Ventilation, ventilatory carbon dioxide and hormonal response during halothane anaesthesia and surgery in children after midazolam premedication.

In 14 intubated, spontaneously breathing children with body weight (bw) ranging from 8.3 to 25.6 kg, the influence of midazolam 0.

The effect of cimetidine on anesthetic metabolism and toxicity.

Because the H2-receptor antagonist cimetidine has been shown to inhibit drug metabolism, the effects of cimetidine on anesthetic metabolism and toxicity were investigated in a rat model. Cimetidine decreased inorganic plasma fluoride production after methoxyflurane administration both in 21% oxygen (P less than 0.001) and in 100% oxygen (P less than 0.

Ventilatory responses to inspiratory mechanical loads in spontaneously breathing children during halothane anaesthesia.

The effect of the addition of two different resistive loads (producing 23 and 36 cmH2O (2.26 and 3.53 kPa) 1(-1) s-1, respectively, at 71 min-1) on minute volume, tidal volume, respiratory rate, duration of inspiration and inspiratory drive was studied in six intubated children during nitrous oxide, oxygen and halothane anaesthesia.

Contrasting effects on halothane hepatotoxicity in the phenobarbital-hypoxia and triiodothyronine model: mechanistic implications.

Factors affecting halothane (H) hepatotoxicity were investigated in two animal models: 1) the phenobarbital-hypoxia model, and 2) the triiodothyronine (T3) model; in the latter we previously have shown that centrilobular necrosis occurs in T3 pretreated rats anesthetized with 1% H, in 21% oxygen for 2 h. Feeding worsens the hepatotoxic effects of H in the T3 model. SGPT levels were higher (P less than 0.

Isoflurane and enflurane-induced hepatic necrosis in triiodothyronine-pretreated rats.

Exposure of triiodothyronine (T3)-pretreated rats to 1.3% isoflurane, 1.8% enflurane, or 1% halothane in 21% oxygen (air) for two hours resulted in hepatic centrilobular necrosis.