F. Lenfant et al., Lidocaine inhibits potassium efflux and hemolysis in erythrocytes during oxidative stress in vitro, GEN PH-VASC, 34(3), 2000, pp. 193-199
Lidocaine is a widely used local anesthetic agent. The aim of this work was
to study the action of lidocaine on human red blood cells exposed to an ox
idative stress in vitro. Blood was obtained from healthy volunteers. After
separation from plasma, the erythrocytes were suspended in phosphate buffer
. Oxidative stress was induced by incubation with a free radical generator,
the 2,2' azobis (2-amidinopropane) hydrochloride (AAPH). Erythrocytes were
incubated with or without lidocaine at two concentrations (36.93 and 73.85
muM) and with or without AAPH (20 mM). Electron paramagnetic resonance (EP
R) spectroscopy was performed to identify the free radical species generate
d by AAPH using the spin trap 5-5'-dimethyI-L-pyroline-N-oxide (DMPO). Diff
erent sets of experiments were run. Potassium efflux was measured by flame
photometry in each group at time 0 min and every 30 min of the experiment f
or 2 h. Hemolysis was studied by the Drabkin method at increasing concentra
tions of AAPH (20, 50, and 100 mM) and with or without lidocaine (36.93 muM
). The oxygen radical absorbance capacity (ORAC) was measured by using allo
phycocyanin (APC) as a fluorescent indicator protein, and the antioxidant c
apacity of lidocaine (36.93 muM) was studied by the analysis of fluorescenc
e of the APC. AAPH was shown to produce alkoxyl free radicals. Oxidative st
ress induced a marked increase in the potassium efflux and the hemolysis th
at was AAPH dose-dependent. Lidocaine inhibited the potassium efflux and de
layed the occurrence of hemolysis. Lidocaine did not show any antioxidant p
roperties for the free radical species generated by AAPH. In this model, li
docaine protects erythrocytes against oxidative stress. This effect is not
explained by a free radical scavenging property. The results may be of grea
t interest in clinical practice such as intravenous regional anesthesia or
the prevention of ischemia-reperfusion injury. (C) 2000 Elsevier Science In
c. All rights reserved.