Background: Hypocapnia induced following the accidental intravenous infusion of a local anesthetic can mitigate anesthetic toxicity, but the effects of hypocapnia induced prior to local anesthetic infusion are unknown. In this study, we examined the effects of prior hypocapnia on bupivacaine-induced cardiotoxicity in rats. Methods: Eighteen Sprague-Dawley rats were randomly divided into two groups: one receiving sevoflurane with normal ventilation (Control Group) and the other receiving sevoflurane with hyperventilation to induce hypocapnia (Hypocapnia Group). After 30 min, both groups received continuous intravenous infusions of 0.25% bupivacaine at 2 mg · kg-1 · min-1. The time taken to reach 25% and 50% reductions in heart rate (HR; HR-25%, HR-50%) and mean arterial pressure (MAP; MAP-25%, MAP-50%) from the start of bupivacaine infusion were recorded. The difference between HR-25% and MAP-25% was calculated. The times of the first ventricular premature beat (VPB) and final systole were also recorded. Results: In the Hypocapnia Group, HR-50%, MAP-25%, and MAP-50% were prolonged compared with the Control Group (P < 0.001). Furthermore, the interval between HR-25% and MAP-25% and the times between the first VPB and final systole were prolonged in the Hypocapnia Group (P < 0.001). Conclusion: In rats under sevoflurane anesthesia, prior hypocapnia delayed the onset of bupivacaine-induced cardiotoxicity. Prior hypocapnia should be avoided during continuous bupivacaine nerve block under general anesthesia, because it may delay the detection of cardiotoxicity.
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