Linked Life Data

12688395

Source:http://linkedlifedata.com/resource/pubmed/id/12688395

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2003-4-11
pubmed:abstractText
To date, there are two pathways discussed as a mechanism of ischemic preconditioning. Activation of protein kinase C by ischemic preconditioning increases adenosine release. The increased adenosine further activates protein kinase C through adenosine A1 receptors, and activated protein kinase C induces an infarct size-reducing effect through the opening of K(ATP) channels (pathway I). Meanwhile, activation of the alpha1b-adrenoceptor through increased interstitial noradrenaline by ischemic preconditioning is also associated with the ischemic preconditioning effect. However, the exact pathway of this is unknown, although it is postulated that protein kinase C and adenosine are cross-talking. Myocardial interstitial noradrenaline levels were measured in Japanese white rabbits using a microdialysis technique. Ischemic preconditioning was elicited by a single episode of 5 min ischemia and 5 min reperfusion. The infarct size was measured in rabbits subjected to 30 min ischemia and 48 h reperfusion. An increase in interstitial noradrenaline by ischemic preconditioning was not inhibited by an adenosine A1 receptor blocker (1,3-dipropyl-8-cyclopentylxanthine), but was inhibited by an adenosine A2 receptor blocker (3,7-dimethyl-1-(2-propynyl) xanthine) or protein kinase C inhibitors (staurosporine and polymyxin B). Interstitial noradrenaline was increased by an adenosine A2 receptor agonist (CGS21680) and the increase was inhibited by a protein kinase C inhibitor. The infarct size-reducing effect of ischemic preconditioning was inhibited by a selective alpha1b-adrenoceptor blocker (chloroethylclonidine) or a protein kinase C inhibitor, and that of tyramine, an inducer of noradrenaline, was inhibited by protein kinase C inhibitor. This suggests the presence of pathway II, indicating ischemic preconditioning --> activation of protein kinase C --> adenosine release --> pre-synaptic adenosine A2 receptors --> activation of protein kinase C in sympathetic nerve --> noradrenaline --> alpha1b-adrenoceptor --> activation of protein kinase C in myocytes --> infarct size-reducing effect. In addition, the ischemic preconditioning effect on infarct size was not inhibited by 1,3-dipropyl-8-cyclopentylxanthine, but was inhibited by 3,7-dimethyl-1-(2-propynyl) xanthine or chloroethylclonidine, suggesting the greater importance of pathway II compared with pathway I. Thus, pathway II plays an important role in the pathogenesis of the infarct size-reducing effect in ischemic preconditioning.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
41 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S39-47
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Cross-talk among noradrenaline, adenosine and protein kinase C in the mechanisms of ischemic preconditioning in rabbits.
pubmed:affiliation
Second Department of Internal Medicine, Gifu University School of Medicine, Gifu, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't