Purpose: The ultra-short-acting μ-opioid receptor agonist, remifentanil, is commonly used in clinical anesthesia; however, there are limited data about the hemodynamic effects of remifentanil itself without anesthetics. We investigated the effects of an ultra-short-acting μ-opioid receptor agonist, remifentanil, on cardiovascular and sympathetic function in conscious rats.
Methods: The mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were recorded during continuous intravenous (i.v.) infusion of remifentanil at a moderate-dose (0.25 and 0.5 μg/kg/min) and a high-dose (1.0 and 2.0 μg/kg/min) in conscious intact and sino-aortic denervated (SAD) rats. Baroreflex sensitivity was examined during remifentanil administration. Rats were administered saline or naloxone to assess the involvement of the μ-opioid receptor in the remifentanil-induced responses.
Results: High-dose remifentanil induced biphasic changes in MAP and HR. Mediated by sympatho-activation, these parameters increased after briefly decreasing once. Subpressor-dose remifentanil enhanced baroreflex sensitivity. Changes in MAP, HR, and RSNA induced by remifentanil were inhibited by naloxone.
Conclusions: High-dose remifentanil decreases MAP and HR transiently and increases these parameters mediated by the activation of sympathetic nerve activity in conscious rats.