|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
4
|
|
pubmed:dateCreated |
2000-8-15
|
|
pubmed:abstractText |
Activation of protein kinase C-linked receptors and subsequent opening of the mitochondrial ATP-sensitive K(+) (mitoK(ATP)) channel are crucial in preconditioning (PC). This study examined whether postinfarct ventricular remodeling interferes with the PC mechanism.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
AIM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Jul
|
|
pubmed:issn |
1524-4539
|
|
pubmed:author |
|
|
pubmed:issnType |
Electronic
|
|
pubmed:day |
25
|
|
pubmed:volume |
102
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
458-63
|
|
pubmed:dateRevised |
2006-11-15
|
|
pubmed:meshHeading |
|
|
pubmed:year |
2000
|
|
pubmed:articleTitle |
Cardioprotective mechanism of ischemic preconditioning is impaired by postinfarct ventricular remodeling through angiotensin II type 1 receptor activation.
|
|
pubmed:affiliation |
Second Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
