Journal of toxicology. Clinical toxicology
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J. Toxicol. Clin. Toxicol. · Jan 1997
Experimental studies of methemoglobinemia due to percutaneous absorption of sodium nitrite.
Methemoglobin formation caused by a liniment solution containing sodium nitrite (30 g/L and 140 g/L) was studied in rats with normal or abraded skin, by measuring the methemoglobin concentration before and after application of liniment solutions with differing nitrite concentration. ⋯ Each of these findings are characteristic of nitrite and they imply the percutaneous absorption of nitrite. Regardless of the nitrite concentration, the methemoglobin concentration was consistently higher in abraded skin than in normal skin.
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J. Toxicol. Clin. Toxicol. · Jan 1997
Historical ArticleAnaleptic use in clinical toxicology: a historical appraisal.
The introduction and increasing popularity of the barbiturates during the first two decades of the 20th century was associated with a new life threatening toxicological problem: the barbiturate overdose. ⋯ Although barbiturate overdose mortality decreased to less than 1% using this strategy, it would take another 20 years before this technique was universally adapted. While analeptic therapies for the treatment of drug overdose have now been abandoned, one of these analeptics, methylphenidate, currently enjoys wide use in the treatment of attention deficit hyperactivity disorder.
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J. Toxicol. Clin. Toxicol. · Jan 1997
Multicenter Study Clinical TrialUnintentional childhood poisoning in athens: a mirror of consumerism?
To estimate the incidence of unintentional childhood injuries resulting from accidental poisonings in the Greater Athens area and to ascertain what fraction of this incidence could be linked to specified conditions, amenable to preventive interventions. ⋯ Unintentional childhood poisoning further reflects an interaction between inappropriate storage of consumer products and suboptimal supervision during the housekeeping hours of the day.
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J. Toxicol. Clin. Toxicol. · Jan 1997
ReviewSites of action of gamma-hydroxybutyrate (GHB)--a neuroactive drug with abuse potential.
This review highlights the biochemistry, pharmacology, and toxicology of the naturally-occurring fatty acid derivative, gamma-hydroxybutyrate (GHB). GHB is derived from gamma-aminobutyric acid (GABA) and is proposed to function as an inhibitory chemical transmitter in the central nervous system. ⋯ When administered in pharmacological doses, its powerful central nervous system depressant effects are readily observed. Although some of the neurophysiological actions of GHB could involve alterations in dopaminergic transmission in the basal ganglia, both its physiological and pharmacological actions are probably mediated through specific brain receptors for GHB. In addition, GHB might mediate some of its effects through interaction with the GABA(B) receptor. Experimentally, GHB has been used as a model for petit mal epilepsy; clinically, it has been used as a general anesthetic and as a drug to treat certain sleep disorders and related conditions. Owing to the purported ability of GHB to induce a state of euphoria, recreational use of this substance is popular. Although no deaths or long-term problems have been associated with GHB abuse, symptoms of GHB intoxication can be severe. The continued potential for GHB abuse makes it imperative for clinical toxicologists to be aware of the effects of this agent. Future research on the mechanism of action of GHB is needed to elucidate both its central nervous system depressant properties and its ability to effect a state of well-being.