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40 adult Wistar rats were divided into two groups depending on the applied anaesthesia. In both groups animals were generally anaesthetized with fentanyl, dehydrobenzperidol administered intraperitoneally and midazolam given intramuscularly. In the second group (SEVO) animals received sevoflurane of 2.2 vol% end-tidal concentration. Intracerebral haematoma was produced through infusion of 100 µl of autologous blood into the striatum. Each group was divided into five subgroups depending on the length of survival period: 1, 3, 7, 14, 21 days. The astrocytic population was studied by means of anti-GFAP staining. Stereological analysis was applied to estimate the numerical density of immunoreactive cells and the distribution of their types. On 7th day of observation the density of GFAP-immunoreactive astrocytes in SEVO was lower (p<0,05) than that in the control group. In the control group, the increase (p<0.05) of per cent of activated astrocytes between the 1st and 3rd survival day was noted, which remained at this level till the end of observation. In SEVO group, the increase (p<0.05) of per cent of activated astrocytes between the 3rd and 7th day and the decrease (p<0.05) between the 14th and 21st survival day were observed. During days of observation the per cent of activated astrocytes was lower (p<0.05) in the SEVO group than that in the control group. Administration of sevoflurane during anaesthesia to animals with intracerebral haemorrhage has evoked not only the delay of the activation of astrocytes but also decrease in its level.
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 effects of propofol and sevoflurane anesthesia on heart rate and respiratory rate, body temperature, plasma Ca, P, Na, K, Mg, creatinine, urea, ALT, APT, ALP, GGT, LDH in rabbits have been assessed. This study was carried out on 12 New Zealand White rabbits. Anesthesia induction was performed using propofol, which was slowly administered via IV injection at a dose of 10 mg/kg. Sevoflurane inhalation was administered at an initial concentration of 5%, followed by 2% for anesthesia maintenance. While causing a decrease in heart rate and respiratory frequency, propofol application but did not affect body temperature and hematocrite value. Sevoflurane did not alter heart rate, although it caused respiratory depression and a decrease in body temperature. Propofol-sevoflurane anesthetic combination caused some alterations in ALT and GGT liver enzymes and plasma phosphorus levels. In the light of the findings, the animals had a reliable and controlled anesthesia with the propofol-sevoflurane combination. However, it should be taken into consideration that this combination may impair the electrolyte balance and cause respiratory depression. Thus it has been concluded that a diligent monitorization and an electrolyte support is essential during the period of anesthesia.
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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