High-dose remifentanil increases blood pressure and heart rate mediated by sympatho-activation in conscious rats

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, r...

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Published inJournal of anesthesia Vol. 27; no. 3; pp. 325 - 332
Main Authors Shirasaka, Tetsuro, Yano, Takeshi, Kunitake, Takato, Tsuneyoshi, Isao
Format Journal Article
LanguageEnglish
Published Japan Springer Japan 01.06.2013
Springer
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Summary: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.
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ISSN:0913-8668
1438-8359
DOI:10.1007/s00540-012-1515-2