THE EFFECTS OF EXOGENOUS EPINEPHRINE ON A CONVULSIVE DOSE OF LIDOCAINE - RELATIONSHIP WITH CEREBRAL-CIRCULATION

Citation
Y. Yamauchi et al., THE EFFECTS OF EXOGENOUS EPINEPHRINE ON A CONVULSIVE DOSE OF LIDOCAINE - RELATIONSHIP WITH CEREBRAL-CIRCULATION, Journal of neurosurgical anesthesiology, 10(3), 1998, pp. 178-187
Citations number
28
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Anesthesiology,Surgery
ISSN journal
0898-4921
Volume
10
Issue
3
Year of publication
1998
Pages
178 - 187
Database
ISI
SICI code
0898-4921(1998)10:3<178:TEOEEO>2.0.ZU;2-U
Abstract
In order to understand why exogenous epinephrine decreases the convuls ive dose of lidocaine. the authors investigated cerebral circulation a nd plasma lidocaine concentrations in Wistar rats under general anesth esia. In the first experiment, baseline evaluations of each rat's elec troencephalogram (EEG), mean arterial pressure (MAP), regional cerebra l blood flow (r-CBF), cerebrospinal fluid (CSF) pressure, and cerebral perfusion pressure (CPP) were made. The rats were then assigned to on e of three groups: Group L (n = 6) received intravenous lidocaine (5 m g/kg/min), Group LE (n = 6) received intravenous lidocaine (5 mg/kg/mi n) and epinephrine (2.5 mu g/kg/min); and Group E (n = 5) received int ravenous epinephrine (2.5 mu g/kg/min). Cumulative doses of lidocaine at the onset of EEG spike activity in Groups L and LE were compared. B lood-brain barrier (BBB) permeability was evaluated by observing extra vasation of Evans blue (EB) dye. In the second experiment, additional rats were allocated to two treatment groups. Group L' (n = 6) received intravenous lidocaine (5 mg/kg/min); Group LE' (n = 6) received intra venous lidocaine (5 mg/kg/min) and epinephrine (2.5 mu g/kg/min). Brai n tissue oxygen partial pressure (PtO2) was monitored during infusion, and arterial and sagittal sinus blood samples were obtained immediate ly after the onset of EEG spike activity to determine plasma lidocaine concentration. The convulsive dose of lidocaine was significantly dec reased when lidocaine was administered with epinephrine (Group L: 61.5 +/- 5.3 mg/kg (mean +/- SD); Group LE: 30.1 +/- 4.0 mg/kg) (p < 0.05) , but there were no significant differences in plasma lidocaine concen tration among these groups. R-CBF. CSF pressure, and CPP immediately b efore EEG spike activity were higher in Group LE than in Group L. Neit her decreased PtO2 nor extravasation of EB was observed in rats treate d with epinephrine and lidocaine, excluding cerebral ischemia and BBB breakdown from possible mechanisms by which epinephrine decreased the convulsive dose of Lidocaine, None of the rats in Group E exhibited EE G findings suggestive of a preconvulsive state, ruling out a convulsiv e effect of epinephrine itself. The results suggest that an increase i n lidocaine supply to the brain caused by increased CBF causes the low cumulative dose of lidocaine at the onset of convulsion in rats given lidocaine plus epinephrine.