Linked Life Data

16456873

Source:http://linkedlifedata.com/resource/pubmed/id/16456873

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-3-1
pubmed:abstractText
Neonatal rat hearts are more tolerant to ischemia compared to adult rat hearts. We hypothesized that opioid receptors and mitochondrial potassium channels are involved in the elevated ischemia tolerance of neonatal rats. Newborn rats were treated by an intraperitoneal injection with sodium chloride (placebo, Pla; n = 7), naloxone (Nal; n = 8), or K+ (ATP) channel blocker 5-hydroxydecanoate (HD; n = 8), or were left untreated (sham; n = 8). Thirty minutes after injection, the rats were sacrificed and hearts were arrested cardioplegically and fixed with aldehyde fixative 90 min after global ischemia at room temperature. For control, newborn rat hearts were fixed immediately after sacrifice. Ventricular tissue blocks were prepared for electron microscopy. Mitochondrial (volume-weighted mean volume of mitochondria) and cardiomyocyte volume (cellular edema index, CEI) were estimated to quantify the ischemic injury. Compared to control myocardium, CEI was increased by 244% +/- 39% in sham, 173% +/- 28% in Nal, 142% +/- 25% in HD, and 101% +/- 24% in Pla (P < 0.05 between groups). Volume-weighted mean volume of mitochondria was increased by 514% +/- 235% in sham, 341% +/- 110% in Nal, 458% +/- 149% in HD, and 175% +/- 70% in Pla. Differences between Pla and other groups were significant (P < 0.01 for all). No significant difference was observed between the other groups. Thus, ischemic injury was smallest with placebo, indicating a mechanism similar to preconditioning induced by the intraperitoneal injection. This response was attenuated by blockade of opioid receptors and mitochondrial potassium channels, suggesting their involvement in the elevated ischemia tolerance of newborn rat hearts.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/5-hydroxydecanoic acid, http://linkedlifedata.com/resource/pubmed/chemical/Bretschneider cardioplegic solution, http://linkedlifedata.com/resource/pubmed/chemical/Decanoic Acids, http://linkedlifedata.com/resource/pubmed/chemical/Glucose, http://linkedlifedata.com/resource/pubmed/chemical/Hydroxy Acids, http://linkedlifedata.com/resource/pubmed/chemical/Mannitol, http://linkedlifedata.com/resource/pubmed/chemical/Naloxone, http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, http://linkedlifedata.com/resource/pubmed/chemical/Potassium Chloride, http://linkedlifedata.com/resource/pubmed/chemical/Procaine, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Opioid, http://linkedlifedata.com/resource/pubmed/chemical/Sodium Chloride, http://linkedlifedata.com/resource/pubmed/chemical/mitochondrial K(ATP) channel
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1552-4884
pubmed:author
pubmed:issnType
Print
pubmed:volume
288
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
297-303
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Myocardial ischemia tolerance in the newborn rat involving opioid receptors and mitochondrial K+ channels.
pubmed:affiliation
Division of Electron Microscopy, Department of Anatomy, University of Göttingen, Göttingen, Germany. cmuehlf@gwdg.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't