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  • Title: Desflurane reduces the gain of thermoregulatory arteriovenous shunt vasoconstriction in humans.
    Author: Kurz A, Xiong J, Sessler DI, Dechert M, Noyes K, Belani K.
    Journal: Anesthesiology; 1995 Dec; 83(6):1212-9. PubMed ID: 8533914.
    Abstract:
    BACKGROUND: Thermoregulatory responses, such as arteriovenous shunt vasoconstriction, provide substantial protection against core hypothermia. A response can be characterized by its threshold (core temperature triggering response), gain (rate at which response intensity increases, once triggered), and maximum response intensity. Reduced gain decreases the efficacy of a thermoregulatory response at a given threshold because response intensity will increase more slowly than usual. The effects of general anesthesia on the gain of arteriovenous shunt vasoconstriction have not been reported. Accordingly, we tested the hypothesis that desflurane decreases the gain of centrally mediated vasoconstriction. METHODS: We studied seven healthy male volunteers. Each was studied twice: (1) desflurane (end-tidal concentration 0.4 minimum alveolar concentration); and (2) control (no anesthesia). Mean skin and fingertip temperatures were controlled at 35.5 degrees C throughout the study. Core temperature was reduced at a rate of 1.5 degrees C/h by central venous infusion of cold fluid. Fingertip arteriovenous shunt flow was measured using venous occlusion volume plethysmography at 1-min intervals. Flow was also evaluated using the perfusion index and laser Doppler flowmetry. Vasoconstriction thresholds were calculated as the core temperatures triggering fingertip flows of 1.0 ml/min (beginning of vasoconstriction) and 0.25 ml/min (intense vasoconstriction). The gain of vasoconstriction was considered to be the slope of the fingertip flow versus core temperature regression within the linear range from 1.0 ml/min to 0.15 ml/min. The minimum observed flow was considered maximum vasoconstriction intensity. Data are presented as means +/- SD; P < 0.01 was considered statistically significant. RESULTS: The vasoconstriction threshold (when defined using a flow of 1.0 ml/min) was reduced from 36.8 +/- 0.3 degrees C to 35.6 +/- 0.3 degrees C by desflurane anesthesia (P < 0.01). Desflurane reduced the gain of vasoconstriction by a factor of three, from 2.4 to 0.8 ml.min-1.degrees C-1 (P < 0.01). Gains, as determined by the perfusion index and laser Doppler flowmetry, were likewise reduced (P < 0.01). The threshold on the control day was only 0.2 +/- 0.1 degrees C less when significant vasoconstriction was defined as a flow of 0.25 ml/min rather than 1.0 ml/min. Because gain was reduced, however, the threshold during desflurane administration was 0.8 +/- 0.2 degrees C less when significant vasoconstriction was defined by a flow of 0.25 ml/min. Minimum flows were comparable and near zero with and without anesthesia. CONCLUSIONS: The threshold reduction (1.2 degrees C/0.4 minimum alveolar concentration) was similar to that observed previously during isoflurane anesthesia. Similarly, it is established already that maximum vasoconstriction intensity is comparable with and without isoflurane anesthesia. However, the data also indicate that even relatively low desflurane concentrations markedly reduce the gain of vasoconstriction. It is likely that reduced gain (i.e., slow onset of vasoconstriction) contributes to core hypothermia in some surgical patients.
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