Urinary Excretion of Bromide in Halothane Anesthesia

Stier, A.; Alter, H; O, Hessler; Rehder, Kai

doi:10.1213/00000539-196411000-00024

Cited by 40 publications

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“…Recently, a number of fluorocarbons were shown to exert carcinogenic potency (24) similar to the known peroxisome proliferators (3). Studies on the metabolism of halothane, a widely used volatile narcotic, have demonstrated perfluoroacetate (PFA) as the main metabolite (25). PFA administration resulted in hepatomegaly and the induction of mitochondrial glycerol-3phosphate dehydrogenase activity (26).…”

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confidence: 99%

Biochemical effects and zonal heterogeneity of peroxisome proliferation induced by perfluorocarboxylic acids in rat liver

et al. 1989

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Rats were treated for 5 to 14 days with perfluoroacetate, perfluorobutyrate and perfluorooctanoate. Alterations in hepatic morphology with special reference to the peroxisomal compartment were investigated by light and electron microscopy following cytochemical staining of catalase activity with the alkaline 3,3'-diaminobenzidine medium. All three compounds induced hepatomegaly and peroxisome proliferation. Perfluorobutyrate and perfluorooctanoate were found to be more active than perfluoroacetate. Perfluorooctanoate-induced peroxisome proliferation was more prevalent in centrilobular than in periportal hepatocytes. Peroxisomes in centrilobular liver cells frequently were of round shape, exhibited diameters of up to 1.5 microns and were predominantly located within smooth endoplasmic reticulum-glycogen areas. In periportal cells, however, clusters of polymorphous peroxisomes ranging from 250 to 1,100 nm in diameter were observed at the periphery of smooth endoplasmic reticulum-glycogen regions. Peroxisome proliferation was accompanied by a change of peroxisomal and mitochondrial enzyme activities, in particular an increase in peroxisomal palmitoyl-CoA oxidation. Significant alterations in the concentration of peroxisomal matrix and membrane polypeptides were also noted. Within the first 2 days, perfluorooctanoate treatment exerted a strong hypolipidemic activity and both compounds perfluorooctanoate and perfluorobutyrate raised the level of hepatic free acid-soluble CoA nearly 10-fold as compared with control livers. The results suggest perfluorinated carboxylic acids to be model substances suitable to correlate biochemical and morphological parameters with the zonal heterogeneity of the peroxisomal compartment in rat liver. Due to the manifold hepatic effects, contact of humans with perfluorinated carboxylic acids or their metabolic precursors may represent a severe health risk.

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confidence: 99%

Biochemical effects and zonal heterogeneity of peroxisome proliferation induced by perfluorocarboxylic acids in rat liver

et al. 1989

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“…The role of the microsomal monooxygenase system in the biotransformation of these com pounds has been substantiated by previous investigators (4,10,21). Recently Rumbaugh et al (18) reported that in rats treated with thyroxine a dose-dependent decrease in hepatic cytochrome P-450 was observed simulta neously, cytochrome c reductase activity was significantly elevated, so that the overall biotransformation rate for ethylmorphine, benzo-[a]-pyrene and aniline was accelerated.…”

Section: Discussionmentioning

confidence: 84%

Effects of Thyroid Dysfunction on the Metabolism of Halothane, Enflurane and Methoxyflurane in Rats

Siegers¹,

Mackenroth²,

Wächter³

et al. 1981

Pharmacology

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The effect of thyroid dysfunction on the metabolism of halothane (100 ppm), enflurane (100 ppm) and methoxyflurane (300 ppm) was investigated during application by inhalation. In male rats the elimination half-lives from the atmosphere of the exposure system amounted to 0.76 h for halothane, 6.84 h for enflurane and 0.64 h for methoxyflurane. Hyperthyroidism due to three daily injections of 0.1 mg/kg triiodothyronine i.p. significantly shortened the half-lives of all three inhalation anesthetics. Hypothyroidism due to operative removal of the thyroid gland affected the metabolism of halothane only as evidenced by a prolongation of the elimination half4ife while enflurane and methoxyflurane half-lives remained unchanged. The observed differences in metabolic rates are explained by different metabolic pathways of the three compounds. They may be important for the manifestation of toxic effects.

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“…Following early studies by Stier et al [40], it became apparent that in man, as well as laboratory animals, halothane underwent biotransformation through at least two differ ent pathways. Studies from a number of work ers have shown that metabolism through both pathways results in the generation of reactive metabolites which bind to liver cell macro molecules; thus, under anaerobic conditions (P |0 2 < 14%), there is increased covalent binding of radiolabellcd halothane to micro somal protein; the degree of binding can be enhanced by pretreatment with cytochrome P450 inducers, such as phenobarbitone and polychlorinated biphenyls [41,42], Under aerobic conditions, there is covalent binding to both microsomal proteins and lipids.…”

Section: Mechanisms Of Halothane Hepatotoxicitymentioning

confidence: 99%

Halothane Hepatitis

Neuberger

1988

Dig Dis

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Urinary Excretion of Bromide in Halothane Anesthesia

Cited by 40 publications

References 0 publications

Biochemical effects and zonal heterogeneity of peroxisome proliferation induced by perfluorocarboxylic acids in rat liver

Biochemical effects and zonal heterogeneity of peroxisome proliferation induced by perfluorocarboxylic acids in rat liver

Effects of Thyroid Dysfunction on the Metabolism of Halothane, Enflurane and Methoxyflurane in Rats

Halothane Hepatitis

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