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ID 110711
Author
Yin, Ruixing Department of Cardiology, Institute of Cardiovascular Diseases, Guangxi Medical University
Yang, Dezhai Department of Cardiology, Institute of Cardiovascular Diseases, Guangxi Medical University
Li, Jiaquan Department of Cardiology, Institute of Cardiovascular Diseases, Guangxi Medical University
Keywords
myocardial infarction
cardiotrophin-1
apoptosis
Content Type
Journal Article
Description
The effects of cardiotrophin-1 on hemodynamics, cardiac function, cardiomyocyte apoptosis, and expression of P53, Fas, Bax and Bcl-2 proteins in myocardium were determined in a rat model of acute myocardial infarction. Twenty-four male Sprague-Dawley rats weighing approximately 310 g were subjected to left coronary artery ligation. Seven days before surgery, the rats were randomized to receive cardiotrophin-1 (treated group) or phosphate-buffered saline (control group). Recombinant rat cardiotrophin-1 (2 μg in 1 ml phosphate-buffered saline) or phosphate-buffered saline (1 ml) was administered daily via the tail vein for 7 days (n=12 for each group). Hemodynamic parameters, apoptotic index, P53, Fas, Bax and Bcl-2 expression in myocardium were measured at 24 hours after coronary ligation. As compared with control animals, rats treated with cardiotrophin-1 had significantly higher mean arterial pressure, left ventricular systolic pressure and the maximum rate of left ventricular pressure rise or fall, and significantly lower left ventricular end-diastolic pressure. Cardiotrophin-1 pretreatment did not affect the heart rate, heart weight, body weight or the ratio of heart weight to body weight. The number of apoptotic cardiomyocytes in cardiotrophin-1 treated group was less than that in control group [(15.8±5.2)% vs (34.6±7.7) %,Plt0.01]. Cardiotrophin-1 pretreatment significantly inhibited P53, Fas and Bax, and increased Bcl-2 expression in myocardium.
Journal Title
The journal of medical investigation : JMI
ISSN
13431420
NCID
AA11166929
Volume
51
Issue
1-2
Start Page
29
End Page
37
Sort Key
29
Published Date
2004-02
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher