The hamster heart: a paradox in itself.

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.