dc.contributor.author | Gross, Eric | |
dc.contributor.author | Peart, Jason | |
dc.contributor.author | Hsu, Anna | |
dc.contributor.author | Auchampach, John | |
dc.contributor.author | Gross, Garrett | |
dc.date.accessioned | 2017-05-03T13:03:44Z | |
dc.date.available | 2017-05-03T13:03:44Z | |
dc.date.issued | 2005 | |
dc.identifier.issn | 03636135 | |
dc.identifier.doi | 10.1152/ajpheart.00918.2004 | |
dc.identifier.uri | http://hdl.handle.net/10072/25842 | |
dc.description.abstract | Selective d-opioid agonists produce delayed cardioprotection that lasts for 24-48 h in rats; however, the maximum length of the cardioprotective window is unclear. In this study, we attempted to prolong the cardioprotective window using a unique d-opioid agonist, fentanyl isothiocyanate (FIT), which binds irreversibly to the -receptor, and determined the role of the phosphatidylinositol 3-kinase (PI3K) pathway as a trigger or end effector of FIT-induced cardioprotection. Initially, male rats were administered FIT (10 姯kg) 10 min before hearts were subjected to 30 min of ischemia and 2 h of reperfusion followed by infarct size (IS) assessment. Acute FIT administration reduced IS when given before ischemia, 5 min before reperfusion, or 10 s after reperfusion compared with control. IS reduction also occurred following a single dose of FIT at 48, 72, 96, and 120 h after administration vs. control, with the maximum effect observed at 96 h. FIT-induced IS reduction at 96 h was completely abolished when the irreversible PI3K inhibitor wortmannin (15 姯kg) was given before FIT during the trigger phase; however, the effect was only partially abrogated when wortmannin was given 96 h later. These data suggest that FIT has a prolonged cardioprotective window greater than that of any previously described cardioprotective agent that requires PI3K primarily in the trigger phase but also partially, as a mediator or end effector | |
dc.description.peerreviewed | Yes | |
dc.description.publicationstatus | Yes | |
dc.language | English | |
dc.language.iso | eng | |
dc.publisher | American Physiological Society | |
dc.publisher.place | United States | |
dc.relation.ispartofstudentpublication | N | |
dc.relation.ispartofpagefrom | H2744 | |
dc.relation.ispartofpageto | H2749 | |
dc.relation.ispartofjournal | American Journal of Physiology: Heart and Circulatory Physiology | |
dc.relation.ispartofvolume | 288 | |
dc.rights.retention | Y | |
dc.subject.fieldofresearch | Zoology | |
dc.subject.fieldofresearch | Medical physiology | |
dc.subject.fieldofresearch | Cardiovascular medicine and haematology | |
dc.subject.fieldofresearchcode | 3109 | |
dc.subject.fieldofresearchcode | 3208 | |
dc.subject.fieldofresearchcode | 3201 | |
dc.title | Extending the cardioprotective window using a novel δ-opioid agonist fentanyl isothiocyanate via the PI3-kinase pathway | |
dc.type | Journal article | |
dc.type.description | C1 - Articles | |
dc.type.code | C - Journal Articles | |
gro.rights.copyright | Self-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information. | |
gro.date.issued | 2015-02-05T03:43:30Z | |
gro.hasfulltext | No Full Text | |
gro.griffith.author | Peart, Jason N. | |