Axonal excitability and conduction alterations caused by levobupivacaine in rat.

In this study, effects of the long-acting amide-type local anesthetic levobupivacaine on axonal conduction and excitability parameters of the rat sciatic nerve were thoroughly examined both in vitro and in vivo. In order to deduce its effects on isolated nerve conduction, compound nerve action potential (CNAP) recordings were performed using the suction method over sciatic nerves of Wistar rats before and after administration of 0.05 % (1.7 mmol L-1) levobupivacaine. Levobupivacaine caused complete CNAP area and amplitude depression by blocking conduction in a time-dependent manner. To assess the influence of levobupivacaine on in vivo excitability properties, threshold-tracking (TT) protocols were performed at sciatic nerves of rats injected with perineural 0.05 % (1.7 mmol L-1) levobupivacaine or vehicle alone. Charge-duration TT results revealed that levobupivacaine increases the rheobase and decreases the strength-duration time constant, suggesting interference of the anesthetic with the opening of Na+ channels. Twenty and 40 % threshold electrotonus curves were found for both groups to follow the same paths, suggesting no significant effect of levobupivacaine on K+ channels for either the fastest or relatively slow conducting fibers. Current-threshold relationship results revealed no significant effect on axonal rectifying channels. However, according to the results of the recovery cycle protocol yielding the pattern of excitability changes following the impulse, potential deviation was found in the recovery characteristics of Na+ channels from the absolute refractory period. Consequently, conduction blockage caused by levobupivacaine may not be due to the passive (capacitive) properties of axon or the conductance of potassium channels but to the decrease in sodium channel conductance.

Electrophysiological alterations in diaphragm muscle caused by abdominal ischemia-reperfusion.

Ischemia-reperfusion injury is the major complication of abdominal aortic surgery, and it mainly affects the lower extremities and remote organs. In the present study, the electrophysiological alterations in diaphragm that underlie the post-operative respiratory dysfunction were investigated. Wistar Albino rats were randomly divided into two groups: SHAM (only laparotomy was performed) and IR (abdominal aorta was clamped for 30min and reperfused for 2h). Following the operational period diaphragm muscles were isolated and electrophysiological experiments were carried out in-vitro. 3nM Ryanodine application, Na+ and K+ current blockage (0.3mM 4-Aminopyridine and 127mM N-methyl-d-glukamine) experiments were also conducted to further reveal any alterations. Twitch and tetanic force were decreased significantly. Action potential overshoot, amplitude and area were increased while diaphragm muscle cells were found to be hyperpolarized significantly. Mechanical alterations were shown to be caused by deterioration of Ca++ homeostasis. At resting state, a decrease in persistent Na+ current was found. The reshaping of action potential, on the other hand, was shown to be due to altered kinetics of Na+ channels and delayed activation of voltage dependent K+ channels.

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

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.