial respiratory rate and transmembrane electrical potential are unaffected by the halogenated anesthetics concentrations capable to inhibit the efflux of calcium.

Animals↗
PubMed1986

L-carnitine effect on halothane-treated mitochondria.

Addition of halothane to the incubation medium is shown to lower respiratory control and transmembrane potential and to increase ATPase activity in isolated rat liver mitochondria. Evidence is presented that L-carnitine is able to substantially decrease the negative effects of halothane on the energy-linked processes of mitochondria. The effects of halothane and the protective action of L-carnitine are discussed in the light of a possible involvement of long-chain acyl CoA in the unpairing of mitochondrial energy-linked functions.

Acyl Coenzyme A↗
PubMed1986

Involvement of long-chain acyl CoA in the antagonistic effects of halothane and L-carnitine on mitochondrial energy-linked processes.

Incubation of rat liver mitochondria in the presence of halothane induced a consistent impairment of mitochondrial oxidative phosphorylation without significantly affecting the steady-state of transmembrane electrical potential. These alterations of mitochondrial energy-linked processes were associated with a consistent accumulation of long-chain acyl CoA. Addition of L-carnitine partially prevented the effects of halothane on oxidative phosphorylation and completely abolished the halothane-induced long-chain acyl CoA accumulation. The possibility is discussed that the damaging action of halothane on mitochondrial functions might be partially ascribed to the noxious action of the excess of long-chain acyl CoA induced the anesthetic.

Acyl Coenzyme A↗