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Conference Paper: Isoflurane preconditioning and propofol postconditioning synergistically enhance STAT3 activation and reduce postischemic myocardial infarction in rats

TitleIsoflurane preconditioning and propofol postconditioning synergistically enhance STAT3 activation and reduce postischemic myocardial infarction in rats
Authors
Issue Date2011
PublisherAmerican Society of Anesthesiologists. The Abstract Archive is located at http://www.asaabstracts.com/strands/asaabstracts/abstractArchive.htm
Citation
The 2011 Annual Meeting of the American Society of Anesthesiologists (ASA 2011), Chicago, IL., 15-19 October 2011. In Abstract Archive of the American Society of Anesthesiologists, 2011, abstract no. A1475 How to Cite?
AbstractBACKGROUND: Isoflurane preconditioning (IsoPC) and propofol anaesthesia have been shown to synergistically attenuate myocardial reperfusion injury in humans (1), but the underlying mechanism is unclear. Recent studies show that the JAK/STAT3 pathway plays an essential role both in cardiac ischemic preconditioning (2) and postconditioning (3). We, therefore, hypothesized that IsoPC and propofol postconditioning (PPostC) may synergistically activate signal transducer and activator of transcription 3 (STAT3) and thus facilitate cardioprotection. METHODS: With ethics approval, adult male SD-rats were subjected to myocardial ischemia-reperfusion injury by occluding the left coronary artery for 30 min followed by 120 min of reperfusion. Rats (n=5-6 per group) were either untreated (control), treated with IsoPC (8% emulsified isoflurane at 2 ml/ kg) for 10 min before inducing ischemia, with intravenous propofol starting from 5 min before reperfusion until 10 min of reperfusion (PPostC), or a combination of IsoPC and PPostC (group IP). At the end of reperfusion, myocardial infarct size (IS) was assessed by triphenyltetrazolium staining and left ventricular tissue was processed for total STAT3 protein and its phosphorylation status at site Tyr705 (p-STAT3) by Western blotting analysis. Data are expressed as mean +/- SEM and were analyzed with ANOVA. RESULTS: Postischemic myocardial IS expressed as percentage of area at risk was 45±7% in the control group and was moderately but significantly reduced by either IsoPC (37±5%) or PPostC (39±3%) (all P<0.05 vs. control). IsoPC and PPostC combination further reduced IS to 20±3% (P<0.01 group IP vs. all other groups). Myocardial total STAT3 protein expression did not significantly differ among groups. The levels of p-STAT3 in the IsoPC and PPostC groups were, respectively, about 1.2-fold and 1.3-fold of that in the control group, but these differences did not reach statistical significance. However, p-STAT3 protein expression in group IP was 1.9-fold of that in the control group (P<0.01 vs. control). CONCLUSIONS: Enhancement of STAT3 phosphorylation/activation may represent an important mechanism by which IsoPC and PPostC synergistically attenuate postischemic myocardial infarct size.
DescriptionTopic: Experimental Circulation: abstract no. A1475
Persistent Identifierhttp://hdl.handle.net/10722/165918

 

DC FieldValueLanguage
dc.contributor.authorXia, Zen_US
dc.contributor.authorQiao, Sen_US
dc.contributor.authorWang, Ten_US
dc.contributor.authorMao, Xen_US
dc.contributor.authorIrwin, MGen_US
dc.date.accessioned2012-09-20T08:25:13Z-
dc.date.available2012-09-20T08:25:13Z-
dc.date.issued2011en_US
dc.identifier.citationThe 2011 Annual Meeting of the American Society of Anesthesiologists (ASA 2011), Chicago, IL., 15-19 October 2011. In Abstract Archive of the American Society of Anesthesiologists, 2011, abstract no. A1475en_US
dc.identifier.urihttp://hdl.handle.net/10722/165918-
dc.descriptionTopic: Experimental Circulation: abstract no. A1475-
dc.description.abstractBACKGROUND: Isoflurane preconditioning (IsoPC) and propofol anaesthesia have been shown to synergistically attenuate myocardial reperfusion injury in humans (1), but the underlying mechanism is unclear. Recent studies show that the JAK/STAT3 pathway plays an essential role both in cardiac ischemic preconditioning (2) and postconditioning (3). We, therefore, hypothesized that IsoPC and propofol postconditioning (PPostC) may synergistically activate signal transducer and activator of transcription 3 (STAT3) and thus facilitate cardioprotection. METHODS: With ethics approval, adult male SD-rats were subjected to myocardial ischemia-reperfusion injury by occluding the left coronary artery for 30 min followed by 120 min of reperfusion. Rats (n=5-6 per group) were either untreated (control), treated with IsoPC (8% emulsified isoflurane at 2 ml/ kg) for 10 min before inducing ischemia, with intravenous propofol starting from 5 min before reperfusion until 10 min of reperfusion (PPostC), or a combination of IsoPC and PPostC (group IP). At the end of reperfusion, myocardial infarct size (IS) was assessed by triphenyltetrazolium staining and left ventricular tissue was processed for total STAT3 protein and its phosphorylation status at site Tyr705 (p-STAT3) by Western blotting analysis. Data are expressed as mean +/- SEM and were analyzed with ANOVA. RESULTS: Postischemic myocardial IS expressed as percentage of area at risk was 45±7% in the control group and was moderately but significantly reduced by either IsoPC (37±5%) or PPostC (39±3%) (all P<0.05 vs. control). IsoPC and PPostC combination further reduced IS to 20±3% (P<0.01 group IP vs. all other groups). Myocardial total STAT3 protein expression did not significantly differ among groups. The levels of p-STAT3 in the IsoPC and PPostC groups were, respectively, about 1.2-fold and 1.3-fold of that in the control group, but these differences did not reach statistical significance. However, p-STAT3 protein expression in group IP was 1.9-fold of that in the control group (P<0.01 vs. control). CONCLUSIONS: Enhancement of STAT3 phosphorylation/activation may represent an important mechanism by which IsoPC and PPostC synergistically attenuate postischemic myocardial infarct size.-
dc.languageengen_US
dc.publisherAmerican Society of Anesthesiologists. The Abstract Archive is located at http://www.asaabstracts.com/strands/asaabstracts/abstractArchive.htm-
dc.relation.ispartofAbstract Archive of the American Society of Anesthesiologistsen_US
dc.titleIsoflurane preconditioning and propofol postconditioning synergistically enhance STAT3 activation and reduce postischemic myocardial infarction in ratsen_US
dc.typeConference_Paperen_US
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hken_US
dc.identifier.emailQiao, S: qiao1983@hku.hken_US
dc.identifier.emailWang, T: wangtt6@hku.hken_US
dc.identifier.emailMao, X: h0994071@hkusuc.hku.hken_US
dc.identifier.emailIrwin, MG: mgirwin@hku.hk-
dc.identifier.authorityXia, Z=rp00532en_US
dc.identifier.authorityIrwin, MG=rp00390en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros209798en_US
dc.publisher.placeUnited States-
dc.customcontrol.immutablesml 130408-

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