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Alterations in sarcoplasmic reticulum function and gene expression in ischemic-reperfused rat heart
R M Temsah1, T Netticadan, D Chapman
1Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6.
The American Journal of Physiology
|August 13, 1999
Summary
Ischemia-reperfusion injury impairs heart function by damaging sarcoplasmic reticulum (SR) Ca(2+) handling and gene expression. Antioxidant treatment may preserve SR function and improve cardiac recovery.
Area of Science:
- Cardiovascular Physiology
- Cellular Biology
- Biochemistry
Background:
- Sarcoplasmic reticulum (SR) Ca(2+) release and pump activity are crucial for cardiac contraction and relaxation.
- Ischemia-reperfusion (I/R) injury significantly impacts myocardial function.
Purpose of the Study:
- To investigate the effects of I/R on SR function, protein content, and gene expression in isolated rat hearts.
- To determine the role of oxyradicals in I/R-induced alterations of SR Ca(2+) handling and gene expression.
Main Methods:
- Isolated rat hearts were subjected to 30 minutes of global ischemia followed by 60 minutes of reperfusion (I/R).
- SR Ca(2+) uptake, Ca(2+) release, ryanodine-binding activities, mRNA levels, and protein content were assessed.
- Hearts were perfused with oxyradical scavengers (superoxide dismutase plus catalase) or oxyradical-generating systems (xanthine/xanthine oxidase, H(2)O(2)).
Main Results:
- I/R hearts exhibited attenuated recovery of contractile function, reduced SR Ca(2+) uptake and release, and decreased ryanodine-binding activities.
- SR Ca(2+) pump ATPase and Ca(2+) release channel mRNA and protein levels were significantly depressed in I/R hearts.
- Antioxidant treatment partially prevented I/R-induced alterations in SR function and gene expression.
Conclusions:
- Oxyradicals contribute to the depression of SR Ca(2+) handling and gene expression in the I/R heart.
- Antioxidant therapy may improve cardiac function recovery by preserving SR function and gene expression following I/R injury.