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Canadian Journal of Anesthesia, Vol 40, 251-256, Copyright © 1993 by Canadian Anesthesiologists' Society
ARTICLES |
M Yokoyama, H Goto, W Ueda, M Hirakawa and K Arakawa
Department of Anesthesiology, University of Kansas Medical Center, Kansas City 66160-7415.
We studied intravenous lidocaine-induced convulsions in rats to determine whether added epinephrine influences the provocation of lidocaine toxicity. Wistar rats (200-250 g) were divided into three groups of ten, depending on the concentration of epinephrine added to lidocaine. Group 1: plain 1.5% lidocaine; Group 2: 1.5% lidocaine with 1:200,000 epinephrine; Group 3: 1.5% lidocaine with 1:100,000 epinephrine. After surgical preparation and recovery from anaesthesia, all rats received a continuous i.v. infusion of lidocaine (15 mg.ml-1) at a rate of 4.0 mg.kg-1 x min-1 until generalized convulsions occurred. The epinephrine-treated animals developed acute hypertension after one minute of lidocaine infusion (105 +/- 2 to 141 +/- 2 mmHg in Group 2 and 103 +/- 2 to 151 +/- 2 mmHg in Group 3). The PaO2 values in the epinephrine groups at the onset of convulsions were decreased significantly (88.3 +/- 1.0 to 84.0 +/- 1.5 mmHg in Group 2 P < 0.05 and 86.9 +/- 1.2 to 78.1 +/- 2.4 mmHg in Group 3 P < 0.01). However, these values were still within physiological ranges. Serum potassium concentrations in all groups were decreased P < 0.05, (4.24 +/- 0.09 to 3.52 +/- 0.12 mEq.L-1 in Group 1, 4.02 +/- 0.09 to 3.63 +/- 0.17 mEq.L-1 in Group 2, and 4.15 +/- 0.10 to 3.69 +/- 0.17 mEq.L-1 in Group 3).(ABSTRACT TRUNCATED AT 250 WORDS)
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