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
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Abstract 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.
AbstractList Rats were administered saline or naloxone to assess the involvement of the μ-opioid receptor in the remifentanil-induced responses.
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. Keywords Remifentanil * Opioid * Sympathetic nerve activity * Sinoaortic-denervated rats
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. 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. 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. High-dose remifentanil decreases MAP and HR transiently and increases these parameters mediated by the activation of sympathetic nerve activity in conscious rats.
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.
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.
Audience Academic
Author Tsuneyoshi, Isao
Shirasaka, Tetsuro
Yano, Takeshi
Kunitake, Takato
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Keywords Sinoaortic-denervated rats
Opioid
Remifentanil
Sympathetic nerve activity
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SSID ssj0006113
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Snippet Purpose The ultra-short-acting μ-opioid receptor agonist, remifentanil, is commonly used in clinical anesthesia; however, there are limited data about the...
The ultra-short-acting μ-opioid receptor agonist, remifentanil, is commonly used in clinical anesthesia; however, there are limited data about the hemodynamic...
Purpose The ultra-short-acting μ-opioid receptor agonist, remifentanil, is commonly used in clinical anesthesia; however, there are limited data about the...
Rats were administered saline or naloxone to assess the involvement of the μ-opioid receptor in the remifentanil-induced responses.
PURPOSEThe ultra-short-acting μ-opioid receptor agonist, remifentanil, is commonly used in clinical anesthesia; however, there are limited data about the...
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pubmed
springer
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SubjectTerms Anesthesiology
Animals
Baroreflex - drug effects
Blood Pressure - drug effects
Complications and side effects
Consciousness - drug effects
Critical Care Medicine
Dosage and administration
Emergency Medicine
Heart beat
Heart Rate - drug effects
Hemodynamics - drug effects
Hypertension
Intensive
Male
Medicine
Medicine & Public Health
Naloxone - pharmacology
Original Article
Pain Medicine
Piperidines - pharmacology
Rats
Rats, Wistar
Receptors, Opioid, mu - agonists
Remifentanil
Risk factors
Sympathetic Nervous System - drug effects
Title High-dose remifentanil increases blood pressure and heart rate mediated by sympatho-activation in conscious rats
URI https://link.springer.com/article/10.1007/s00540-012-1515-2
https://www.ncbi.nlm.nih.gov/pubmed/23132182
https://search.proquest.com/docview/1367880719
Volume 27
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