• Tetsuro Shirasaka, Takeshi Yano, Takato Kunitake, and Isao Tsuneyoshi.
• Department of Anesthesiology and Intensive Care, Faculty of Medicine, University of Miyazaki, 5200 Kihara Kiyotake, Miyazaki, Japan. shirasak@med.miyazaki-u.ac.jp
• J Anesth. 2013 Jun 1; 27 (3): 325-32.

PurposeThe 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.MethodsThe 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.ResultsHigh-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.ConclusionsHigh-dose remifentanil decreases MAP and HR transiently and increases these parameters mediated by the activation of sympathetic nerve activity in conscious rats.

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