Search PubMed⌕ Search

Biomedical subjects

G G Harrison

Publications and source records attributed to G G Harrison.

At least 109 records · Page 6Linked to original sources

An investigation into the hepatic cytochrome P-450 catalysed metabolism of the anaesthetic fluroxene (2,2,2-trifluoroethyl vinyl ether).

The role of the different cytochromes P-450 in the metabolism of the anaesthetic agent fluroxene, and the mechanism of production of toxic effects seen after pre-treatment of the animals with pehnobarbital prior to anaesthesia, have been investigated. Male rats were anaesthetized with fluroxene, or with 2,2,2-trifluroethyl ethyl ether, or with ethyl vinyl ether in an attempt to ascertain the in vivo toxic effects of the three anaesthetic agents. The resultant hepatic histology is reported. A study of the binding and metabolism of fluroxene by isolated rat hepatic microsomes was also made. We conclude that it is elevated levels of cytochrome P-450 which potentiate the toxicity of fluroxene anaesthesia in phenobarbital treated animals and that cytochrome P-448 does not bind or metabolize fluroxene. The potential toxicity of the fluroxene molecule is considered to reside in the trifluoroethyl moiety, while the vinyl group of fluroxene appears to play a role in the observed liver damage.

Allylisopropylacetamide↗

Anaesthetic-induced malignant hyperpyrexia: a suggested method of treatment.

Experiments in susceptible Landrace pigs have shown that procaine blocks the initiation of anaesthetic-induced malignant hyperpyrexia by both halothane and succinylcholine. Pretreatment with curare prevents only the trigger action of succinylcholine. In a preliminary study procaine was used to treat the established syndrome in five pigs, two of which survived. On the basis of these findings a treatment regimen can be suggested for patients who develop malignant hyperpyrexia.

Acidosis↗

Multiple halothane exposure and hepatic bromsulphthalein clearance.

Multiple exposures to halothane have been shown to have delayed effects on bromsulphthalein (B.S.P.) clearance. Rats were exposed to repeated halothane anaesthetics, and their livers were subsequently isolated and perfused. B.S.P. retention in the perfusate of these isolated livers was greatly increased one to three weeks after the last halothane exposure. In similarly pretreated animals at the same time period the B.S.P.-glutathione conjugating enzyme activity in homogenates of the livers was found to be depressed. These findings did not occur after multiple diethyl ether exposures or following a single exposure to halothane.

Animals↗