Neural bloodflow regulation in rat tongue by chorda-lingual nerve stimulation

Objectives:The present study was designed to investigate the mechanisms underlying vasodilatation in rat tongue, evoked by electrical stimulation of the peripheral cut end of the chorda-lingual nerve (CLN). Methods:Eighty six rats were deeply anesthetized with urethane and cervically vago-sympathectomized. One femoral vein was canulated to allow drug injection. The anesthetized rats were intubated, paralyzed by intravenous injection of pancuronium brobide and artificially ventilated via the tracheal cannula with a mixture of 50% air-50% O2. Dynamic changes in tongue blood flow (TBF) by electrical stimulation (10-40 V, 2ms, 10 Hz, 10s) or capsaicin (10mM) application to CLN were monitored with laser Doppler flowmetry (LDF), and maximum TBF increases were compared before and after each drug injection. Results: Electrical stimulation of CLN ipsilarterally induced TBF increases in a stimulus intensity-dependent manner. Capsaicin application on CLN didn't elicit TBF increases. Pyrilamine, histamine H1 blocker, had no effect on TBF increases by electrical CLN stimulation. These results indicated they contained no antidromic vasodilator mechanism by sensory nerve fibers via vanilloid and histamine type 1 receptor. TBF vasodilator responses were also markedly reduced by the autonomic ganglionic blocker, hexamethonium, and by the muscarinic receptor blocker, atropine, suggesting that they were mediated via a parasympathetic autonomic ganglion, and that the final neuron was partly cholinergic. Further, a-adrenergic receptor blocker, phentolamine, enhanced TBF increases, indicating that they contained vasoconstriction evoked by sympathetic nerve fiber. Conclusion: The present study demonstrates that vasodilatation in the tongue, evoked by electrical stimulation of the peripheral cut end of CLN consists of both vasodilator responses by parasympathetic nerve and vasoconstrictor response by sympathetic nerve, but not antidromic vasodilator mechanism by sensory nerve. This study was supported by a Grant-in -Aid for Scientific Research from the Japan Society for the Promotion of Science (19592401)