Decreased carotid arterial resistance in cats in response to trigeminal stimulation

• Published in: Journal of neurosurgery Vol. 61; no. 2; p. 307
• Main Authors: Lambert, G A, Bogduk, N, Goadsby, P J, Duckworth, J W, Lance, J W
• Format: Journal Article
• Language: English
• Published: United States 01.08.1984
• Subjects: Animals; Blood Pressure; Carotid Arteries - innervation; Carotid Arteries - physiology; Cats; Electric Stimulation; Trigeminal Nerve - anatomy & histology; Trigeminal Nerve - physiology; Vascular Resistance
• ISSN: 0022-3085
• DOI: 10.3171/jns.1984.61.2.0307

Stimulation of the trigeminal nerve or ganglion in the cat caused a frequency-dependent reduction in carotid vascular resistance. Systemic arterial blood pressure (SABP) decreased at low frequencies (0.2 to 5 sec-1) and increased at higher frequencies, thus increasing carotid blood flow at the higher frequencies. The effect on resistance was predominantly ipsilateral and was unaltered by cervical sympathectomy, but was abolished or substantially reduced by section of the trigeminal root proximal to the ganglion. Diminution of carotid vascular resistance was replicated by stimulation of the greater superficial petrosal (GSP) nerve without any change in SABP. Section of the seventh cranial nerve reduced or abolished the response to stimulation of the trigeminal nerve but not that from the GSP nerve. The trigeminal response was prevented by ganglion-blocking drugs in seven out of eight cats. The resistance response was unaffected by noradrenergic, cholinergic, serotonergic, and histamine-2 blocking agents. No neural connection could be demonstrated between the GSP and the trigeminal ganglion, and the vascular response to GSP stimulation persisted after trigeminal section. It is concluded that activation of the trigeminal system increases carotid blood flow by a pathway involving the seventh cranial nerve, the GSP and Vidian nerves, and a parasympathetic synapse employing an unconventional transmitter. A varying proportion of the response (greatest in the third division) may be mediated by antidromic activation of trigeminal nerves. These findings may have clinical implications for the vascular changes of migraine and other facial pain.