Relationship between α-actinin and cardiac function in rats with myocardial ischemia-reperfusion / 南方医科大学学报
Journal of Southern Medical University
; (12): 970-974, 2011.
Article
in Chinese
| WPRIM (Western Pacific)
| ID: wpr-332505
Responsible library:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To explore the relationship between α-actinin content and cardiac function in rats during myocardial ischemia-reperfusion.</p><p><b>METHODS</b>Thirty-two rats were randomized equally into sham-operated group, 30 min ischemia group, 1 h ischemia group, and 1 h ischemia with 2 h reperfusion group. Acute myocardial ischemia was induced in the 3 ischemia groups by ligation of the left anterior descending coronary artery, and the cardiac functions were evaluated. The myocardial contents of α-actinin was measured by immunohistochemistry, and phospholipase C (PLC) and phosphatidylinositol-3-kinase (PI3K) contents were determined by ELISA after the operations.</p><p><b>RESULTS</b>The left ventricular systolic pressure (LVSP), +dp/dt max, and -dp/dt max tended to decrease during myocardial ischemia, and increased after reperfusion, and the left ventricular end-diastolic pressure (LVEDP) showed reverse changes. The levels of α-actinin decreased with prolonged ischemia, showing a significant difference in 1 h ischemia group from those in the other 3 groups. PI3K and PLC contents were significantly increased with prolonged myocardial ischemia. Stimulation by LY-294002 and U-73122 caused enhanced contraction of single cardiomyocytes, and also increased the fluorescence intensity of α-actinin in the cardiomyocytes compared with that in 1 h ischemia group.</p><p><b>CONCLUSIONS</b>The cardiac dysfunction during acute ischemia-reperfusion in rats may be related with the changes of myocardial α-actinin content, which are probably a result of increased PI3K and PLC contents in the ischemic myocardium.</p>
Full text:
Available
Database:
WPRIM (Western Pacific)
Main subject:
Type C Phospholipases
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Actinin
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Myocardial Reperfusion Injury
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Rats, Wistar
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Myocardial Ischemia
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Phosphatidylinositol 3-Kinase
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Metabolism
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Myocardium
Limits:
Animals
Language:
Chinese
Journal:
Journal of Southern Medical University
Year:
2011
Document type:
Article