Remifentanil has been well known to cause much more significant bradycardia and hypotension as compared with other opioids. However, the underlying mechanism is still poorly understood. The present study hypothesized that remifentanil led to bradycardia and hypotension with distinct mechanisms and aimed to test this hypothesis. Testing the hypothesis would broaden our understanding the underlying mechanism of remifentanil and may provide some guidance in the use of remifentanil clinically. Mean arterial pressure and heart rate were measured before and at the indicated time after drug treatment in the anesthetized rabbits. In the vagotomy group, bilateral vagus in the neck was exposed and one section of the vagus severed respectively. Remifentanil caused slight but significant bradycardia immediately which recovered entirely within one minute. On the other hand, bolus injection of remifentanil led to severe hypotension which sustained for more than five minutes. Bilateral vagotomy could delay the recovery of remifentanil-mediated bradycardia but did not affect remifentanil-evoked hypotension significantly. Pretreatment with naloxone, a non-specific opioid receptor antagonist could entirely prevent the remifentanil-mediated hypotension but only partially reversed remifentanil-mediated bradycardia. Remifentanil induces bradycardia and hypotension with distinct physiological and biochemical mechanisms. Remifentanil-induced bradycardia is mediated by opioid receptor-dependent and -independent pathways; however, remifentanil-induced hypotension is only through opioid receptor-dependent pathway.
Key words: Remifentanil, bradycardia, hypotension, opioid receptor, hemodynamic effect.
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