Preservation of amino acids during long term ischemia and subsequent reflow with supplementation of L-arginine, the nitric oxide precursor, in the rat heart.

We investigated whether L-arginine, used in heart preservation to limit endothelial damage, may influence the pool of amino acids during long term ischemia and reflow. Isolated isovolumic rat hearts (n = 23) were submitted to 8 h of hypothermic ischemia after cardioplegic arrest with the Centre de Résonance Magnétique Biologique et Médicale (CRMBM) solution with or without L-arginine (Arg and No Arg groups respectively). Hearts were freeze-clamped after ischemia (n = 11) or submitted to 60 min of reflow (n = 12) and freeze-clamped.

L-arginine during long-term ischemia: effects on cardiac function, energetic metabolism and endothelial damage.

Background: We have evaluated the addition of L-arginine, a precursor of nitric oxide, to a cardioplegic solution (named CRMBM) designed for long-term heart preservation.

Methods: Isolated isovolumic-perfused rat hearts (n = 22) were arrested with the CRMBM solution either with (Arg) or without L-arginine (2 mmol/L) (Arg group, n = 12, vs control group n = 10), submitted to 8 hours of cold storage (4 degrees C) in the solution, and then reperfused for 60 minutes at 37 degrees C. In 11 hearts, we evaluated the quality of cardiac preservation with P-31 magnetic resonance spectroscopy and the measure of function and cellular integrity.

Metabolic and functional effects of low-potassium cardioplegic solutions for long-term heart preservation.

Cardioplegic solutions used to arrest the heart during open heart surgery and cardiac transplantation are based on potassium as a cardioplegic agent in a concentration range of 15-35 mM. However, high to moderate K+ concentrations increase Ca2+ influx and impair endothelial function. We have therefore evaluated the possible advantage of a lower potassium concentration in a new cardioplegic solution (named CRMBM solution) designed for long-term heart preservation.