Anesthesia and analgesia
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Anesthesia and analgesia · Jan 2005
Individual effect-site concentrations of propofol are similar at loss of consciousness and at awakening.
Reported effect-site concentrations of propofol at loss of consciousness and recovery of consciousness vary widely. Thus, no single concentration based on a population average will prove optimal for individual patients. We therefore tested the hypothesis that individual propofol effect-site concentrations at loss and return of consciousness are similar. ⋯ The target effect-site propofol concentration was 2.0 +/- 0.9 at loss of consciousness and 1.8 +/- 0.7 at return of consciousness (P <0.001). The average difference between individual effect-site concentrations at return and loss of consciousness was only 0.17 +/- 0.32 microg/mL (95% confidence interval for the difference 0.09-0.25 microg/mL). Our results thus suggest that individual titration to loss of consciousness is an alternative to dosing propofol on the basis of average population requirements.
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Anesthesia and analgesia · Jan 2005
Anesthetic preconditioning: the role of free radicals in sevoflurane-induced attenuation of mitochondrial electron transport in Guinea pig isolated hearts.
Cardioprotection by anesthetic preconditioning (APC) can be abolished by nitric oxide (NO*) synthase inhibitors or by reactive oxygen species (ROS) scavengers. We previously reported attenuated mitochondrial electron transport (ET) and increased ROS generation during preconditioning sevoflurane exposure as part of the triggering mechanism of APC. We hypothesized that NO* and other ROS mediate anesthetic-induced ET attenuation. ⋯ Both this NADH increase and the cardioprotection by APC on reperfusion were prevented by superoxide dismutase, catalase, and glutathione and by N(G)-nitro-L-arginine-methyl-ester. Thus, ROS and NO*, or reaction products including peroxynitrite, mediate sevoflurane-induced ET attenuation. This may lead to a positive feedback mechanism with augmented ROS generation to trigger APC secondary to altered mitochondrial function.