Heat-shock response is associated with enhanced postischemic ventricular recovery

Area of Science:

• Cardiovascular Physiology
• Cellular Stress Response
• Biochemistry

Background:

• Hyperthermia induces heat-shock proteins and thermotolerance in cells.
• Thermotolerant cells exhibit resistance to oxidative stress.
• The protective effects of hyperthermia on the heart during ischemia-reperfusion are not fully understood.

Purpose of the Study:

• To investigate the protective effects of hyperthermia on rat hearts subjected to ischemia and reperfusion.
• To determine if heat-shock preconditioning enhances myocardial recovery and reduces injury.

Main Methods:

• Rats were exposed to mild hyperthermia (42°C for 15 minutes).
• Hearts were isolated 24 hours later and subjected to perfusion, ischemia, and reperfusion.
• Contractility, creatine kinase release, and ultrastructural damage were assessed.
• Myocardial catalase activity was measured biochemically.

Main Results:

• Heat-shocked hearts showed significantly improved recovery of contractility within 5 minutes of reperfusion compared to controls.
• Creatine kinase release, an indicator of reperfusion injury, was significantly reduced in heat-shocked hearts.
• Ultrastructural analysis revealed less mitochondrial membrane damage in heat-shocked hearts.
• Catalase activity was significantly increased in heat-shocked hearts (137 U/mg protein) versus controls (64.8 U/mg protein).

Conclusions:

• Hyperthermic preconditioning confers significant protection to the myocardium during the reperfusion phase following ischemia.
• This protection is associated with reduced cellular damage and improved functional recovery.
• Increased myocardial catalase activity is a key mechanism mediating the protective effects of hyperthermia during ischemia-reperfusion.