Halothane In Rats Research Articles

Analysis of fetal development in rats following maternal exposure to subanesthetic concentrations of halothane

AbstractPregnant Sprague‐Dawley rats were exposed to 50, 100, 200, 800, 1600, or 3200 ppm halothane on days 8, 9, 10, 11, and 12 of pregnancy. This did not result in increased fetal death and resorption rates, growth retardation, or an increased frequency of skeletal anomalies. When rats were exposed to 1600 ppm halothane on days 1–21 of pregnancy fetal growth was retarded but the differences in the number of centers of ossification in the skeletons were not significant. Skeletal anomalies including supplementary ribs, defective or delayed ossification of sternebrae, and missing centers of ossification in the lower parts of the limbs were seen in some fetuses in all groups but the frequency was not treatment related. Our results indicate that in Sprague‐Dawley rats halothane is not teratogenic or otherwise fetotoxic at subanesthetic concentrations.

Interaction of ketamine and halothane in rats

Interaction of ketamine and halothane in rats

Ultrastructural evidence of the hepatotoxic effect of halothane in rats following in-utero exposure.

Eight pregnant Sprague-Dawley rates were exposed to 10 ppm halothane 8 hours/day and 5 days/week throughout pregnancy. Liver samples were obtained from the pups for electron microscopy. Degenerative changes such as myelin-figure formation, focal-cytoplasmic degradation; fatty changes and cellular necrosis were observed. Leukocytic infiltration and phagocytosis of the cellular debris by Kupffer cells were also evident. The present investigation has demonstrated the hepatotoxic effects of halothane on the foetal liver. The role of halothane as an occupational hazard is considered.

Interaction of ketamine and halothane in rats.

The interaction of intramuscularly injected ketamine and its N-demethylated metabolite (metabolite I) with halothane was evaluated in rats. Five, 10, 20, or 50 mg/kg of ketamine alone or 20, 50, or 100 mg/kg of metabolite I alone produced less than 10 minutes of hypnosis. However, halothane anesthetic requirement (i.e., MAC) was depressed in a dose-dependent fashion as much as 56% 1-2 hours and as much as 14% 5-6 hours after injection of ketamine, 50 mg/kg, im. The reduction in MAC was correlated with brain levels of ketamine or metabolite I, suggesting a ketamine:metabolite I potency ration of 3:1. The half-life of ketamine in plasma and brain was longer in the presence of halothane than when ketamine was given alone. It is concluded that ketamine is not a short-acting drug and that concomitant use with halothane would be expected to prolong further the duration of its action on the central nervous system.

Teratogenicity of Halothane in Rats

Teratogenicity of Halothane in Rats