TRIGEMINAL AUTONOMIC PATHWAYS INVOLVED IN NOCICEPTION-INDUCED REFLEX CARDIOVASCULAR-RESPONSES

Reflex cardiovascular responses elicited by noxious ore-facial stimula tion are well known but the neural pathways that underlie trigeminal c ardiovascular reflex reactions remain to be elucidated. In previous st udies, we have shown that noxious electrical stimulation of the mandib ular incisor in the anesthetized rat elicits increases in mean arteria l blood pressure and heart rate (Alien, G.V., Barbrick, B. and Esser, M.J., Trigeminal parabrachial connections: possible pathway for nocice ption-induced cardiovascular reflex responses, Brain Res., 715 (1996) 125-135). In this study, microinjections of the presynaptic blocker, c obalt chloride, or the anesthetic agent, Lidocaine, were made into sel ected brainstem sites to identify neural pathways that are involved in mediation of the reflex presser responses. Ipsilateral and bilateral injections of chemical blocker into the dorsomedial spinal trigeminal nucleus, pars caudalis, lateral parabrachial nucleus and the rostral v entral lateral medulla/caudal A5 region attenuated the reflex cardiova scular response. Bilateral injections of cobalt chloride into the dors omedial subnucleus caudalis resulted in 70-100% attenuation of the ref lex presser response. Bilateral injections of cobalt chloride and/or l idocaine into the lateral parabrachial nucleus or the rostral ventral lateral medulla/A5 region resulted in 43-57% and 44-100% attenuation o f the reflex presser response, respectively. There were no significant differences in the degree or duration of attenuation of the reflex pr esser responses produced by cobalt chloride compared to that produced by lidocaine injections. The reflex presser responses usually returned to baseline levels approximately 60 min following injection of the ch emical blocker substance. The results indicate that noxious electrical stimulation of the mandibular incisor elicits a reflex increase in me an arterial blood pressure which is initially mediated in the dorsomed ial spinal trigeminal nucleus, pars caudalis and is subsequently media ted in the lateral parabrachial nucleus and the rostral ventral latera l medulla/caudal A5 region. (C) 1997 Elsevier Science B.V.