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Updated: Jun 24, 2026
A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
Published on: July 17, 2012
[Study on the expression of activin-A in myocardial ischemia postconditioning]
Ling-Jun Zhang1, He Huang, Ping-Xi Pan
1Department of Cardiology, West China Hospital, Sichuan University, Chengdu 610041, China.
Objective:
To analyze the relationship between the hydroxy free radical (* OH) and the activity of lactate dehydrogenase (LDH) and to study the potential role of activin-A in myocardial ischemia postconditioning for the protection of myocardium.
Methods:
Forty healthy adult Sprague-Dawley rats (gender unconcerned) were randomly divided into four different groups (n = 10 in each group): sham-operation, ischemia (I), ischemia/reperfusion (I/R) and ischemia postconditioning (postcon). In anesthetized open-chest rats, the left anterior descending artery (LAD) was ligated. Sham operation: the surgical procedure was identical to other groups, but the LAD was ligated for only 30 min, and not occluded. Ischemia: the LAD was occluded for 30 min; Ischemia/reperfusion: the LAD was occluded for 30 min and reperfused for 1 h; Postconditioning: after LAD occlusion for 30 min, at the start of reperfusion, three cycles of 30 s reperfusion and 30 s LAD re-occlusion preceded the 1h of reperfusion. The expression of activin-A in myocardium was detected by ELISA in all groups. The ability of suppression on the hydroxy free radical (* OH) and the activity of lactate dehydrogenase (LDH) in myocardium taken from each group were measured by spectrophotometer.
Results:
Compared with the sham-operated group, the expression of activin-A was significantly elevated in ischemia, ischemia/reperfusion and postconditiong groups, with the highest in the ischemia/reperfusion group. And postconditioning significantly decreased the expression of activin-A in the ischemia/ reperfusion injured myocardium [(343.05 +/- 25.8) microg/mg protein vs (470.6 +/- 33.1) microg/mg protein, P < 0.05]. The expression of activin-A was negatively correlated with the ability of suppression on the hydroxy free radical and LDH separately.
Conclusion:
The result indicated that activin-A was involved in myocardial ischemia/reperfusion injury, and down-regulation of activin-A might be one of the cardioprotective mechanisms of postconditioning.