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The rat is the most frequently used animal in scientific inquiry conducted for the purpose of advancing basic knowledge that may lead to an improvement in the results of treatment. Understanding of the pharmacological properties of inhalation anaesthetics, in combination with monitoring of their concentration in the inspired and end-tidal gas, together provide safe and precise control of the depth of the anaesthesia. However, accurate application of the inhalation method of anaesthesia requires special equipment for the delivery and effective scavenging of inhalation anaesthetics.
The aim of this study was to evaluate midazolam as an intravenous induction agent for inhalation anaesthesia in the routine castration of dogs. Investigations concerned the dose required for induction as well as its effects on the dog’s general condition, arterial blood gas and acid-base balance. A total of 24 male dogs of various breeds were studied, ranging in age from 1 to 11 years and in weight from 5 to 27 kg. Dogs were recruited at the Department and Clinics of Animal Surgery, University of Life Sciences in Lublin, Poland. The dogs were premedicated intramuscularly with xylazine and atropine sulphate at dose rates of 2 mg/kg and 0.05 mg/kg respectively. Twenty minutes after premedication, midazolam was administered by intravenous infusion. Intravenous midazolam proved useful as an induction agent for inhalation anaesthesia. The dose used was dependent on the animal’s reaction. The induction of anaesthesia with midazolam was successful and enabled endotracheal intubation and inhalation anaesthesia with a halothane-oxygen mixture. The application of midazolam with halothane, however, led to transitory disturbances in systemic acid-base balance due to gas exchange abnormalities. The median effective dose of midazolam for the induction of anaesthesia was 0.46 mg/kg i.v. Postoperatively, a full recovery of consciousness and motor functions was rapidly achieved in all dogs. Further studies on midazolam as an intravenous induction agent for inhalation anaesthesia in the dog are warranted.
The relationship between DNA damage and repair of peripheral blood leukocytes, liver, kidney and brain cells was investigated in Swiss albino mice (Mas musculus L.) after exposure to sevoflurane (2.4 vol% for 2 h daily, for 3 days). Genetic damage of mouse cells was investigated by the comet assay and micronucleus test. To perform the comet assay, mice were divided into a control group and 4 groups of exposed mice sacrificed on day 3 of the experiment, at 0,2,6 or 24 h after the last exposure to sevoflurane. Mean tail length (TL), tail moment (TM), and tail intensity (TI) values were significantly higher in exposed mice (all examined organs) than in the control group. Significant DNA damage immediately after exposure to sevoflurane was observed in leukocytes. Damage induction in the liver, kidney, and brain occurred 6 h later than in leukocytes, as expected according to the toxicokinetics of the drug, where blood is the first compartment to absorb sevoflurane. However, none of the tested tissues revealed signs of repair until 24 h after the exposure. To distinguish the unrepaired genome damage in vivo, the micronucleus test was applied. Number of micronuclei in reticulocytes showed a statistically significant increase, as compared with the control group at all observed times after the treatment.
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