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Biomedical subjects

L Congiu

Publications and source records attributed to L Congiu.

At least 37 records · Page 2Linked to original sources
PubMed1979

A biological approach to two forms of human self-injury.

One hundred cases of self-injury, comprising 39 self-cutters and 61 self-poisoners, were interviewed when they became able to describe the act: 83 in a casualty department, 17 in a hospital. Standardized recordings were made of their feeling state before and after the act, together with an account of the social circumstances under which it occurred. The information was obtained in a way which allowed comparison with existing animal data on self-injury, although comparisons were made between what is known of animal behavior in this area and human feelings as reported by these subjects. The results indicate similarities between what is known of animal self-injury and self-cutting in man in the form of the injury, in the social situation preceding the act, and in the agitation preceding it. Similarities also exist, but are less close, for the self-poisoners. The most obvious effect of the act is a reduction in tension; this may constitute its physiological value.

Adolescent↗
PubMed1976

Early investigations on the effect of methyl mercuric chloride upon DMN-acute hepatotoxicity.

Acute toxicity induced by DMN was partially prevented by previously administering methyl mercuric chloride (MMC), a chemical inhibitor of the drug metabolizing enzyme system (DMES). We have studied the early changes occurring during the course of DMN-intoxication, namely disaggregation of polysomal profiles and necrosis, evaluated morphologically and by the release of S-GPT.

Alanine Transaminase↗
PubMed1976

Influence of lead nitrate on dimethylnitrosamine intoxication.

The effect of lead nitrate, an inhibitor of the hepatic drug-metabolizing enzyme system upon the acute, hepatotoxicity of dimethylnitrosamine (DMN) was studied. Lead pretreatment significantly prevented polysomal disaggregation induced by the nitrosamine. Cell necrosis, evaluated morphologically and by the release of serum glutamic-pyruvic transaminase (GPT), was also diminished. The metabolism of DMN in rats pretreated with lead nitrate was investigated by following its clearance from blood and by determining, in vitro the demethylation of the nitrosamine. Lead increased, although not significantly, the clearance of DMN from blood, but it lowered the activity of DMN-demethylase 24 h after its administration. Finally, lead lowered the lethal effects of DMN. The mechanism by which lead influenced DMN toxicity is discussed.

Animals↗
PubMed1976

Protection by cerium chloride on CCl4-induced hepatotoxicity.

Pretreatment of rats with cerium chloride, an inhibitor of the DMES, protect against CCl4 intoxication. The protection was obtained against the fatty infiltration in the liver, the decrease of triglyceride secretion from the liver into the plasma compartment, the polysomal disaggregation and the rise of serum transaminases.

Alanine Transaminase↗
PubMed1976

Bromobenzene hepatotoxicity in lead pretreated rats.

We have studied the levels of hepatic GSH in animals intoxicated with bromobenzene. A marked decrease of hepatic GSH was observed in poisoned rats. Such decrease was prevented by previous administration of lead nitrate, an inhibitor of DMES. In the rats treated with lead nitrate alone a rise in hepatic GSH was observed. Such protection was further observed by histological examination. The mechanism of protection exerted by lead nitrate against bromobenzene intoxication is discussed.

Animals↗
PubMedDate not supplied

Protection by lead nitrate against carbon tetrachloride hepatotoxicity.

Pretreatment with lead nitrate of rats intoxicated with CCl4 exerted a significant protective effect against several damaging effects of the haloalkane. Liver microsomal lipid peroxidation, one of the earliest phenomena in CCl4 intoxication, was clearly inhibited by pretreating the rats with lead. The heavy metal also ameliorated the polyribosomal disaggregation caused by CCl4. Fatty infiltration in the liver, measured by the triglyceride content in the organ, was less pronounced in CCl4-poisoned rats pretreated with lead than in animals treated with the haloalkane alone. Lipid metabolism was also studied by means of Triton WR 1339-induced hypertriglyceridemia to examine the state of triglyceride secretion from liver into plasma; the higher level of plasma triglyceride in the lead-pretreated rats further strengthened the results obtained on the secretion experiments. Finally, CCl4-induced liver necrosis, as measured by serum transaminases and histological examination, was partially prevented by lead. The mechanism by which lead, an inhibitor of the drug-metabolizing enzyme system, interferes with CCl4 intoxication, is disccused.

Alanine Transaminase↗
PubMedDate not supplied

[Participation of tachykinins in experimental models of lung damage].

In the present investigation a possible involvement of tachykinins during sulfur dioxide-(SO2) and metabisulfite-(MBS) induced bronchoconstriction, and paraquat (PQ)-induced mortality was studied. SO2 (250ppm) inhalation and MBS (3mM) perfusion induced a marked decrease of compliance and conductance in the isolated and perfused lung. SO2-induced bronchoconstriction was associated with release of Calcitonin Gene Related Peptide, suggesting activation of capsaicin sensitive sensory nerves. Pretreatment of animals with capsaicin, in order to deplete the tachykinin content of sensory nerves, significantly reduced SO2- and MBS-induced bronchoconstriction. PQ (25mg/Kg) treatment induced high mortality (75%) after 3 weeks. Pretreatment with capsaicin significantly protected versus PQ induced mortality (25%). The results suggest that tachykinin content in the respiratory airways participate to SO2- and MBS-induced bronchoconstriction and PQ mortality.

Animals↗
PubMedDate not supplied

[Mechanisms of tolerance to sulfur dioxide and sodium metabisulfite].

Inhalation of sulphur dioxide (250 ppm), (SO2) or sodium metabisulfite (80 mM) (MBS) aerosol or perfusion with MBS (3 mM) induced a reduction in compliance and conductance in the isolated, perfused and ventilated guinea pig lung. Pretreatment of the lung with sodium sulfite (3 mM), a dissolution product of SO2 and MBS, reduced the bronchoconstriction induced by SO2 and MBS. Bronchoconstriction induced by SO2 and MBS in associated to increased levels of Calcitonin gene-Related Peptide (CGRP) in the perfusate effinent, indicating activation of sensory nerves. The release of CGRP induced by SO2 and MBS was not affected by sodium sulfite. Sulfite treatment did not modify lung reactivity towards acethylcholine, bradykinin, serotonin, histamine and substance P (fragment 5-11). An inhibitory effect by sulfite was observed on bronchoconstriction induced by neurokinin A (fragment 4-10). Since bronchoconstriction induced by SO2 and MBS appears to be mediated by neurokinin A release and action, sulfite may act by affecting its signal transduction pathway. In conclusion, the results indicate that during exposure to some environmental and occupational pollutants, e.g. SO2 and MBS, critical modifications of sulfhydryl groups on smooth muscle receptors may occur. We hypothesise this as a possible step in the development of tolerance and hyperreactivity.

Administration, Inhalation↗