Study of pathways of trigemino-cardiovascular reflex and central control

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Electrical stimulation of the trigeminal nerve caused hypotension and bradycardia in rabbits at the stimulus frequency of 5 Hz and strengths of 5 mA and 20 mA. Activities of the sympathetic nerve decreased when blood pressure fell. In this study, we examined brainstem pathways mediating hemodynamics elicited by trigeminal stimulation.Adult white rabbits were used. Under urethane and α-chloralose anesthesia, animals were ventilated artificially. At the stimulus frequency of 50 Hz, blood pressure fell at first and then rose. It took 4.2 s from the beginning of stimulation to the peak of high pressure, and 11.6 s to the peak of low pressure. This discrepancy suggested that pathways of suppressor response and depressor response were different. In the next experiment, effects of inhalation anesthetics (isoflurane and sevoflurane) on cardiovascular and autonomic changes generated by electrical stimulation of the mental- nerve were evaluated. At lower concentration, stimulation of the mental nerve caused a decrease in sympathetic nervous activity and at higher concentration, it caused an increase in sympathetic nerve activity. We hypothesized that there were two systems that controlled sympathetic nervous activity i.e. a suppressor system and a depressor system and that sensitivities of these systems to inhalation agents were different. Furthermore, we made small lesions in spinal trigeminal complex (STC), rostral ventrolateral medulla (RVLM), caudal ventrolateral medulla (CVLM) by highly localized heating. After making lesions in STC, depressor response elicited by trigeminal electrical stimulation became little but suppressor response did not change. It suggested that there were two pathways in medulla. After making lesions in RVLM and CVLM, responses did not change. It seemed that these regions were not important in conduction of trigeminal stimulation.