Dexmedetomidine augments the effect of lidocaine: power spectrum and nerve conduction velocity distribution study

Nizamettin Dalkilic, Seckin Tuncer, Ilksen Burat, Nizamettin Dalkilic, Seckin Tuncer, Ilksen Burat

Abstract

Background: In this study, the individual and combined inhibitory effects of dexmedetomidine and lidocaine on the conduction group of isolated nerve were investigated by determining conduction velocity distribution (CVD) and power spectrum.

Methods: Electrophysiological compound action potential (CAP) recordings were conducted on isolated rat sciatic nerve before (Con) and 20 minutes after exposure to 1 mM lidocaine (Lido), 21pM dexmedetomidine (Dex) and their combination (Lido + Dex). Then for CVD, mathematical model and for power spectrum Fast Fourier analysis were conducted.

Results: Dexmedetomidine alone made no significant difference in shape and duration of CAPs as compared to Con, on the other hand lidocaine depresses amplitude and prolongs the duration of CAPs, but not more than combination of dexmedetomidine and lidocaine can do. Lidocaine caused a shift in the CVD histogram to relatively slower conducting group significantly while dexmedetomidine did not cause any significant change as compared to Control. Lidocaine, when combined with dexmedetomidine revealed a remarkable effect on the whole CVD histogram by causing almost complete blockage of fast conducting nerve fibers. The relative number of fibers in CVD is conserved for separate applications of anesthetics, but not for their combination. As in CVD, power spectrum shifted from higher to lower frequency region by lidocaine and significantly for lidocaine combined with dexmedetomidine application. Shifts for dexmedetomidine applied group were seen beggarly.

Conclusions: We have concluded that dexmedetomidine alone did not influence nerve conduction, but when it is used with lidocaine it augments neural conduction blockage effect, especially on fast conducting nerve fibers.

Keywords: Conduction velocity distribution; Dexmedetomidine; Lidocaine; Neural conduction blockage; Power spectrum.

Figures

Figure 1
Figure 1
Sample CAP traces from a single nerve for each groups (Con, Lido, Dex, Lido + Dex) recorded 40 mm away from the stimulating electrodes.
Figure 2
Figure 2
Estimated separate CVD histograms of Lido, Dex and Lido + Dex groups. For comparison, in each graph, Con histogram is also given in the same conduction velocity (m/s) axis with Dex (A), Lido (B) and Lido+Dex (C). Each bin represents percent relative number of fiber of that conduction velocity class. Values are given as mean ± SEM (N = 7).
Figure 3
Figure 3
Estimated CVD histograms of Lido and Dex groups. Histograms are given in the same conduction velocity (m/s) axis comparatively. Each bin represents percent relative number of fiber of that conduction velocity class. Values are given as mean ± SEM (N = 7).
Figure 4
Figure 4
Recalculated conduction velocity distribution of three subgroups for four experimental group of constituted conduction subgroups as described in the Methods (slow:8-28 m/s; medium:29-52 m/s; fast:53-79 m/s) for the groups Con, Dex, Lido and Lido + Dex. * represents the significance when compared to the Con group while # represents the significance when compared to the Lido group at a level of p < 0.05.
Figure 5
Figure 5
The effect of lidocaine, dexmedetomidine and lidocaine + dexmedetomidine combination on CAP waveform power spectra. Graphs show the % relative power vs. frequency relationship related to CAPs for control (A) and three different drug groups (B,C,D). Frequency axis is divided into 17 bins.

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