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Article: In vitro electrophysiologic effects of morphine in rabbit ventricular myocytes

TitleIn vitro electrophysiologic effects of morphine in rabbit ventricular myocytes
Authors
Issue Date2005
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.org
Citation
Anesthesiology, 2005, v. 103 n. 2, p. 280-286 How to Cite?
AbstractBackground: Morphine is widely used in patients undergoing surgical operations and is also reported to mediate cardioprotection of preconditioning. The current study determined effects of morphine at therapeutic to pharmacologic concentrations on cardiac action potential, L-type Ca2+ current (ICa.L), delayed rectifier K+ current (IK), and inward rectifier K+ current (IK1) in isolated rabbit ventricular myocytes. Methods: Ventricular myocytes were enzymatically isolated from rabbit hearts. Action potential and membrane currents were recorded in current and voltage clamp modes. Results: Morphine at concentrations from 0.01 to 1 μM significantly prolonged cardiac action potential, and at 0.1 and 1 μM slightly but significantly hyperpolarized the resting membrane potential. In addition, morphine at 0.1 μM significantly augmented ICa.L (at + 10 mV) from 5.9 ± 1.9 to 7.3 ± 1.7 pA/pF (by 23%; P < 0.05 vs. control) and increased IK1 (at -60 mV) from 2.8 ± 1.0 to 3.5 ± 0.9 pA/pF (by 27%; P < 0.05 vs. control). Five μM naltrindole (a selective δ-opioid receptor antagonist) or 5 μM norbinaltorphimine (a selective κ-opioid receptor antagonist) prevented the increase in ICa.L induced by morphine, but 5 μM CTOP (a selective μ-opioid receptor antagonist) did not. The three types of opioid antagonists did not affect the augmentation of IK1 by morphine. Morphine had no effect on IK. Conclusions: These results indicate that morphine prolongs action potential duration by increasing ICa.L, an effect mediated by δ- and κ-opioid receptors. It also hyperpolarizes cardiac resting membrane potential by increasing IK1, which is not mediated by opioid receptors. © 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/85494
ISSN
2015 Impact Factor: 5.264
2015 SCImago Journal Rankings: 2.162
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXiao, GSen_HK
dc.contributor.authorZhou, JJen_HK
dc.contributor.authorWang, GYen_HK
dc.contributor.authorCao, CMen_HK
dc.contributor.authorLi, GRen_HK
dc.contributor.authorWong, TMen_HK
dc.date.accessioned2010-09-06T09:05:44Z-
dc.date.available2010-09-06T09:05:44Z-
dc.date.issued2005en_HK
dc.identifier.citationAnesthesiology, 2005, v. 103 n. 2, p. 280-286en_HK
dc.identifier.issn0003-3022en_HK
dc.identifier.urihttp://hdl.handle.net/10722/85494-
dc.description.abstractBackground: Morphine is widely used in patients undergoing surgical operations and is also reported to mediate cardioprotection of preconditioning. The current study determined effects of morphine at therapeutic to pharmacologic concentrations on cardiac action potential, L-type Ca2+ current (ICa.L), delayed rectifier K+ current (IK), and inward rectifier K+ current (IK1) in isolated rabbit ventricular myocytes. Methods: Ventricular myocytes were enzymatically isolated from rabbit hearts. Action potential and membrane currents were recorded in current and voltage clamp modes. Results: Morphine at concentrations from 0.01 to 1 μM significantly prolonged cardiac action potential, and at 0.1 and 1 μM slightly but significantly hyperpolarized the resting membrane potential. In addition, morphine at 0.1 μM significantly augmented ICa.L (at + 10 mV) from 5.9 ± 1.9 to 7.3 ± 1.7 pA/pF (by 23%; P < 0.05 vs. control) and increased IK1 (at -60 mV) from 2.8 ± 1.0 to 3.5 ± 0.9 pA/pF (by 27%; P < 0.05 vs. control). Five μM naltrindole (a selective δ-opioid receptor antagonist) or 5 μM norbinaltorphimine (a selective κ-opioid receptor antagonist) prevented the increase in ICa.L induced by morphine, but 5 μM CTOP (a selective μ-opioid receptor antagonist) did not. The three types of opioid antagonists did not affect the augmentation of IK1 by morphine. Morphine had no effect on IK. Conclusions: These results indicate that morphine prolongs action potential duration by increasing ICa.L, an effect mediated by δ- and κ-opioid receptors. It also hyperpolarizes cardiac resting membrane potential by increasing IK1, which is not mediated by opioid receptors. © 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.orgen_HK
dc.relation.ispartofAnesthesiologyen_HK
dc.rightsAnesthesiology. Copyright © Lippincott Williams & Wilkins.en_HK
dc.subject.meshAction Potentials - drug effectsen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCalcium - metabolismen_HK
dc.subject.meshCalcium Channels, L-Type - drug effects - physiologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMorphine - pharmacologyen_HK
dc.subject.meshMyocytes, Cardiac - drug effects - physiologyen_HK
dc.subject.meshNaltrexone - analogs & derivatives - pharmacologyen_HK
dc.subject.meshPotassium Channels - drug effects - physiologyen_HK
dc.subject.meshRabbitsen_HK
dc.titleIn vitro electrophysiologic effects of morphine in rabbit ventricular myocytesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0003-3022&volume=103&issue=2&spage=280&epage=286&date=2005&atitle=In+vitro+electrophysiologic+effects+of+morphine+in+rabbit+ventricular+myocytesen_HK
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_HK
dc.identifier.authorityLi, GR=rp00476en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/00000542-200508000-00011en_HK
dc.identifier.pmid16052110-
dc.identifier.scopuseid_2-s2.0-23044477453en_HK
dc.identifier.hkuros112631en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-23044477453&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume103en_HK
dc.identifier.issue2en_HK
dc.identifier.spage280en_HK
dc.identifier.epage286en_HK
dc.identifier.isiWOS:000230983800010-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXiao, GS=8695315100en_HK
dc.identifier.scopusauthoridZhou, JJ=7405545441en_HK
dc.identifier.scopusauthoridWang, GY=7407149992en_HK
dc.identifier.scopusauthoridCao, CM=7401501737en_HK
dc.identifier.scopusauthoridLi, GR=7408462932en_HK
dc.identifier.scopusauthoridWong, TM=7403531434en_HK

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