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Article: Remifentanil preconditioning reduces hepatic ischemia-reperfusion injury in rats via inducible nitric oxide synthase expression

TitleRemifentanil preconditioning reduces hepatic ischemia-reperfusion injury in rats via inducible nitric oxide synthase expression
Authors
Issue Date2011
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.org
Citation
Anesthesiology, 2011, v. 114 n. 5, p. 1036-1047 How to Cite?
AbstractBACKGROUND: Opioid preconditioning against ischemia reperfusion injury has been well studied in myocardial and neuronal tissues. The objective of this study was to determine whether remifentanil could attenuate hepatic injury and to investigate the mechanisms. METHODS: A rat model of hepatic ischemia reperfusion injury and a hepatocyte hypoxia reoxygenation (HR) injury model were used, respectively, in two series of experiments. Remifentanil was administered before ischemia or hypoxia and the experiments were repeated with previous administration of naloxone, L-arginine and N-omega-nitro-L-arginine methyl ester, a nonselective opioid receptor antagonist, a nitric oxide donor, and nitric oxide synthase (NOS) inhibitor, respectively. Serum aminotransferase, cytokines, and hepatic lipid peroxidation were measured. Histopathology examination and apoptotic cell detection were assessed. For the in vitro study, cell viability, intracellular nitric oxide, apoptosis, and NOS expression were evaluated. RESULTS: Remifentanil and L-arginine pretreatment reduced concentrations of serum aminotransferases and cytokines, decreased the concentrations of hepatic malondialdehyde and myeloperoxidase activity, and increased superoxide dismutase, nitric oxide, and inducible NOS expression in vivo. Decreased histologic damage and apoptosis were also seen in these two groups. These changes were prevented by previous administration of N-omega-nitro-L-arginine methyl ester but not naloxone. There was an increase in inducible NOS protein expression but not endogenous NOS in remifentanil and L-arginine pretreated groups compared with control, naloxone, and N-omega-nitro-L-arginine methyl ester groups. CONCLUSION: Pretreatment with remifentanil can attenuate liver injury both in vivo and in vitro. Inducible NOS but not opioid receptors partly mediate this effect by exhausting reactive oxygen species and attenuating the inflammatory response. Copyright © 2011, the American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins. Anesthesiology.
Persistent Identifierhttp://hdl.handle.net/10722/138934
ISSN
2021 Impact Factor: 8.986
2020 SCImago Journal Rankings: 1.874
ISI Accession Number ID
Funding AgencyGrant Number
Shanghai Rising-Star Program, Shanghai, China08QA14007
Science and Technology Commission of Shanghai, Shanghai, China10411952000
Funding Information:

Received from the Department of Anesthesiology, Eastern Hepatobiliary Surgery Hospital, Shanghai, China. Submitted for publication March 10, 2010. Accepted for publication December 2, 2010. Supported by Grant 08QA14007 from the Shanghai Rising-Star Program, Shanghai, China, and Grant 10411952000 from key program of Science and Technology Commission of Shanghai, Shanghai, China. Drs. Yang and Tao contributed equally to this work.

References

 

DC FieldValueLanguage
dc.contributor.authorYang, LQen_US
dc.contributor.authorTao, KMen_US
dc.contributor.authorLiu, YTen_US
dc.contributor.authorCheung, CWen_US
dc.contributor.authorIrwin, MGen_US
dc.contributor.authorWong, GTCen_US
dc.contributor.authorLv, Hen_US
dc.contributor.authorSong, JGen_US
dc.contributor.authorWu, FXen_US
dc.contributor.authorYu, WF-
dc.date.accessioned2011-09-23T05:42:19Z-
dc.date.available2011-09-23T05:42:19Z-
dc.date.issued2011en_US
dc.identifier.citationAnesthesiology, 2011, v. 114 n. 5, p. 1036-1047en_US
dc.identifier.issn0003-3022-
dc.identifier.urihttp://hdl.handle.net/10722/138934-
dc.description.abstractBACKGROUND: Opioid preconditioning against ischemia reperfusion injury has been well studied in myocardial and neuronal tissues. The objective of this study was to determine whether remifentanil could attenuate hepatic injury and to investigate the mechanisms. METHODS: A rat model of hepatic ischemia reperfusion injury and a hepatocyte hypoxia reoxygenation (HR) injury model were used, respectively, in two series of experiments. Remifentanil was administered before ischemia or hypoxia and the experiments were repeated with previous administration of naloxone, L-arginine and N-omega-nitro-L-arginine methyl ester, a nonselective opioid receptor antagonist, a nitric oxide donor, and nitric oxide synthase (NOS) inhibitor, respectively. Serum aminotransferase, cytokines, and hepatic lipid peroxidation were measured. Histopathology examination and apoptotic cell detection were assessed. For the in vitro study, cell viability, intracellular nitric oxide, apoptosis, and NOS expression were evaluated. RESULTS: Remifentanil and L-arginine pretreatment reduced concentrations of serum aminotransferases and cytokines, decreased the concentrations of hepatic malondialdehyde and myeloperoxidase activity, and increased superoxide dismutase, nitric oxide, and inducible NOS expression in vivo. Decreased histologic damage and apoptosis were also seen in these two groups. These changes were prevented by previous administration of N-omega-nitro-L-arginine methyl ester but not naloxone. There was an increase in inducible NOS protein expression but not endogenous NOS in remifentanil and L-arginine pretreated groups compared with control, naloxone, and N-omega-nitro-L-arginine methyl ester groups. CONCLUSION: Pretreatment with remifentanil can attenuate liver injury both in vivo and in vitro. Inducible NOS but not opioid receptors partly mediate this effect by exhausting reactive oxygen species and attenuating the inflammatory response. Copyright © 2011, the American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins. Anesthesiology.-
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.org-
dc.relation.ispartofAnesthesiologyen_US
dc.subject.meshAnalgesics, Opioid - metabolism - therapeutic use-
dc.subject.meshIschemic Preconditioning-
dc.subject.meshLiver - blood supply - drug effects - metabolism-
dc.subject.meshLiver Diseases - metabolism - prevention and control-
dc.subject.meshNitric Oxide Synthase - drug effects - metabolism-
dc.titleRemifentanil preconditioning reduces hepatic ischemia-reperfusion injury in rats via inducible nitric oxide synthase expressionen_US
dc.typeArticleen_US
dc.identifier.emailCheung, CW: cheucw@hku.hken_US
dc.identifier.emailWong, GTC: gordon@hku.hken_US
dc.identifier.emailYu, WF: ywf808@sohu.com-
dc.identifier.authorityCheung, CW=rp00244en_US
dc.identifier.authorityWong, GTC=rp00523en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1097/ALN.0b013e3182104956-
dc.identifier.pmid21383616-
dc.identifier.scopuseid_2-s2.0-79955466532-
dc.identifier.hkuros193527en_US
dc.identifier.hkuros216263-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79955466532&selection=ref&src=s&origin=recordpage-
dc.identifier.volume114-
dc.identifier.issue5en_US
dc.identifier.spage1036en_US
dc.identifier.epage1047en_US
dc.identifier.isiWOS:000289980200008-
dc.publisher.placeUnited States-
dc.identifier.issnl0003-3022-

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