Isoflurane and Enflurane-Induced Hepatic Necrosis in Triiodothyronine-Pretreated Rats

Berman, M. L.; Kuhnert, L.; Phythyon, James M.; Holaday, Duncan A.

doi:10.1097/00132586-198308000-00008

Cited by 4 publications

(4 citation statements)

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“…107,108 In the case of acute iron overload in hyperthyroid animals, the enhanced hepatotoxicity observed also is associated with the severe oxidative stress status established in the tissue, that is related to an impairment of Kupffer cell phagocytosis and particleinduced respiratory burst activity. 109 In agreement with these studies, thyroid hormone-induced sensitization to hepatotoxicity also has been reported for halothane, [110][111][112] isoflurane and enflurane, 111 carbon tetrachloride, 113 thioacetamide, 114 1,1-dichloroethylene, 115,116 and chloroform. 117 Moreover, a hypothyroid state induced by methimazole or PTU administration and thyroidectomy substantially reduces the development of liver injury associated with thioacetamide intoxication, 114 cold organ storage in liver transplantation, 108 or that produced by the exposure of rats chronically treated with ethanol to low O 2 tensions.…”

Section: Thyroid Hormone-induced Oxidative Stress In Mansupporting

confidence: 76%

Energy metabolism, thyroid calorigenesis, and oxidative stress: functional and cytotoxic consequences

Videla

2000

Redox Report

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Section: Thyroid Hormone-induced Oxidative Stress In Mansupporting

confidence: 76%

Energy metabolism, thyroid calorigenesis, and oxidative stress: functional and cytotoxic consequences

Videla

2000

Redox Report

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“…It is well established that the hepatotoxicity of a variety of substances such as lindane [138], halothane [139], isoflurane and enflurane [140], carbon tetrachloride [141] and chloroform [142], which seems to be linked to the development of an oxidative stress condition, is enhanced by hyperthyroid state. The mechanism for liver toxicity of anesthetic agents such as isoflurane, enflurane and halothane in hyperthyroid state has been scarcely investigated.…”

Section: Potentation Of Xenobiotic Hepatotoxicitymentioning

confidence: 99%

Thyroid hormone-induced oxidative stress

Venditti

Meo

2006

Cell. Mol. Life Sci.

339

230

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Hypermetabolic state in hyperthyroidism is associated with tissue oxidative injury. Available data indicate that hyperthyroid tissues exhibit an increased ROS and RNS production. The increased mitochondrial ROS generation is a side effect of the enhanced level of electron carriers, by which hyperthyroid tissues increase their metabolic capacity. Investigations of antioxidant defence system have returned controversial results. Moreover, other thyroid hormone-linked biochemical changes increase tissue susceptibility to oxidative challenge, which exacerbates the injury and dysfunction they suffer under stressful conditions. Mitochondria, as a primary target for oxidative stress, might account for hyperthyroidism linked tissue dysfunction. This is consistent with the inverse relationship found between functional recovery of ischemic hyperthyroid hearts and mitochondrial oxidative damage and respiration impairment. However, thyroid hormone-activated mitochondrial mechanisms provide protection against excessive tissue dysfunction, including increased expression of uncoupling proteins, proteolytic enzymes and transcriptional coactivator PGC-1, and stimulate opening of permeability transition pores.

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“…Rats pretreated with triiodothyronine showed increased hepatic necrosis following halogenated anaesthetics such as halothane, enflurane and isoflurane (Berman et al 1983). Halogenated anaesthetics are commonly used in patients undergoing thyroid surgery, because they allow rapid recovery and only moderate increases in concentrations of plasma thyroid hormones (Oyama et al 1979).…”

Section: Therapeutic Implicationsmentioning

confidence: 99%

Clinical Pharmacokinetics and Endocrine Disorders Therapeutic Implications

O’Connor

Feely

1987

Clinical Pharmacokinetics

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Endocrine disorders are common and produce widespread changes in cellular and organ function. Alterations in the sensitivity of patients with thyroid disorders to digoxin, anticoagulants and sedatives have been recognised for many years. Many of the recently documented kinetic alterations in endocrine patients are explicable on the basis of disease-induced changes in hepatic drug metabolism, protein binding and renal function. In hyperthyroidism the rate of absorption of paracetamol, propranolol and oxazepam is increased due to increased gastrointestinal motility. The volume of distribution of propranolol and digoxin is increased and there is decreased binding of both basic and acidic drugs as a consequence of alterations in alpha 1-acid glycoprotein and albumin concentration. The rate of glucuronidation of paracetamol and oxazepam is increased in hyperthyroidism. While oxidative metabolism of antipyrine, propranolol, metoprolol and theophylline is enhanced, the clearance of a number of other agents, including diazepam, warfarin, antithyroid drugs and phenytoin, is unaltered. The systemic clearance of propranolol is enhanced as a consequence of a 50% increase in liver blood flow. The rate of elimination of a number of endogenous substances, including cortisol, thyroid hormones and insulin, also appear to be enhanced. Hyperthyroidism has a variable effect on renal function, with a possible increase in digoxin elimination, but no effect on the clearance of renally excreted beta-blockers, atenolol, sotalol and nadolol. These kinetic changes suggest that individualization and higher than normal dosage of propranolol is necessary to control hyperthyroidism, and in thyrotoxic atrial fibrillation higher doses of digoxin or additional therapy with beta-blockers, or verapamil, may be indicated. The increased sensitivity of thyrotoxic patients to warfarin suggest care with dosage and frequent monitoring of response are warranted. Less information is available concerning hypothyroidism, but there is a general trend for decreased absorption of paracetamol and propranolol. In addition, the volume of distribution of digoxin is reduced, as is renal clearance. Limited studies suggest no alteration in the glucuronidation of oxazepam, but antipyrine clearance appears to be reduced. Steady-state propranolol concentrations are elevated in hypothyroidism and there appears to be a decreased metabolism of thyroid hormones and cortisol. Preliminary information suggests the binding of propranolol is increased. Thus, in the treatment of hypothyroid patients, a lower dosage of propranolol may be required.(ABSTRACT TRUNCATED AT 400 WORDS)

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Isoflurane and Enflurane-Induced Hepatic Necrosis in Triiodothyronine-Pretreated Rats

Cited by 4 publications

References 0 publications

Energy metabolism, thyroid calorigenesis, and oxidative stress: functional and cytotoxic consequences

Energy metabolism, thyroid calorigenesis, and oxidative stress: functional and cytotoxic consequences

Thyroid hormone-induced oxidative stress

Clinical Pharmacokinetics and Endocrine Disorders Therapeutic Implications

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