The Threshold and Gain of Thermoregulatory Vasoconstriction Differs During Anesthesia in the Dependent and Upper Arms in the Lateral Position Robert Greif, MD*, Sonja Laciny, MD†, Angela Rajek, MD‡, Anthony G. Doufas, MD, PhD§, and Daniel I. Sessler, MD§ *Department of Anesthesiology and Intensive Care Medicine, Donauspital/SMZO; †Private practice, Vienna, Austria; ‡Department of Cardiothoracic and Vascular Anesthesia, University of Vienna, Austria; §Department of Anesthesiology, University of Louisville, Kentucky; and §OUTCOMES RESEARCH™ Institute, Louisville, Kentucky, and Ludwig Boltzmann Institute, University of Vienna, Austria Increased intraluminal pressure may help maintain va- sodilation in a dependent arm even after hypothermia triggers centrally mediated thermoregulatory vasocon- striction. We therefore tested the hypotheses that the threshold (triggering core temperature) and gain (in- crease in vasoconstriction per degree centigrade) of cold-induced vasoconstriction is reduced in the depen- dent arm during anesthesia. Anesthesia was main- tained with 0.4 minimum alveolar anesthetic concen- tration of desflurane in 10 volunteers in the left-lateral position. Mean skin temperature was reduced to 31°C to decrease core body temperature. Fingertip blood flow in both arms was measured, as was core body tem- perature.The vasoconstriction threshold was slightly, but significantly, less in the dependent arm (36.2°C  0.3°C, mean  sd) than in the upper arm (36.5°C  0.3°C). However, the gain of vasoconstriction in the de- pendent arm was 2.3-fold greater than in the upper arm. Consequently, intense vasoconstriction (i.e., a fingertip blood flow of 0.15 mL/min) occurred at similar core temperatures. In the lateral position, the vasoconstric- tion threshold was reduced in the dependent arm; how- ever, gain was also increased in the dependent arm. The thermoregulatory system may thus recognize that hy- drostatic forces reduce the vasoconstriction threshold and may compensate by sufficiently augmenting gain. (Anesth Analg 2002;94:1019 –22) T hermoregulatory vasoconstriction is the primary defense against cold stress (1). This vasoconstric- tor response is defined by its threshold (trigger- ing core temperature) and gain (incremental reduction in blood flow as temperature decreases below the threshold) (2). The substantial concentration-dependent effects of general anesthetics (3–5) and sedatives (6 – 8) on vasoconstriction and other thermoregulatory thresholds are well established. However, factors other than anes- thetic type and concentration also influence vasocon- striction thresholds. For example, noxious stimulation increases the vasoconstriction threshold during anesthe- sia (9). Nitrous oxide similarly reduced the vasoconstric- tion threshold less than expected (10). Both effects may be mediated by sympathetic nervous system activation. An additional factor that may influence thermoreg- ulatory responses is patient position. For example, blood pressure in unanesthetized humans remains un- changed in the lateral position (11) but decreases in the anesthetized individual (12). Furthermore, body temperature is altered by postural shifts in unanesthe- tized subjects. It is also well established that barore- ceptor loading promotes hypothermia by reducing the vasoconstriction threshold (13). Blood pressure in a dependent arm during anesthe- sia exceeds that in the upper arm because of hydro- static forces. It seems likely that increased intralumi- nal pressure will, at least for a time, maintain vasodilation in the dependent arm even after hypo- thermia triggers a central thermoregulatory vasocon- strictor response. If so, the threshold and gain of va- soconstriction in the dependent arm would decrease. Supported by NIH Grant GM 58273 (Bethesda, MD), the Joseph Drown Foundation (Los Angeles, CA), and the Commonwealth of Kentucky Research Challenge Trust Fund (Louisville). Tyco, Inc. (St. Louis, MO) donated the thermocouples we used. Dr. Sessler is a consultant for Radiant Medical, Inc. and ThermaMed, GmbH. Accepted for publication December 14, 2001. Address correspondence and reprint requests to Daniel I. Sessler, MD, Outcomes Research Institute, 501 E. Broadway Ave., Louisville, KY 40202. Address e-mail to sessler@louisville.edu. ©2002 by the International Anesthesia Research Society 0003-2999/02 Anesth Analg 2002;94:1019–22 1019