File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Remifentanil preconditioning confers cardioprotection via cardiac κ- and δ-opioid receptors

TitleRemifentanil preconditioning confers cardioprotection via cardiac κ- and δ-opioid receptors
Authors
Issue Date2005
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.org
Citation
Anesthesiology, 2005, v. 102 n. 2, p. 371-378 How to Cite?
AbstractBackground: Remifentanil preconditioning (RPC) reduces the infarct size in anesthetized rat hearts, and this effect seems to be mediated by all three types of opioid receptors (ORs). Because there is evidence of only κ- and δ- but not μ-ORs in the rat heart, the authors investigated whether RPC confers cardioprotection via cardiac κ- and δ-OR as well as via extracardiac μ-OR agonist activity. The authors also investigated the involvement of signaling mechanisms, namely protein kinase C and mitochondrial adenosine triphosphate-sensitive potassium (KATP) channels. Methods: The hearts of male Sprague-Dawley rats weighing 190-210 g were removed, mounted on a Langendorff apparatus, and perfused retrogradely at 100 cm H2O with Krebs-Ringer's solution. All hearts were subjected to 30 min of ischemia and 2 h of reperfusion. The study consisted of three series of experiments on the effect of ischemic preconditioning or RPC (10, 50, and 100 ng/ml remifentanil) after blockade of OR subtypes (δ-OR antagonist naltrindol, κ-OR antagonist nor-binaltorphimine, and μ-OR antagonist CTOP). The involvement of protein kinase C or the KATP channel in the cardioprotection of RPC was also investigated using specific blockers in each group. RPC was produced by three cycles of 5-min perfusion of remifentanil in Krebs-Ringer's solution interspersed with a 5-min reperfusion with Krebs solution only. Infarct size, as a percentage of the area at risk, was determined by 2,3,5-triphenyltetrazolium staining. Results: Infarct size as a percentage of the area at risk was significantly reduced after RFC from 51.9 ± 5.0% (control, n = 8) to 36.2 ± 10.0% (100 ng/ml RPC, n = 8, P < 0.01). This effect was stopped by pretreatment with naltrindol (52.3 ± 5.2%) and nor-binaltorphimine (43.5 ± 6.0%) but not CTOP (37.1 ± 6.0%). Chelerythrine and GF109203X, both protein kinase C inhibitors, abolished the effects of RPC or ischemic preconditioning on infarct size as a percentage of area at risk. 5-Hydroxydecanoate (a selective mitochondrial KATP channel blocker) also abolished the cardioprotection of RPC and IPC, but HMR-1098 (a selective inhibitor of the sarcolemmal KATP channel) did not. Conclusion: Cardiac δ- and κ- but not μ-ORs mediate the cardioprotection produced by RPC. Both protein kinase C and the mitochondrial KATP channel were involved in this effect.
Persistent Identifierhttp://hdl.handle.net/10722/145538
ISSN
2015 Impact Factor: 5.264
2015 SCImago Journal Rankings: 2.162
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, Yen_HK
dc.contributor.authorIrwin, MGen_HK
dc.contributor.authorTak, MWen_HK
dc.contributor.authorChen, Men_HK
dc.contributor.authorCao, CMen_HK
dc.date.accessioned2012-02-28T01:53:17Z-
dc.date.available2012-02-28T01:53:17Z-
dc.date.issued2005en_HK
dc.identifier.citationAnesthesiology, 2005, v. 102 n. 2, p. 371-378en_HK
dc.identifier.issn0003-3022en_HK
dc.identifier.urihttp://hdl.handle.net/10722/145538-
dc.description.abstractBackground: Remifentanil preconditioning (RPC) reduces the infarct size in anesthetized rat hearts, and this effect seems to be mediated by all three types of opioid receptors (ORs). Because there is evidence of only κ- and δ- but not μ-ORs in the rat heart, the authors investigated whether RPC confers cardioprotection via cardiac κ- and δ-OR as well as via extracardiac μ-OR agonist activity. The authors also investigated the involvement of signaling mechanisms, namely protein kinase C and mitochondrial adenosine triphosphate-sensitive potassium (KATP) channels. Methods: The hearts of male Sprague-Dawley rats weighing 190-210 g were removed, mounted on a Langendorff apparatus, and perfused retrogradely at 100 cm H2O with Krebs-Ringer's solution. All hearts were subjected to 30 min of ischemia and 2 h of reperfusion. The study consisted of three series of experiments on the effect of ischemic preconditioning or RPC (10, 50, and 100 ng/ml remifentanil) after blockade of OR subtypes (δ-OR antagonist naltrindol, κ-OR antagonist nor-binaltorphimine, and μ-OR antagonist CTOP). The involvement of protein kinase C or the KATP channel in the cardioprotection of RPC was also investigated using specific blockers in each group. RPC was produced by three cycles of 5-min perfusion of remifentanil in Krebs-Ringer's solution interspersed with a 5-min reperfusion with Krebs solution only. Infarct size, as a percentage of the area at risk, was determined by 2,3,5-triphenyltetrazolium staining. Results: Infarct size as a percentage of the area at risk was significantly reduced after RFC from 51.9 ± 5.0% (control, n = 8) to 36.2 ± 10.0% (100 ng/ml RPC, n = 8, P < 0.01). This effect was stopped by pretreatment with naltrindol (52.3 ± 5.2%) and nor-binaltorphimine (43.5 ± 6.0%) but not CTOP (37.1 ± 6.0%). Chelerythrine and GF109203X, both protein kinase C inhibitors, abolished the effects of RPC or ischemic preconditioning on infarct size as a percentage of area at risk. 5-Hydroxydecanoate (a selective mitochondrial KATP channel blocker) also abolished the cardioprotection of RPC and IPC, but HMR-1098 (a selective inhibitor of the sarcolemmal KATP channel) did not. Conclusion: Cardiac δ- and κ- but not μ-ORs mediate the cardioprotection produced by RPC. Both protein kinase C and the mitochondrial KATP channel were involved in this effect.en_HK
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.orgen_HK
dc.relation.ispartofAnesthesiologyen_HK
dc.subject.meshCardiotonic Agents - pharmacology - therapeutic use-
dc.subject.meshIschemic Preconditioning, Myocardial - methods-
dc.subject.meshPiperidines - pharmacology - therapeutic use-
dc.subject.meshReceptors, Opioid, delta - antagonists and inhibitors - physiology-
dc.subject.meshReceptors, Opioid, kappa - antagonists and inhibitors - physiology-
dc.titleRemifentanil preconditioning confers cardioprotection via cardiac κ- and δ-opioid receptorsen_HK
dc.typeArticleen_HK
dc.identifier.emailIrwin, MG:mgirwin@hku.hken_HK
dc.identifier.authorityIrwin, MG=rp00390en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1097/00000542-200502000-00020en_HK
dc.identifier.pmid15681953-
dc.identifier.scopuseid_2-s2.0-13244265918en_HK
dc.identifier.hkuros97324en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-13244265918&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume102en_HK
dc.identifier.issue2en_HK
dc.identifier.spage371en_HK
dc.identifier.epage378en_HK
dc.identifier.isiWOS:000226755300018-
dc.publisher.placeUnited Statesen_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats