dc.contributor.author | Headrick, JP | |
dc.contributor.author | Gauthier, NS | |
dc.contributor.author | Morrison, R | |
dc.contributor.author | Matherne, GP | |
dc.date.accessioned | 2017-05-03T13:44:13Z | |
dc.date.available | 2017-05-03T13:44:13Z | |
dc.date.issued | 2000 | |
dc.identifier.issn | 0363-6135 | |
dc.identifier.uri | http://hdl.handle.net/10072/3466 | |
dc.description.abstract | We studied the role of mitochondrial ATP-sensitive K+(KATP) channels in modifying functional responses to 20 min global ischemia and 30 min reperfusion in wild-type mouse hearts and in hearts with ~250-fold overexpression of functionally coupled A1-adenosine receptors (A1ARs). In wild-type hearts, time to onset of contracture (TOC) was 303 ᠲ4 s, with a peak contracture of 89 ᠵ mmHg. Diastolic pressure remained elevated at 52 ᠶ mmHg after reperfusion, and developed pressure recovered to 40 ᠶ% of preischemia. A1AR overexpression markedly prolonged TOC to 517 ᠸ4 s, reduced contracture to 64 ᠶ mmHg, and improved recovery of diastolic (to 9 ᠴ mmHg) and developed pressure (to 82 ᠸ%). 5-Hydroxydecanoate (5-HD; 100 卩, a mitochondrial KATPblocker, did not alter ischemic contracture in wild-type hearts, but increased diastolic pressure to 69 ᠸ mmHg and reduced developed pressure to 10 ᠵ% during reperfusion. In transgenic hearts, 5-HD reduced TOC to 348 ᠱ8 s, increased postischemic contracture to 53 ᠴ mmHg, and reduced recovery of developed pressure to 22 ᠴ%. In summary, these data are the first to demonstrate that endogenous activation of KATP channels improves tolerance to ischemia-reperfusion in murine myocardium. This functional protection occurs without modification of ischemic contracture. The data also support a role for mitochondrial KATP channel activation in the pronounced cardioprotection afforded by overexpression of myocardial A1ARs. | |
dc.description.peerreviewed | Yes | |
dc.description.publicationstatus | Yes | |
dc.language | English | |
dc.language.iso | eng | |
dc.publisher | American Physiological Society | |
dc.publisher.place | USA | |
dc.publisher.uri | http://ajpheart.physiology.org/content/279/4/H1690 | |
dc.relation.ispartofpagefrom | H1690 | |
dc.relation.ispartofpageto | H1697 | |
dc.relation.ispartofjournal | American Journal of Physiology: Heart and Circulatory Physiology | |
dc.relation.ispartofvolume | 279 | |
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 | Cardioprotection by KATP channels in wild-type hearts and hearts overexpressing A1 adenosine receptors | |
dc.type | Journal article | |
dc.type.description | C1 - Articles | |
dc.type.code | C - Journal Articles | |
gro.faculty | Griffith Health, School of Medical Science | |
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 | 2015-02-05T03:42:49Z | |
gro.hasfulltext | No Full Text | |
gro.griffith.author | Headrick, John P. | |