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Na+/Ca++ exchanger and myocardial ischemia/reperfusion.
1Department of Medicine, Jikei University, School of Medicine, Tokyo, Japan.
Japanese Heart Journal
|March 25, 1999
Summary
Myocardial hypoxia and ischemia cause cellular injury by altering ion balance, particularly sodium and calcium. Inhibiting the sodium-calcium exchanger may offer new treatments for heart disease.
Area of Science:
- Cardiovascular Physiology
- Cellular Biology
- Biochemistry
Background:
- Myocardial hypoxia and ischemia disrupt cellular energy (ATP) and pH, leading to ionic imbalances.
- Elevated intracellular calcium (Ca++) during these events causes significant cellular injury and irreversible damage upon reperfusion.
- Increased intracellular sodium (Na+) correlates with Ca++ overload, implicating ion exchange mechanisms.
Purpose of the Study:
- To elucidate the role of the sodium-calcium exchanger in myocardial injury during hypoxia/ischemia and reoxygenation/reperfusion.
- To explore the therapeutic potential of targeting the sodium-calcium exchanger for ischemic heart disease.
Main Methods:
- Review of experimental evidence on ion transport during hypoxia/ischemia.
- Analysis of the role of Na+/H+ exchange in Na+ influx.
- Investigation of the Na+/Ca++ exchanger's function in Ca++ overload.
Main Results:
- Intracellular acidosis drives Na+ influx via Na+/H+ exchange during hypoxia/ischemia.
- Accumulated intracellular Na+ activates the Na+/Ca++ exchanger, leading to Ca++ overload.
- The Na+/Ca++ exchanger is critical for myocardial damage during ischemic events and reperfusion.
Conclusions:
- The Na+/Ca++ exchanger is a key mediator of cellular injury and death in the heart during ischemia and reperfusion.
- Recent cloning and functional studies of the Na+/Ca++ exchanger provide a foundation for therapeutic strategies.
- Inhibitors of the Na+/Ca++ exchanger hold promise for treating ischemic heart disease.