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Alterations in arterial PaCO2 can influence local anesthetic toxicity. The objective of this study was to evaluate the effect of stress-induced changes in PaCO2 and PaO2 on the seizure threshold of lidocaine and articaine. Lidocaine (2% with 1 ∶ 100,000 epinephrine) or articaine (4% with 1 ∶ 100,000 epinephrine) was administered intravenously under rest or stress conditions to 36 rats separated into 4 groups. Propranolol and prazosin were administered preoperatively to minimize cardiovascular effects of epinephrine. Mean arterial pressure (MAP), heart rate (HR), and arterial pH, PaCO2, and PaO2 were measured. Results showed no differences in MAP, HR, or pH. Stress significantly increased the latency period for the first tonic-clonic seizure induced by a toxic dose of both lidocaine and articaine (P < .05). Seizures were brought on more rapidly by articaine. No significant difference between toxic doses of lidocaine and articaine was noted. Stress raised the seizure threshold dose for both drugs and significantly (P < .01) increased arterial PaO2 from 94.0 ± 1.90 mm Hg to 113.0 ± 2.20 mm Hg, and reduced PaCO2 from 36.0 ± 0.77 mm Hg to 27.0 ± 0.98 mm Hg. In conclusion, reduction in PaCO2 and/or increase in PaO2 raised the seizure threshold of lidocaine and articaine. This study also confirmed that lidocaine and articaine have equipotent central nervous system toxicity.

Keywords: Lidocaine; Articaine; Local anesthetic toxicity
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Copyright: 2010 by the American Dental Society of Anesthesiology

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eISSN: 1878-7177

ISSN: 0003-3006

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