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 in | Journal of anesthesia Vol. 27; no. 3; pp. 325 - 332 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Japan
Springer Japan
01.06.2013
Springer |
Subjects | |
Online Access | Get full text |
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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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0913-8668 1438-8359 |
DOI: | 10.1007/s00540-012-1515-2 |