The in vitro effects of remifentanil and fentanyl on isolated human right atria and saphenous veins

Duman, Ateş; Şahin, Ayşe; Atalık, Kısmet Esra Nurullahoğlu; Öğün, Cemile Öztin; Ulusoy, Hasan; Durgut, Kadir; Ökesli, Selmin

doi:10.1016/s1053-0770(03)00151-4

Cited by 22 publications

(16 citation statements)

References 23 publications

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“…It also induces a dose-dependent increase in systemic arterial vasodilation in humans with total artificial heart implants 10 . Remifentanil and fentanyl induce concentration-dependent relaxation in human saphenous vein strips 11 and radial artery rings 12 . Fentanyl, alfentanil, and sufentanil induce vasodilation by direct action on the peripheral vascular smooth muscle in the isolated canine hind limb, while increased administration causes a progressive decrease in peripheral resistance 13 .…”

Section: Discussionmentioning

confidence: 99%

General anaesthesia induction using general anaesthetic agents and opioid analgesics increases Perfusion Index (PI) and decreases Pleth Variability Index (PVI): Observational clinical study

Mizuno

Morita

Kakinuma

et al. 2012

Sri Lankan J Anaesthesiol

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Section: Discussionmentioning

confidence: 99%

General anaesthesia induction using general anaesthetic agents and opioid analgesics increases Perfusion Index (PI) and decreases Pleth Variability Index (PVI): Observational clinical study

Mizuno

Morita

Kakinuma

et al. 2012

Sri Lankan J Anaesthesiol

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“…These findings indicate direct cardioprotection since neither remifentanil nor sufentanil produced direct inotropic or lusitropic effects in human atrial myocardium. The absence of inotropic or lusitropic effects of fentanyl in human atrial tissue is less clear, however [102, 103]. …”

Section: Opioid-induced Cardioprotection In Humansmentioning

confidence: 99%

Opioid-induced Cardioprotection

Tanaka¹,

Kersten²,

Riess³

2014

CPD

103

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Ischemic heart disease and myocardial infarction continue to be leading causes of cardiovascular morbidity and mortality. Activation of opioid, adenosine, bradykinin, adrenergic and other G-protein coupled receptors have been found to be cardioprotective. κ- and/or δ-opioid receptor activation is involved in direct myocardial protection, while the role of μ-opioid receptors seems less clear. In addition, differential affinities to the three opioid-receptor subtypes by various agonists and cross-talk among different G-protein coupled receptors render conclusions regarding opioid-mediated cardioprotection challenging. The present review will focus on the protective effects of endogenously released opioid peptides as well as exogenously administered opioids such as morphine, fentanyl, remifentanil, butorphanol, and methadone against myocardial ischemia/reperfusion injury. Receptor heterodimerization and cross-talk as well as interactions with other cardioprotective techniques will be discussed. Implications for opioid-induced cardioprotection in humans and for future drug development to improve myocardial salvage will be provided.

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“…The number of studies using isolated human vessels 122, 144,146,151,168,183,193,202,223,[302][303][304][305][306][307][308] is increasing, and they have reported both similarities and differences in vascular responsiveness to general anesthetics between humans and animals. However, as discussed above, the underlying mechanisms are not entirely clear.…”

Section: Investigations With Human Vesselsmentioning

confidence: 99%

“…However, as discussed above, the direct action of volatile anesthetics on arterial VSMCs may contribute to the prolonged systemic hypotension observed during the postanesthesia period. 157,158,294,303,305,307,308,[317][318][319] Again, on consideration of possible species differences, further studies using human capacitance vessels, as well as human systemic resistance vessels, would be essential to evaluate a possibility that the direct (i.e., nonneural) actions of general anesthetics on VSMCs contribute to systemic hypotension during their administration. 2 In previous studies with isolated mesenteric veins, 157,158,317 halothane, enflurane, and isoflurane inhibited the contractile response to norepi- nephrine.…”

Section: Investigations With Systemic Resistance and Capacitance Vesselsmentioning

confidence: 99%

General Anesthetics and Vascular Smooth Muscle

Akata

2007

Anesthesiology

101

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General anesthetics threaten cardiovascular stability by causing changes in cardiac function, vascular reactivity, and cardiovascular reflexes and significantly alter distribution of cardiac output to various organs. Their overall impact is often systemic hypotension, which is attributable to myocardial depression, peripheral vasodilation, and attenuated sympathetic nervous system activity. However, one could be more causative than the others, depending on anesthetic agents and cardiovascular factors inherent in patients (e.g., coexisting heart disease). It is generally believed that most general anesthetics attenuate sympathetic nervous system outflow from the central nervous system, thereby decreasing vascular resistance in peripheral circulations. Indeed, in previous in vivo studies, during administration of various general anesthetics, vascular resistance was decreased in most peripheral circulations; however, it was unaffected or increased in some peripheral circulations. General anesthetics may act directly on vascular smooth muscle and/or endothelial cells in various vascular beds, influencing total peripheral and/or regional vascular resistance, and hence organ blood flow. This article reviews previously reported direct (i.e., nonneural) vascular actions of general anesthetics and discusses their underlying mechanisms, their in vivo relevance, and the future of research for general anesthetic vascular pharmacology.

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The in vitro effects of remifentanil and fentanyl on isolated human right atria and saphenous veins

Cited by 22 publications

References 23 publications

General anaesthesia induction using general anaesthetic agents and opioid analgesics increases Perfusion Index (PI) and decreases Pleth Variability Index (PVI): Observational clinical study

General anaesthesia induction using general anaesthetic agents and opioid analgesics increases Perfusion Index (PI) and decreases Pleth Variability Index (PVI): Observational clinical study

Opioid-induced Cardioprotection

General Anesthetics and Vascular Smooth Muscle

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