Ischemic heart arrest: nitrogenous metabolism in energy-depleted human myocardium.
Seventeen patients undergoing radical correction of Fallot's tetrad or defects of interventricular septum were investigated. Needle biopsies from the left ventricular apex region were obtained at the 1st min after cross-clamping of the aorta and at the end of cardiac arrest to determine adenosine triphosphate (ATP), glutamate, aspartate, alanine and ammonia. The losses of ATP during clamping period were related to decrease in glutamate. The fall in ATP by more than 20% of the initial level was accompanied by a significant decrease in aspartate, an accumulation of alanine and ammonia in cardiac tissue but did not affect glutamine content. The data obtained prove the participation of specific nitrogenous compounds of human heart, and especially glutamate, in response to energy depletion during ischemia.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000409:Alanine / Q000378:metabolism; D000641:Ammonia / Q000378:metabolism; D001224:Aspartic Acid / Q000378:metabolism; D004734:Energy Metabolism; D005971:Glutamates / Q000378:metabolism; D018698:Glutamic Acid; D006324:Heart Arrest, Induced; D006345:Heart Septal Defects, Ventricular / Q000601:surgery; D006801:Humans; D009206:Myocardium / Q000378:metabolism*; D009584:Nitrogen / Q000378:metabolism*; D013771:Tetralogy of Fallot / Q000601:surgery
D005971:Glutamates; D001224:Aspartic Acid; D018698:Glutamic Acid; D000641:Ammonia; D000255:Adenosine Triphosphate; D009584:Nitrogen; D000409:Alanine