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The hamster heart: a paradox in itself
1Division of Pharmacology, Central Drug Research Institute, Lucknow, 226001, India.
Insights
The hamster heart resists calcium paradox injury, unlike rat hearts, by maintaining high energy phosphates and preventing calcium overload. This highlights the hamster
Area of Science:
- Cardiovascular Physiology
- Myocardial Injury Mechanisms
- Comparative Cardiac Pathophysiology
Background:
- The calcium paradox describes irreversible myocardial damage upon reperfusion with calcium after calcium-free perfusion.
- Understanding the protective mechanisms in hearts resistant to this paradox is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the roles of creatine kinase (CK), high-energy phosphates, and calcium (Ca2+) influx in rat myocardial injury during the calcium paradox.
- To compare these mechanisms between rat and hamster hearts, identifying factors contributing to the hamster's resistance.
Main Methods:
- Isolated rat and hamster hearts were perfused using the Langendorff mode.
- Hearts underwent perfusion with Ca(2+)-free Tyrode solution followed by reperfusion with normal Tyrode solution.
- High-energy phosphate levels were monitored using 31P-NMR, CK release was measured in perfusate, and 45Ca influx was assessed in papillary muscles.
Main Results:
- Rat hearts showed significant decline in high-energy phosphates, massive CK release, and increased Ca2+ influx upon reperfusion.
- Hamster hearts maintained high-energy phosphates, prevented CK release, and exhibited no rise in Ca2+ influx.
- These findings indicate distinct responses to calcium reperfusion between rat and hamster myocardium.
Conclusions:
- The hamster heart possesses superior calcium homeostasis, protecting it from calcium overload and the calcium paradox.
- Creatine kinase, high-energy phosphates, and calcium influx are key determinants of myocardial injury susceptibility during the calcium paradox.
Abstract:
Perfusion of all mammalian heart muscle except hamster with Ca(2+)-free Tyrode and thereafter reperfusion with normal Tyrode causes irreversible damage, the calcium paradox. Our study aims at deciphering the role of creatine kinase, high energy phosphates and Ca(2+)influx in the genesis of myocardial injury in the rat and comparing it with the hamster. Isolated hearts from hamster and rats were perfused in the Langendorff mode at 37 degrees C for 30 min with normal Tyrode, for 15 min with Ca(2+)-free Tyrode and thereafter for 30 min of reperfusion with normal Tyrode. The 'high energy phosphate compound' levels were monitored by(31)P-NMR, creatine kinase (CK) release was measured in the perfusate.(45)Ca influx was estimated in the papillary muscle. We observed that in the rat heart: (a) high energy phosphate levels declined significantly within 1 min of Ca(2+)reperfusion; (b) a massive release of CK occurred upon Ca(2+)reperfusion; (c) there was a significant increase of Ca(2+)influx. In the hamster heart, there was preservation of high energy phosphates, CK release was prevented completely and no rise in(45)Ca influx was observed upon Ca(2+)reperfusion. These results suggest that the hamster heart has a remarkable capacity for Ca(2+)homeostasis which protects the heart from Ca(2+)overload.