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

Abstract

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.

Sevofluran, Isofluran ve Propofol’ün tiroid fonksiyonlarına etkileri

“…Acil operasyona alınan tiroid bezi disfonksiyonu olan hastalarda özellikle kardiyovasküler sistem olmak üzere birçok organ etkilenmektedir [7,8]. Bu komplikasyonlar; tiroid hormonlarının direkt metabolizma ve kardiyak etkilerinin yanında, cerrahi stres ve anesteziye yanıt sonucunda hormon seviyelerindeki değişimlere ve anesteziklerin metabolizmasındaki değişimlere de bağlıdır [9,10].…”

Effect of Hyperthyroidism on the in Vitro Metabolism and Covalent Binding of 1,1-Dichloroethylene in Rat Liver Microsomes

“…Conversely, hyperthyroidism attenuates the toxicity of bromobenzene, and has only a minor effect on acetaminophen injury (Smith et al, 1983;Raheja et al, 1982). In rats, hyperthyroidism has been shown to alter pharmacokinetic parameters such as elimination halflives, label excretion, or metabolite concentrations of these toxicants (Siegers et al, 1981;Kanz et al, 1994;Raheja et al, 1982). Based on alterations in circulating metabolite concentration, Siegers et al (1 983) proposed that the hyperthyroid-induced potentiation of halothane hepatotoxicity was due to an enhanced bioactivation.…”