On the other hand, lidocaine, when combined with dexmedetomidine, manifests a remarkable effect on the whole CVD, causing almost complete conduction blockage of fast conducting nerve fibers.
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.
The chamber myocardium becomes fast conducting myocardium whereas the non-chamber myocardium retains slow conduction, thereby participating in the establishment of synchronized beating in the embryonic heart [4].
It is estimated that the high interfacial conductivity is mainly attributed to the highly-disordered microstructures with structural defects in interfacial regions which provide fast conducting pathways.
Relay neurons in the dLGN receive signals from fast conducting Y-like retinal axons and in turn, send signals to the VC along their own fast conducting axons [2].
So, the SFAP of fast conducting fibers' duration are smaller, while the that of slowly conducting fibers are relatively longer and hence have lower frequency component.
These include low-threshold nociceptors that are connected to fast conducting A-delta pain fibers, and high-threshold nociceptors that conduct impulses in slow (unmyelinated) C fibers.
Gasser showed that fast conducting myelinated A-fibers were involved in pain responses, together with slower conducting C-fibers (Gasser, 1941).
Lidocaine, when combined with dexmedetomidine revealed a remarkable effect on the whole CVD histogram by causing almost complete blockage of fast conducting nerve fibers.
