Izvorni znanstveni članak

https://doi.org/10.1515/acph-2017-0025

Axonal excitability and conduction alterations caused by levobupivacaine in rat

SEÇKİN TUNCER ; N.E. University, Meram Faculty of Medicine, Biophysics Department, Konya, Turkey
TÜLAY TUNCER PEKER ; Ankara University, Faculty of Medicine, Anesthesiology Department, Ankara, Turkey
İLKSEN BURAT ; N.E. University, Meram Faculty of Medicine, Biophysics Department, Konya, Turkey
ERHAN KIZILTAN ; Başkent University, Faculty of Medicine, Physiology Department, Ankara, Turkey
BARKIN İLHAN ; N.E. University, Meram Faculty of Medicine, Biophysics Department, Konya, Turkey
NİZAMETTİN DALKILIÇ ; N.E. University, Meram Faculty of Medicine, Biophysics Department, Konya, Turkey

Sažetak

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.

Ključne riječi

levobupivacaine; nerve conduction; excitability; threshold electrotonus

Hrčak ID:

181330

URI

https://hrcak.srce.hr/181330

Datum izdavanja:

30.9.2017.

Posjeta: 1.689 *