Abstract:
:Neurophysiologic and local cerebral metabolic mapping techniques indicate that seizures associated with lidocaine toxicity originate in subcortical brain structures. Normally local cerebral blood flow (l-CBF) is quantitatively coupled to local cerebral metabolic rate for glucose (l-CMRg). In the present study the response of l-CBF to a lidocaine-induced preconvulsive state (localized seizure activity in the absence of a grand mal seizure) was evaluated in rats anesthetized with 60% nitrous oxide. Lidocaine administered as a bolus (20 mg/kg) followed by an infusion (4 mg/kg) over 5.5 min resulted in progressive alteration in the electroencephalogram (EEG). L-CBF was studied with the 14C-iodoantipyrine autographic method when the preconvulsive EEG pattern consisted of a repetitive spike and wave complex at a frequency of 14 +/- 1 X min-1 complexes, superimposed on practically isoelectric background activity. Under these conditions high doses of lidocaine significantly (P less than 0.05) decreased (range -30% to -68%) l-CBF in 71% of the 34 brain regions studied. The greatest exception to this trend for l-CBF to decrease was observed in the limbic system wherein l-CBF remained within control ranges in eight of the 11 structures evaluated. Qualitative comparison of lidocaine l-CBF changes with l-CMRg changes obtained under similar conditions indicated a general trend for local flow and metabolism to decrease in parallel. Exceptions to this were confined to certain limbic areas (amygdala and hippocampus) in which increases in l-CMRg were more than 100% greater than slight (P greater than 0.05) increases in l-CBF.(ABSTRACT TRUNCATED AT 250 WORDS)
journal_name
Anesthesiologyjournal_title
Anesthesiologyauthors
Tommasino C,Maekawa T,Shapiro HMdoi
10.1097/00000542-198606000-00016subject
Has Abstractpub_date
1986-06-01 00:00:00pages
771-7issue
6eissn
0003-3022issn
1528-1175journal_volume
64pub_type
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