Anesthesiology
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Hepatic oxygen supply and uptake were assessed in phenobarbital-pretreated male Sprague-Dawley rats receiving subanesthetic doses of thiopental, halothane, enflurane, or isoflurane combined with hypoxia (approximately 0.5 MAC and 12% oxygen) for the purpose of evaluating the role of these combinations in hepatic blood flow alterations and the concomitant hepatic oxygen supply and uptake. Hepatic blood flow was measured using microspheres; hepatic oxygen supply and consumption was calculated from measured hepatic blood flow and oxygen content in hepatic arterial, portal venous, and hepatic venous blood. In all anesthetic groups, total hepatic blood flow did not change from the control value. ⋯ Oxygen content in hepatic venous blood correlated well with hepatic oxygen supply/consumption ratio in all five groups. These results show that, during exposure to mild hypoxia, a sub-MAC dose of isoflurane maintains the relationship of hepatic oxygen supply to uptake better than thiopental, halothane, or enflurane. However, a subanesthetic dose of halothane did not aggravate liver hypoxia specifically, compared with thiopental or enflurane.
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Comparative Study Clinical Trial Controlled Clinical Trial
The minimum alveolar concentration (MAC) of sevoflurane in humans.
Forty surgical patients were divided into two groups and anesthetized with either sevoflurane and oxygen or sevoflurane, oxygen, and nitrous oxide. The minimum alveolar concentration (MAC) for sevoflurane required to prevent movement in response to surgical incision in healthy patients was 1.71 +/- 0.07% (SE). ⋯ The reduction in sevoflurane MAC was 61.4%. The AD95 for sevoflurane with 63.5% end-tidal nitrous oxide was 0.94%.
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The authors determined the accuracy of the Ohmeda 3700 (version J) pulse oximeter in healthy volunteers rendered hypoxic (SaO2 from 60-98%) by breathing mixtures of O2 in N2. When equipped with an ear probe, the pulse oximeter reading (y) reliably predicted arterial saturation (x) under steady-state conditions (y = 1.05x - 4.66, r = 0.98) as well as when oxygen saturation was rapidly decreasing (y = 1.05x - 6.38, r = 0.96). Conversely, when equipped with a finger probe, the oximeter tended to significantly underestimate steady-state arterial saturation (y = 1.21x - 19.1, r = 0.98, P less than 0.001). ⋯ Despite the close correlation between steady-state oximeter readings and arterial saturation, the 99% prediction limits for both the ear and finger probes (version XJ1) were +/- 8%. Finger probe readings did not reliably reflect radial arterial oxygenation during rapid desaturation (y = 0.55x + 45.2, r = 0.78). This may be related to the time required to "arterialize" the blood in the finger; during acute resaturation, we found that the ear- to finger-probe delay was 24.0 +/- 2.3 s (means +/- SE, P less than 0.001).