Inhibition of cold-induced vasoconstriction with ketanserin

The role of serotonin, thromboxane A2, and prostacyclin in cold-stimulated vasoconstriction was studied in 11 volunteers randomly pretreated with placebo, antagonists to serotonin (ketanserin, 40 mg), cyclooxygenase (ibuprofen, 800 mg), or thromboxane synthetase (ketoconazole, 400 mg). With an ambient temperature of 27 degrees, the hand and distal arm of one side were immersed in iced slush for 2 min. At the end of this time there was a fall in skin temperature from 31.2 to 12.2 degrees. Six minutes later with ketanserin treatment, temperature rose 4.5 degrees above placebo (P less than 0.05). In the noncooled side, ketanserin led to a rise in baseline temperature of 2.3 degrees (P less than 0.05), and increased plethysmographic finger flow to 2.08% delta vol/sec contrasted with 1.00% delta vol/sec in the placebo group (P less than 0.05). During cold immersion, temperature of this side fell 0.5 degrees, and flow decreased to 0.17% delta vol/sec. With ketanserin, temperature did not fall and flow was 0.85% delta vol/sec (P less than 0.05). Ketanserin accelerated recovery of temperature and flow (P less than 0.05). Plasma serotonin levels were constant. Ibuprofen and ketoconazole reduced baseline thromboxane B2 levels from 30 pg to 18 and 20 pg/ml (P less than 0.05), respectively, but did not influence temperature or flow. Results show that serotonin and perhaps alpha-adrenoreceptors, but not prostanoids, modulate resting skin flow and cold-induced vasoconstriction.