Suppression and augmentation of trigeminal depressor response

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Decrease in cerebral blood flow is one of the most common complications in dental practice. Trigeminal stimulation plays an important role and baroreflex seems to participate in this complication. Therefore we examined hemodynamic responses and autonomic nerve activities (renal sympathetic nerve activity : RSNA, vagal nerve activity : VNA) when we stimulated trigeminal nerve and evoked arterial baroreflex. In addition, we examined effects of some agents (propofol, fentanyl, isoflurane and phentolamine) on hemodynamic response and autonomic nerve activity during stimuli of trigeminal nerve.This study was performed on rabbits. Arterial baroreflex was evoked with stimuli of aortic depressor nerve (ADN). Low frequency stimulation (5 Hz) of infraorbital nerve (ION) reduced mean arterial blood pressure (MAP), heart rate (HR) and RSNA significantly. High frequency stimulation (25 Hz) of ION caused a biphasic change, an early fall of MAP and a subsequent rise of MAP. Change of RSNA was also biphasic.To examine the effect of arterial baroreflex, simultaneous stimuli of ION (5 Hz) and ADN were performed. Depressor response evoked with simultaneous stimuli was greater than that evoked with ION alone. On the other hand, during stimuli of ION (25 Hz) and ADN, presser response which was observed during stimulation of ION alone was suppressed significantly. Change of RSNA was similar to the change of MAP.Propofol suppressed presser response during stimuli of ION and fentanyl suppressed depressor response in dosage dependence. Combination of propofol and fentanyl suppressed depressor and presser responses but arterial baroreflex still remained. Isoflurane suppressed changes of MAP and RSNA during stimuli of ION, but decrease in MAP before stimuli of ION was remarkable and arterial baroreflex was suppressed. Phentolamine suppressed presser and depressor response, but the change of RSNA was observed similarly before administration.