Qh. Hogan et al., EFFECTS OF LIDOCAINE AND BUPIVACAINE ON ISOLATED RABBIT MESENTERIC CAPACITANCE VEINS, REGIONAL ANESTHESIA AND PAIN MEDICINE, 23(4), 1998, pp. 409-417
Background and Objectives. The direct effects of circulating lidocaine
and bupivacaine on splanchnic capacitance veins have not been examine
d previously. This article reports on the effects of clinically releva
nt concentrations of lidocaine and bupivacaine on adrenergic responsiv
eness of isolated rabbit mesenteric veins and examines the mechanism o
f changes. Methods. Rings of ileal mesenteric capacitance veins were s
uspended in tissue baths for isometric tension measurements. Effects o
f lidocaine and bupivacaine on contractile responses to adrenergic ner
ve stimulation, exogenous norepinephrine (10(-6) M NE), and potassium
chloride (80 mM KCl) were examined in endothelium-intact, L-NAME (10(-
4) M) treated or denuded veins. Results. Constriction in response to a
drenergic nerve stimulation was attenuated by lidocaine and bupivacain
e in a dose-dependent manner, with the potency of bupivacaine being hi
gher than lidocaine. Unstimulated or potassium-constricted veins with
and without endothelium were unaffected by lidocaine (0.25-100 mu g/mL
) and bupivacaine (0.1-100 mu g/mL). In veins preconstricted by exogen
ously administered NE, a cumulative increase of both anesthetics produ
ced no effect at low doses, an augmentation of constriction to NE at 5
-20 mu g/mL bupivacaine and 20-100 mu g/mL lidocaine, and minimal effe
ct at 50-100 mu g/mL bupivacaine. These actions persisted in denuded o
r L-NAME treated veins. Nonincremental delivery of high concentrations
of lidocaine or bupivacaine produced relaxation of NE and potassium-c
onstricted rings in the absence and presence of L-NAME. Conclusions. L
idocaine and bupivacaine in concentrations typical during uncomplicate
d regional anesthesia inhibit adrenergic neurotransmission in rabbit m
esenteric capacitance veins and produce modest venodilatation. Higher
doses, resembling concentrations during accidental intravascular injec
tion, result in substantial loss in vasomotor control of these capacit
ance vessels, which may contribute to hemodynamic effects.