Functional roles played by the sympathetic supply to lip blood vessels in the cat

In the anesthetized cat we used laser-Doppler flowmetry to investigate the part played by cervical superior sympathetic trunk (CST) fibers in the control of blood vessels in an orofacial area (the lower lip). The blood flow increase (antidromic vasodilatation) elicited by inferior alveolar nerve (IAN) stimulation was not affected by ongoing repetitive CST stimulation over the frequency range examined (0.2–10 Hz), although reflex parasympathetic vasodilatation was attenuated. The vasoconstrictor responses elicited by IAN stimulation in some preparations were reduced in a frequency-dependent manner (at 0.2–1 Hz) during ongoing CST stimulation (and replaced by vasodilator responses). The vasoconstrictor response evoked directly by brief CST stimulation was attenuated, but not transformed to a vasodilator response, by ongoing CST stimulation. Thus in the cat lower lip 1) sympathetic stimulation attenuated one type of vasodilator response (parasympathetic-mediated vasodilatation), but not another (antidromic vasodilatation), and 2) ongoing sympathetic (CST) stimulation at low frequencies (<1 Hz) prevented further sympathetic-mediated vasoconstriction.

Sensitization of nociceptive C-fibers in zinc-deficient rats

A marked decrease in zinc concentration was observed in plasma (P < 0.001), hindpaw skin (P < 0.01), and dorsal skin (P < 0.01) in zinc-deficient rats (rats fed a zinc-deficient diet for 3 wk), compared with the control rats fed the same zinc-deficient diet supplemented with ZnCO3 (50 mg/kg diet). The threshold intensity needed to elicit vasodilatation in the hindpaw skin of the zinc-deficient rats on electrical stimulation of the saphenous nerve in a peripheral direction was markedly lower (P < 0.01) than that in the control rats. No difference was observed between control (n = 5) and zinc-deficient rats (n = 5) in the magnitude of the plasma extravasation evoked by either histamine or substance P. There was no difference between control and zinc-deficient rats in terms of the dose-response curve for release of histamine by substance P. Prostaglandin E2 (PGE2) concentration in the hindpaw skin of the zinc-deficient rats was nearly fourfold higher (P < 0.01) than that of the control rats, whereas no difference in the leukotriene B4 level in the hindpaw skin was observed between control and zinc-deficient rats. From the present study, it seems likely that an increased level of PGE2 in the vicinity of the nociceptive C-fiber terminals in the hindpaw skin of zinc-deficient rats may sensitize the terminals of the nociceptive C-fibers of the saphenous afferent nerve in the hindpaw and thus facilitate the production of antidromic vasodilatation.