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
Case ReportsPlacental transfer of N-acetylcysteine following human maternal acetaminophen toxicity.
To determine whether the antidote for acetaminophen poisoning, N-acetylcysteine, administered to pregnant women with acetaminophen toxicity, crosses the placenta and can be measured in the newborn circulation following delivery. ⋯ This is the first study documenting placental transfer of N-acetylcysteine in humans and provides impetus for research establishing a direct antidotal effect of N-acetylcysteine in the fetus.
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J. Toxicol. Clin. Toxicol. · Jan 1997
Multicenter StudyProspective multicenter evaluation of tramadol exposure.
Tramadol is a novel analgesic possessing both opiate and noradrenergic effects. Its low potential for abuse suggests increasing use, but there are limited data on the toxicity in overdose. ⋯ This study suggests significant neurologic toxicity from tramadol overdose. Serious cardiovascular toxicity was not seen.
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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.