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Biomedical subjects

V A Peduto

Publications and source records attributed to V A Peduto.

At least 19 recordsLinked to original sources
PubMed1992

[Systemic poisoning caused by percutaneous absorption of mineral spirit].

Owing to a car accident, the clothes of a injured joiner were permeated with a timber impregnating product containing 51.8% of mineral spirit (a mixture of naphthenes, aromatic and aliphatic hydrocarbons). Despite a short-lasting skin exposure (approximately 40 minutes), dermal contact has caused full thickness burns that, in their turn, have made easier the percutaneous absorption and the storage of organic solvents in subcutaneous tissue depots. Twenty-four hours later, clinical findings of neurologic involvement have arisen, that have got worse when the peripheral tissue perfusion has got better by the adequate replacement of lost blood.

Adult↗
PubMed1991

Biochemical and electrophysiologic evidence that propofol enhances GABAergic transmission in the rat brain.

The influence of propofol, a new intravenous anesthetic agent, on brain gamma-aminobutyric acid (GABA)-ergic transmission has been investigated both in vitro and in vivo. In vitro, propofol, like benzodiazepines, 1) markedly enhanced 3H-GABA binding in cortical membrane preparations; 2) potentiated muscimol-induced stimulation of 36Cl- uptake in membrane vesicle preparations (the propofol potentiating effect was antagonized by bicuculline); and 3) inhibited 35S-TBPS binding to unwashed membrane preparations from rat cerebral cortex. Finally, propofol failed to displace 3H-flunitrazepam from its binding site, indicating that its site of action in brain is different from that of benzodiazepines. In vivo, the effect of propofol was studied using single-unit recording of the electrical activity of both nondopaminergic neurons in the pars reticulata of the substantia nigra (PR neurons) and of dopaminergic neurons in the pars compacta of the substantia nigra (DA neurons). PR neurons are known to be inhibited by GABA-mimetic drugs and benzodiazepines, whereas DA neurons are tonically inhibited by PR neurons. The intravenous administration of propofol, in a fat emulsion formulation, produced a brief dose-dependent inhibition of the firing rate of PR neurons. The dose producing 50% inhibition of the firing rate was calculated to be 1.2 +/- 0.1 mg/kg. The inhibitory effect lasted less than 5 min. Repeated injections of propofol reproduced the same inhibitory response, whereas continuous infusion (0.5 mg.kg-1.min-1) produced a persistent inhibition of neuronal firing. The inhibitory effect of propofol on PR neurons was potentiated by diazepam and reversed by picrotoxin and bicuculline but was not influenced by the benzodiazepine antagonist Ro 15-1788. These findings suggest that propofol exerts a GABA-mimetic action on PR neurons by acting on a site distinct from the benzodiazepine recognition site. Unlike benzodiazepines, propofol inhibited the firing rate of DA neurons with a potency proportional to its inhibitory effect on PR neurons. The inhibition of DA neurons was reversed by bicuculline and picrotoxin. The results suggest that propofol enhances the inhibitory control over DA neurons by strionigral GABAergic neurons.

Animals↗
PubMed1989

[Poisoning caused by chronic exposure to volatile anesthetics. Molecular mechanisms and risk anesthetics].

The possible molecular mechanisms potentially inducing occupational disease among operating room personnel were examined; and the really dangerous anaesthetic agents were identified. As concerns the molecular mechanisms of parenchymatous injury, we surveyed: those connected with free radicals and biological reactive intermediates produced during halothane and nitrous oxide biotransformation; those coming from inorganic fluoride produced during biotransformation of any halogenated anaesthetic agent, and from inorganic bromide released during halothane metabolism; and, finally, those linked to vitamin B12 inactivation from nitrous oxide. Halothane and nitrous oxide can be considered as really dangerous anaesthetic agents for operating room personnel, and enflurane as an agent with marginal toxic power. On the contrary, isoflurane is a safe, useful compound, totally devoided of viscerotoxic effects. From data examined it is possible to conclude that an isoflurane-oxygen-air anaesthesia is safe for operating room personnel more than a balanced anaesthesia with intravenous drugs and nitrous oxide as maintenance.

Air Pollutants, Occupational↗
PubMed1988

Bilateral extensive skin necrosis of the lower limbs following prolonged epidural blockade.

Skin necrosis has not been described as a complication following epidural sympathetic blockade. We report a case of bilateral extensive skin necrosis of the lower limbs after a 48-hour lumbar epidural blockade in a 71-year-old patient with right hemiplegia and mitral valve regurgitation, without any preoperative clinical evidence of peripheral vascular disease or diabetes, who underwent transurethral prostatectomy.

Aged↗
PubMed1988

[Isoflurane pollution in operating rooms].

In three operating rooms of a Sardinian hospital, the Authors have measured the air levels of isoflurane using static samplers. Anaesthetic mean daily concentrations ranged from 3.5 to 41.5 ppm in room A, from 4.1 to 24.4 ppm in room B, from 9.5 to 30.4 ppm in room C above all depending on the length and the number of surgical operations. The Authors emphasize the need of suitable prevention measures.

Air Pollutants, Occupational↗
PubMed1986

Liver function following hypovolemic hypotension in rats anaesthetized with halothane or enflurane.

Rats which had approximately 25-30% of their calculated blood volume removed were exposed to halothane (1%) or enflurane (2%) in 33% oxygen for 30 min. Hepatic function was evaluated by determining, at various time intervals, serum activities of glutamic-oxalacetic and glutamic-pyruvic transaminase, acid phosphatase and gamma-glutamyl-transpeptidase. In this model serum enzyme activities and animal mortality were significantly increased when hypovolemic hypotension was induced during halothane anaesthesia. The same events did not occur in bleeding animals anaesthetized with enflurane. The marked disparity in hepatic dysfunction and mortality between halothane and enflurane-anaesthetized rats during hypovolemic hypotension may be explained by the more pronounced decrease of oxygen available for the liver and production of reductive toxic intermediates in animals exposed to halothane.

Anesthesia↗
PubMed1983

Analgesic interaction between nitrous oxide and delta-9-tetrahydrocannabinol in the rat.

The analgesic activities of a 75:25% nitrous oxide-oxygen mixture administered for 15 min, of delta-9-tetrahydrocannabinol (THC) 10 mg kg-1 i.p., and of a combination of both, were evaluated in the rat by tail-flick and hot-plate tests. The nitrous oxide-oxygen mixture produced a significant increase in the pain threshold. The analgesic activity of THC was similar in extent but of longer duration than that of nitrous oxide. The cannabinoid also induced some locomotor and behavioural modifications. When both THC and the nitrous oxide-oxygen mixture were administered, a significant potentiation of the analgesic response was produced, without modification of the locomotor and behavioural responses that were induced by THC alone. Such mixtures may prove of value in the control of chronic pain in man.

Analgesia↗
PubMed1983

Stimulation of drug-metabolizing enzymes by nitrous oxide in the rat.

Wistar male rats were subchronically (150 h continuously) or chronically (5 h daily for 15 days) exposed to a 50% nitrous oxide/oxygen mixture. As an index of enzyme induction liver N-demethylase and benzo(a)pyrene-hydroxylase activities, serum gamma-glutamyltranspeptidase activity, urinary d-glucaric acid and pentobarbital sleeping time were evaluated in comparison with a control group. No effect was observed after subchronic exposure to the anaesthetic gas. Chronic exposure, on the contrary, decreased pentobarbital sleeping time, increased urinary d-glucaric acid, liver N-demethylase and serum gamma-glutamyltranspeptidase activities. No increase of liver benzo(a)pyrene-hydroxylase was observed. Chronic nitrous oxide exposure under appropriate conditions can modify some enzymes, metabolizing drugs and xenobiotic compounds.

Animals↗
PubMed1982

[Effects of nitrous oxide on the female gonad in the rat].

Female rats have been exposed (24 hours for 15 days) to N2O 60% in normo-oxic blend of N2 and O2. Vaginal smears have been observed daily. At the end of the experiment the ovaries have been removed and the following morphological parameters have been statistically evaluated: number of evolutive follicles and corpora lutea, amount of interstitial tissue. Our results seem to account for a remarkable toxic effect of N2O on the rat gonad. Such effect is testified by alterations of the oestrous cycle and, at the ovary, a decrease in the number of evolutive follicles and functioning corpora lutea and by a sharp increase of atretic phenomena.

Animals↗
PubMed1980

Analgesic effect of aprotinin in the rat and its inhibition by naloxone.

Experiments were performed on rats using two analgesimetric tests (tail-flick; hot-plate) before and after injection i.v. of graded doses of aprotinin (12.5, 25.0 and 50 KIU g-1). A dose-related analgesic effect was noted with both tests. Prior administration of naloxone 0.001 mg g-1 i.p. inhibited the analgesic action.

Analgesia↗