In animal experiments halothane induces a decrease in CVR (Harp et al. 1976, Todd and Drummond 1984b), an increase in CBF (McDowall et al. 1963, Theye and Michenfelder 1968a, Smith and Wollman 1972, Smith 1973, Harp et al. 1976, Stullken et al. 1977, Todd and Drummond 1984b, Scheller et al. 1984), and a decrease in CMRO2 (McDowall et al. 1963, Theye and Michenfelder 1968a, Smith 1973, Harp et al. 1976, Stullken et al. 1977, Todd and Drummond 1984b). The changes in CVR and CBF give rise to an increase in CBV and ICP (Fitch and McDowall 1971, DiGiovanni et al. 1974, Drummond et al. 1983a, Todd and Drummond 1984b). The increase in CBF is dependent on the age. Thus, the increase in CBF is more pronounced in young animals (Hoffman et al. 1982a). The increase in CBF occurs few minutes after induction, and is recorded before any change in CMRO2 (Albrecht et al. 1977). During halothane administration over several hours a normalization of CBF occurs, and at the same time a moderate increase in CVR and CMRO2 are observed (Albrecht et al. 1983). According to Warner et al. (1985), this cerebrovascular adaptation to prolonged halothane administration is not related to changes in CSF-pH, which is unchanged. Simultaneous administration of nitrous oxide give rise to an increase in CBF, and a decrease in CVR.
KeywordsNitrous Oxide Cerebral Autoregulation Isoflurane Anaesthesia Halothane Anaesthesia Inhalation Anaesthetics
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