Remifentanil but not sufentanil induces cardioprotection in human ischemic heart muscle in vitro.
Cardioprotection
Ischemia–reperfusion injury; remifentanil
Sufentanil
Journal
BMC pharmacology & toxicology
ISSN: 2050-6511
Titre abrégé: BMC Pharmacol Toxicol
Pays: England
ID NLM: 101590449
Informations de publication
Date de publication:
20 04 2023
20 04 2023
Historique:
received:
18
05
2022
accepted:
07
03
2023
medline:
24
4
2023
pubmed:
21
4
2023
entrez:
20
04
2023
Statut:
epublish
Résumé
Previous studies on animal models have suggested that δ-opioid receptor (OR) signaling is the primary pathway responsible for opioids' cardioprotective effect. We hypothesize that the μ-OR's activation protects the human heart muscle. We performed the experiments on muscular trabeculae obtained from the right atrial appendages of 104 consecutive patients subjected to coronary artery bypass surgery. Two trabeculae from each patient were studied simultaneously and exposed to 60 min of hypoxia with subsequent 60 min of reoxygenation. Remifentanil (5 μM or 50 μM) or sufentanil (40 μM or 400 μM) was used from the time of reoxygenation. Trabeculae contractility was assessed as the maximal amplitude of the contraction at baseline, after 60 min of hypoxia, during reoxygenation, and after norepinephrine application. During reperfusion, the application of remifentanil improved cardiomyocytes' function as compared to the control group (time from reperfusion: 15 min: 39.8% vs. 21.7%, p = 0.01; 30 min: 41.4% vs. 21.8%, p = 0.01; 60 min: 42.7% vs. 26.9%, p = 0.04; after norepinephrine: 64.7% vs. 43.2%, p = 0.03). The application of sufentanil did not influence cardiomyocyte function as can be seen when comparing the results of the experimental and control group. Remifentanil, but not sufentanil, induces a cardioprotective effect on human right atria muscle in in vitro conditions, manifested as the increased amplitude of their contraction during reperfusion after 60 min of ischemia.
Sections du résumé
BACKGROUND
Previous studies on animal models have suggested that δ-opioid receptor (OR) signaling is the primary pathway responsible for opioids' cardioprotective effect. We hypothesize that the μ-OR's activation protects the human heart muscle.
METHODS
We performed the experiments on muscular trabeculae obtained from the right atrial appendages of 104 consecutive patients subjected to coronary artery bypass surgery. Two trabeculae from each patient were studied simultaneously and exposed to 60 min of hypoxia with subsequent 60 min of reoxygenation. Remifentanil (5 μM or 50 μM) or sufentanil (40 μM or 400 μM) was used from the time of reoxygenation. Trabeculae contractility was assessed as the maximal amplitude of the contraction at baseline, after 60 min of hypoxia, during reoxygenation, and after norepinephrine application.
RESULTS
During reperfusion, the application of remifentanil improved cardiomyocytes' function as compared to the control group (time from reperfusion: 15 min: 39.8% vs. 21.7%, p = 0.01; 30 min: 41.4% vs. 21.8%, p = 0.01; 60 min: 42.7% vs. 26.9%, p = 0.04; after norepinephrine: 64.7% vs. 43.2%, p = 0.03). The application of sufentanil did not influence cardiomyocyte function as can be seen when comparing the results of the experimental and control group.
CONCLUSIONS
Remifentanil, but not sufentanil, induces a cardioprotective effect on human right atria muscle in in vitro conditions, manifested as the increased amplitude of their contraction during reperfusion after 60 min of ischemia.
Identifiants
pubmed: 37081569
doi: 10.1186/s40360-023-00660-3
pii: 10.1186/s40360-023-00660-3
pmc: PMC10120098
doi:
Substances chimiques
Remifentanil
P10582JYYK
Norepinephrine
X4W3ENH1CV
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
25Informations de copyright
© 2023. The Author(s).
Références
J Cardiothorac Vasc Anesth. 2003 Aug;17(4):465-9
pubmed: 12968234
Cell Cycle. 2021 Feb;20(4):383-391
pubmed: 33475463
Acta Anaesthesiol Scand. 2011 Jul;55(6):758-64
pubmed: 21615344
Am J Cardiol. 2004 May 15;93(10):1295-7
pubmed: 15135709
Circulation. 1998 Apr 7;97(13):1282-9
pubmed: 9570199
Am J Physiol Heart Circ Physiol. 2001 Jan;280(1):H384-91
pubmed: 11123255
J Cardiothorac Vasc Anesth. 2010 Oct;24(5):790-6
pubmed: 20056436
Lancet. 2019 Oct 19;394(10207):1415-1424
pubmed: 31500849
Sci Signal. 2010 Jul 20;3(131):ra54
pubmed: 20647592
J Am Coll Cardiol. 2000 Dec;36(7):2296-302
pubmed: 11127476
Cardiol J. 2017;24(4):419-426
pubmed: 27734456
Circulation. 1986 Nov;74(5):1124-36
pubmed: 3769170
Br J Anaesth. 2011 Jul;107(1):8-18
pubmed: 21613279
Lancet. 1993 Jul 31;342(8866):276-7
pubmed: 8101304
Lab Anim. 2018 Jun;52(3):271-279
pubmed: 28776458
Acta Anaesthesiol Scand. 2004 Oct;48(9):1155-62
pubmed: 15352962
Can J Physiol Pharmacol. 2018 Jan;96(1):80-87
pubmed: 28881154
Anesthesiology. 2008 Aug;109(2):308-17
pubmed: 18648240
Aging (Albany NY). 2020 Jun 25;12(14):13924-13938
pubmed: 32584786
Anesthesiology. 2004 Oct;101(4):918-23
pubmed: 15448525
Am J Physiol. 1995 May;268(5 Pt 2):H2157-61
pubmed: 7771566
Int Immunopharmacol. 2012 Jul;13(3):341-6
pubmed: 22561119
Nan Fang Yi Ke Da Xue Xue Bao. 2009 Aug;29(8):1554-6
pubmed: 19726290
Biochim Biophys Acta. 1989 Dec 11;987(1):69-74
pubmed: 2557082
Br J Pharmacol. 2015 Apr;172(8):2026-50
pubmed: 25521834
N Engl J Med. 2015 Oct 8;373(15):1408-17
pubmed: 26436207
Heart Fail Rev. 2007 Dec;12(3-4):235-44
pubmed: 17520362
Ann Transl Med. 2020 Apr;8(8):551
pubmed: 32411774
Exp Gerontol. 2014 Feb;50:72-81
pubmed: 24316036
J Toxicol Sci. 2021;46(6):263-271
pubmed: 34078833
Cardiovasc Res. 2009 Jul 15;83(2):234-46
pubmed: 19398470
Anesthesiology. 2005 Feb;102(2):371-8
pubmed: 15681953
J Cardiothorac Vasc Anesth. 2011 Dec;25(6):926-30
pubmed: 21514843
Curr Pharm Des. 2014;20(36):5696-705
pubmed: 24502571
Interact Cardiovasc Thorac Surg. 2014 Mar;18(3):308-12
pubmed: 24336785
Anesth Analg. 2001 Sep;93(3):543-9
pubmed: 11524316
Anesth Analg. 1995 Sep;81(3):619-23
pubmed: 7653833
J Mol Cell Cardiol. 1997 Aug;29(8):2187-95
pubmed: 9281450