Calcium-free cardioplegia--pro.

Area of Science:

• Cardiology
• Biochemistry
• Cardiovascular Surgery

Background:

• Myocardial ischemia compromises heart energy supply via anaerobic glycolysis.
• Optimizing buffer capacity pre-ischemia can improve energy supply.
• Extracellular sodium (Na+) and calcium (Ca2+) reduction are key for improving ischemia tolerance.

Purpose of the Study:

• To evaluate the efficacy of the HTK cardioplegic solution for improving myocardial ischemia tolerance.
• To assess the impact of varying calcium and magnesium concentrations on myocardial recovery.
• To investigate the role of quinine in mitigating calcium paradox.

Main Methods:

• Comparison of myocardial ATP decay velocity in pure ischemia versus HTK solution.
• Assessment of metabolic, morphological, and functional recovery after prolonged ischemia (300 min) at controlled temperatures.
• Evaluation of HTK solution's protective efficacy with varying Ca2+ and Mg2+ concentrations.
• Investigation of calcium paradox induction and prevention under different infusion conditions.

Main Results:

• HTK solution delayed myocardial ATP decay by 7-8 times compared to pure ischemia.
• Good myocardial recovery was observed after 300 min of ischemia at 23°C, especially with quinine.
• Adding 50 µmol/L Ca2+ reduced HTK's protective efficacy but also mitigated calcium paradox risk.
• Calcium paradox was observed at 35°C but not at lower temperatures or with added Ca2+.
• Intermittent cardioplegic reperfusion delayed recovery, but adding Ca2+ or reducing Mg2+ improved outcomes.

Conclusions:

• HTK cardioplegia effectively improves myocardial ATP preservation and recovery during ischemia.
• Careful control of temperature, infusion duration, and ionic composition (Ca2+, Mg2+) is crucial for HTK efficacy and preventing adverse effects.
• Further research is needed to explore membrane stabilization mechanisms for enhanced cardioprotection.