COOLING AUGMENTS HUMAN SAPHENOUS-VEIN REACTIVITY TO ELECTRICAL-STIMULATION

Human saphenous veins were obtained at operation and assayed immediate ly (n = 10). The veins were cut into rings, suspended in organ chamber s, and connected to force transducers for recording of isometric tensi on. One ring served as control; others were treated with either the al pha(1)-adrenoceptor antagonist prazosin (Pz, 3 x 10(-7) M) or the alph a(2)-adrenoceptor antagonist rauwolscine (Rw(1), 10(-7) M). Cooling fr om 37 degrees to 24 degrees C had no significant effect on the resting tone of quiescent rings. Electrical stimulation (0.2-16 Hz) caused fr equency-dependent contractions in control vessels. The contractions we re inhibited by Pz (p < 0.001) and by Rw (p < 0.001). In control rings , cooling potentiated contractions evoked at all frequencies. Similar augmentations were induced by cooling in rings treated with the alpha( 1)-antagonist Pz. In contrast, rings treated with Rw before being elec trically stimulated showed no significant change in contractile force when cooled. The data indicate that in the human saphenous vein, both alpha(1)- and alpha(2)-adrenoceptors are innervated, contributing to c ontractile response evoked by neuronal excitation. Cold augments saphe nous vein reactivity to endogenously released norepinephrine (NE) by a n apparent increase in the responsiveness of alpha(2)-adrenoceptors to agonists. This relationship between temperature and adrenoceptor resp onsiveness is consistent with the hypothesized role of alpha(2)-adreno ceptors in cold-induced vasospasm.