Abstract
Since hypothermic conditions augment sensitivity to vasoactive amines like serotonin (5-HT) and 5-HT is associated with the etiology of Raynaud's phenomenon, this amine perhaps plays a role in cold-induced vasoconstriction. To determine if 5-HT participated in normal peripheral cooling and if ketanserin (KET), a 5-HT blocker, modulated such cooling, four groups of New Zealand white rabbits ( N = 33) were studied. The femoral artery was cannulated to allow perfusion of a hindlimb. Thermistors were implanted in the footpad and rectum. The hindfoot was exposed to a 15 °C bath for 30 min, while footpad and rectal temperatures were recorded. During cold exposure, 5-HT (5 × 10 −2 M, group 1), KET (0.1 mg/kg) + 5-HT (group 2), KET (group 3), or saline (group 4) was perfused through the hindlimb. Groups 2 and 3 were also pretreated with KET (0.1 mg/kg perfused over 30 min). The rabbit footpad cooled rapidly when exposed to exogenous 5-HT (group 1). KET treatment in the presence of exogenous 5-HT (group 2) was associated with a significantly ( P < 0.05) reduced cooling rate. KET treatment in the absence of exogenous 5-HT (group 3) was also associated with a significantly ( P < 0.05) elevated limb temperature when compared to controls (group 4). This suggested that endogenous 5-HT participated in limb cooling. Therefore, as noted for Raynaud's disease, 5-HT may also influence peripheral cooling of tissues free of such pathologies. Since KET treatment did not significantly alter rectal temperature in comparison to controls (39.18 ± 0.95 vs 38.97 ± 0.97 °C), such treatment with mild cold exposure may have potential in the regulation of peripheral temperature without increasing the risk of hypothermia.
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