Effects of 2 mg.kg⁻¹ of intravenous lidocaine on the latency of two different doses of rocuronium and on the hemodynamic response to orotracheal intubation.

BACKGROUND AND OBJECTIVES: Lidocaine potentiates the effects of neuromuscular blockers and attenuates the hemodynamic response to orotracheal intubation. The objective of the present study was to test the effects of lidocaine on the latency of two different doses of rocuronium and on the hemodynamic response to intubation. METHODS: Eighty patients were distributed in 4 groups: Groups 1 and 2 received 0.6 mg.kg(-1) of rocuronium; patients in Group 2 also received 2 mg.kg(-1) of lidocaine before intubation. Patients in Groups 3 and 4 received 1.2 mg.kg(-1) of rocuronium; patients in Group 4 received additional 2 mg.kg(-1) of lidocaine. The latency of the neuromuscular blockade was measured by acceleromyography. Hemodynamic evaluation was performed at baseline, immediately before, and 1 minute after orotracheal intubation (OI). RESULTS: Statistically significant differences were not observed between the latency from 0.6 mg.kg(-1) and 1.2 mg.kg(-1) of rocuronium in patients who received lidocaine before induction and those who did not. The latency in patients who received 0.6 mg.kg(-1) of rocuronium with lidocaine was statistically similar to that of those who received 1.2 mg.kg(-1) rocuronium independently of whether lidocaine was administered or not. Patients who did not receive lidocaine before induction showed the same increases in systolic, diastolic, and mean arterial pressure and heart rate after OI, which was not observed in those patients who received lidocaine. CONCLUSIONS: Intravenous lidocaine before anesthetic induction was capable of attenuating the hemodynamic response associated to OI maneuvers, but it did not reduce the latency of the neuromuscular blockade produced by two different doses of rocuronium.

Activation of presynaptic NMDA receptors coupled to NaV1.8-resistant sodium channel C-fibers causes retrograde mechanical nociceptor sensitization.

The present study investigated whether activation of presynaptic N-methyl-d-aspartate (NMDA) receptors in the spinal cord produces a retrograde nociceptor sensitization (hypernociception) to mechanical nonnoxious stimulus. By using an electronic version of the von Frey hair test (pressure meter), s.c. intraplantar administration of prostaglandin E(2) (PGE(2)) (50-400 ng per paw) evoked a dose-related ipsilateral paw hypernociception. In contrast, intrathecal (i.t.) administration of NMDA (5-80 ng) and PGE(2) (15-150 ng) evoked dose-related bilateral paw hypernociception. The s.c. intraplantar administration of dipyrone (80-320 microg per paw) or morphine (3 and 9 microg per paw), usually used to antagonize peripheral PGE(2) (100 ng per paw), induced hypernociception and also antagonized the ipsilateral (without affecting the contralateral) paw hypernociception induced by i.t. injections of NMDA (40 ng) or PGE(2) (50 ng). These doses of drugs did not modify the basal mechanical sensitivity of control paws. This result shows that intraspinal NMDA or PGE(2) produces sensitization of the primary sensory neuron in response to mechanical stimulation. In a second series of experiments it was shown that the i.t. treatment with NaV1.8 (SNS/PN3) sodium channel antisense oligodeoxynucleotides, but not mismatch oligodeoxynucleotides, decreased the mRNA expression of sodium tetrodotoxin-resistant channels on the dorsal root ganglia and abolished the mechanical hypernociception induced by i.t. administration of NMDA. Thus, our results support the suggestion that glutamate release in the spinal cord during inflammation causes retrograde hypernociception of nociceptors associated with sodium tetrodotoxin-resistant channels in primary nociceptive sensory neurons.