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Conference Paper: Effects of glucose concentration on propofol cardioprotection against ischemia-reperfusion injury in isolated rat hearts

TitleEffects of glucose concentration on propofol cardioprotection against ischemia-reperfusion injury in isolated rat hearts
Authors
KeywordsBiology
Issue Date2013
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The 2013 Annual Meeting of Experimental Biology (EB 2013), Boston, MA., 28 March-1 April 2013. In The FASEB Journal, 2013, v. 27 meeting abstracts, no. lb620 How to Cite?
AbstractThe anesthetic propofol protects against myocardial ischemia-reperfusion injury (IRI) by reducing reactive oxygen species (ROS)-induced oxidative stress. However, its cardioprotection in patients is inconsistent. We postulated that low glucose(LG) as seen during tight glycemic control promotes cardiac ROS formation through enhancing fatty acid(FA) oxidation during IRI and unmasks propofol cardioprotection. Rat hearts were isolated and randomly assigned to be perfused with Krebs-Henseleit solution with glucose at 5.5 mmol/l (LG) in the absence or presence of propofol (5ug/ml) or propofol with trimetazidine (TMZ) unknown to inhibit FA oxidation, or with glucose at 8 mmol/L (group G) in the absence or presence of propofol or propofol plus TMZ. Hearts were subjected to 35 min of global ischemia and 60 min of reperfusion. Myocardial infarct size(IS) was higher in LG than in G group (P<0.05), accompanied with reduced left ventricular (LV) developed pressure and increases in postischemic cardiac contracture. Cardiac 15-F2t-isoprostane was higher in LG that was associated with higher cardiac lipid transporter CD36 protein expression than in G group. Propofol reduced IS and improved cardiac function and reduced cardiac CD36 in G but not in LG group. TMZ facilitated propofol cardioprotection in LG. During IRI, LG through enhancing fatty acid oxidation and oxidative stress compromised propofol cardioprotection.
Persistent Identifierhttp://hdl.handle.net/10722/190355
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorTao, MZen_US
dc.contributor.authorLiu, HMen_US
dc.contributor.authorZhang, Pen_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2013-09-17T15:20:17Z-
dc.date.available2013-09-17T15:20:17Z-
dc.date.issued2013en_US
dc.identifier.citationThe 2013 Annual Meeting of Experimental Biology (EB 2013), Boston, MA., 28 March-1 April 2013. In The FASEB Journal, 2013, v. 27 meeting abstracts, no. lb620en_US
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/190355-
dc.description.abstractThe anesthetic propofol protects against myocardial ischemia-reperfusion injury (IRI) by reducing reactive oxygen species (ROS)-induced oxidative stress. However, its cardioprotection in patients is inconsistent. We postulated that low glucose(LG) as seen during tight glycemic control promotes cardiac ROS formation through enhancing fatty acid(FA) oxidation during IRI and unmasks propofol cardioprotection. Rat hearts were isolated and randomly assigned to be perfused with Krebs-Henseleit solution with glucose at 5.5 mmol/l (LG) in the absence or presence of propofol (5ug/ml) or propofol with trimetazidine (TMZ) unknown to inhibit FA oxidation, or with glucose at 8 mmol/L (group G) in the absence or presence of propofol or propofol plus TMZ. Hearts were subjected to 35 min of global ischemia and 60 min of reperfusion. Myocardial infarct size(IS) was higher in LG than in G group (P<0.05), accompanied with reduced left ventricular (LV) developed pressure and increases in postischemic cardiac contracture. Cardiac 15-F2t-isoprostane was higher in LG that was associated with higher cardiac lipid transporter CD36 protein expression than in G group. Propofol reduced IS and improved cardiac function and reduced cardiac CD36 in G but not in LG group. TMZ facilitated propofol cardioprotection in LG. During IRI, LG through enhancing fatty acid oxidation and oxidative stress compromised propofol cardioprotection.-
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journalen_US
dc.subjectBiology-
dc.titleEffects of glucose concentration on propofol cardioprotection against ischemia-reperfusion injury in isolated rat heartsen_US
dc.typeConference_Paperen_US
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros221909en_US
dc.identifier.volume27en_US
dc.identifier.issuemeeting abstracts-
dc.publisher.placeUnited States-

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