In addition to the cerulospinal noradrenergic mechanism, the cerulospinal glutamatergic pathway and both NMDA and non-NMDA receptors in the spinal cord may mediate fentanyl-induced muscular rigidity in the rat.

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We have measured electromyographic (EMG) and systemic arterial pressure (SAP) signals during fentanyl-induced muscular rigidity in adult male Sprague-Dawley rats anaesthetized initially with ketamine 120 mg kg-1 i.p. during controlled ventilation. Fentanyl 100 micrograms kg-1 i.v. induced significant increase in EMG activity, recorded from the sacrococcygeus dorsi lateralis muscle. Power spectral analysis revealed that this was produced by an increase in the root mean square and a decrease in the mean power frequency values of the signals, signifying recruitment and synchronous activation of motor units. Together with transient hypotension and bradycardia, power spectral analysis of the SAP signals demonstrated a reduced but maintained power density of the frequency components that represent respiratory, baroreceptor and vasomotor activities. All these effects were only demonstrated unequivocally in rats maintained by i.v. infusion of ketamine until 10 min before the administration of fentanyl. We conclude that analysis of the temporal alterations in the spectral components of the EMG and SAP signals in rats during mechanical ventilation provides a sensitive method of measuring fentanyl-induced muscular rigidity and the accompanying alterations in haemodynamic variables.