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J Physiol Volume 510, Number 3, 915-921, August 1, 1998
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The Journal of Physiology (1998), 510.3, pp. 915-921
© Copyright 1998 The Physiological Society

Sympathetic attenuation of parasympathetic vasodilatation in oro-facial areas in the cat

Hiroshi Izumi and Yutaka Ito *

Departments of Physiology and * Anaesthesiology, Tohoku University School of Dentistry, Sendai 980-8575, Japan

  1. The present study was designed to examine the interaction between sympathetic and parasympathetic influences on blood flow in oro-facial areas such as lower lip, palate and submandibular gland (SMG) and in the common carotid artery (CCA) in anaesthetized cats.

  2. Section of the ipsilateral superior cervical sympathetic trunk (CST) increased the basal CCA blood flow significantly. The control level with the nerve intact was comparable with that seen at 0·5-1 Hz CST stimulation, suggesting a spontaneous discharge of around 0·5-1 Hz in the CST fibres innervating the beds supplied by the CCA. The basal blood flow at all sites examined was reduced by CST stimulation in a frequency-dependent manner.

  3. Electrical stimulation of the central end of the lingual nerve (LN) evoked blood flow increases in the lower lip and palate. These blood flow increases were markedly reduced by concurrent CST stimulation in a manner that was frequency dependent, but not simply related to the vasoconstrictor effect of CST stimulation. This effect of CST stimulation was not observed in tongue or SMG, even though CST stimulation evoked vasoconstriction in these tissues. A significant reduction in the level of CCA blood flow attained during LN stimulation was observed on repetitive CST stimulation only at 10 Hz, indicating that this response behaved in a fashion different from that seen in the lower lip, palate, tongue and SMG.

  4. The present study suggests that concurrent repetitive CST stimulation reduces parasympathetically mediated blood flow increases in certain oro-facial areas (such as the lower lip and palate), but not in the tongue and SMG. This inhibitory action was not a simple additive effect (between vasoconstriction and vasodilatation) and it disappeared rapidly after the cessation of CST stimulation.



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