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Table of Contents
Year : 2011  |  Volume : 14  |  Issue : 3  |  Page : 242-243
Remifentanil: Much ado about something

Department of Internal Medicine/Critical Care, Medwin Hospital, Nampally, Hyderabad, AP, India

Click here for correspondence address and email

Date of Web Publication20-Aug-2011

How to cite this article:
Gude D. Remifentanil: Much ado about something. Ann Card Anaesth 2011;14:242-3

How to cite this URL:
Gude D. Remifentanil: Much ado about something. Ann Card Anaesth [serial online] 2011 [cited 2021 Oct 16];14:242-3. Available from:

The Editor,

Having read with great interest the article by Ruggeri et al. on remifentanil, [1] We would like to discuss more about the drug. An ultra-short-acting phenylpiperidine derivative and a selective μ opioid receptor agonist, remifentanil seems to deserve the recent limelight it is attracting. In the ischemia/reperfusion (I/R) injury, remifentanil demonstrated both pre- and post-conditioning cardioprotection. Regardless of the timing and duration of administration, it significantly reduced myocardial infarct size. Extracellular signal related protein kinases (ERK1/2) get activated in response to I/R, oxidative stress, and hypoxia, and have an established role in the anti-apoptotic defense network. Remifentanil increases the phosphorylation of ERK 1/2 and anti-apoptotic proteins in I/R. It is through this phosphorylation that remifentanil prevents apoptosis [inhibits the detrimental conformational changes in Bcl-2-associated X protein (Bax) and cytochrome c-induced caspase activation]. Remifentanil preserves gene expressions of SR (serine/arginine-rich) proteins and plays a key role in regulating the intracellular Ca2+ concentration via Ca2+ cycling proteins such as Ryanodine receptor (RyR), sarcoplasmic-reticulum Ca 2+ ATPase (SERCA2a), Phospholamban (PLB), and Calsequestrin (CSQ). [2] Apart from enhancing myofilament Ca 2+ sensitivity, remifentanil decreases intracellular Ca 2+ transient in myocytes by coupling to a Gi-protein, which may explain its negative inotropism. Also, remifentanil stimulates d and k opioid receptors activating protein kinase C (PKC) and opening mitochondrial KATP channel, which are of paramount significance in cardioprotection in ischemic and pharmacological preconditioning. Diabetes is shown to have mitigating effects on remifentanil-induced cardioprotection against I/R, probably mediated through the reduced recovery of the activities of proteins involved in anti-apoptotic pathways and the abnormal expression of SR genes.

Adding remifentanil to the standard anesthesia regimen (like fentanyl and propofol) reduced demonstrably the degree of myocardial damage [lower CK-MB, Cardiac troponin-I (cTnI), Ischemia modified albumin (IMA) and heart-type fatty acid binding protein (hFABP)] and the time to tracheal extubation. [3] The pharmacokinetic properties, hemodynamic stability and peri-operative control of stress response to cardiac surgery of remifentanil are comparable to fentanyl/morphine. Also, if Patient-Controlled-Analgesia (PCA) morphine is contraindicated after coronary artery bypass graft (CABG), PCA-remifentanil is a safe alternative.

Remifentanil may inhibit both intra-atrial conduction and sinus-node automaticity (no effect on atrioventricular node conduction). Although a decrease in heart rate, bradyarrhythmias and asystole need to be watched out for, a study showed that cardiac output (monitored with FloTrac/Vigileo) is not impaired, despite a decrease in arterial pressure. Also, a continuous infusion of remifentanil does not affect systolic and diastolic left ventricular function in young healthy subjects during spontaneous breathing.

The hepatoprotective potential has been established in a study where remifentanil and l-arginine pretreatment (before I/R insult) reduced the concentrations of serum aminotransferases and cytokines, decreased the concentrations of hepatic malondialdehyde and myeloperoxidase activity, and increased superoxide dismutase, nitric oxide, and inducible nitric oxide synthase (NOS) expression in vivo. The histologic damage and apoptosis were considerably decreased as well. [4]

Decreased delta opioid receptor (DOR) mRNA levels in the dorsal root ganglia mediate remifentanil-induced nociception, which may be reversed by increasing enkephalin levels in the spinal cord and the periphery. [5] Lithium chloride has also shown benefit in reducing its incisional hyperalgesia.

Remifentanil certainly holds promise and lives up to the hype.

   References Top

1.Ruggeri L, Landoni G, Guarracino F, Scolletta S, Bignami E, Zangrillo A. Remifentanil in critically ill cardiac patients. Ann Card Anaesth 2011;14:6-12.  Back to cited text no. 1
[PUBMED]  Medknow Journal  
2.Kim HS, Cho JE, Hong SW, Kim SO, Shim JK, Kwak YL. Remifentanil protects myocardium through activation of anti-apoptotic pathways of survival in ischemia-reperfused rat heart. Physiol Res 2010;59:347-56.  Back to cited text no. 2
3.Wong GT, Huang Z, Ji S, Irwin MG, Kim HS, Cho JE, et al. Remifentanil reduces the release of biochemical markers of myocardial damage after coronary artery bypass surgery: A randomized trial. J Cardiothorac Vasc Anesth 2010;24:790-6.  Back to cited text no. 3
4.Yang LQ, Tao KM, Liu YT, Cheung CW, Irwin MG, Wong GT, et al. Remifentanil preconditioning reduces hepatic ischemia-reperfusion injury in rats via inducible nitric oxide synthase expression. Anesthesiology 2011 Mar 4. [In Press].  Back to cited text no. 4
5.Cabañero D, Célérier E, García-Nogales P, Mata M, Roques BP, Maldonado R, et al. The pro-nociceptive effects of remifentanil or surgical injury in mice are associated with a decrease in delta-opioid receptor mRNA levels: Prevention of the nociceptive response by on-site delivery of enkephalins. Pain 2009;141:88-96.  Back to cited text no. 5

Correspondence Address:
Dilip Gude
AMC, 3rd Floor, Medwin Hospital, Chirag Ali Lane, Nampally, Hyderabad, AP - 500 001
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.84039

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