Mass spectrometry and phosphorus-31 nuclear magnetic resonance demonstrate additive myocardial protection by potassium cardioplegia and hypothermia during global ischemia.
Previous studies from this laboratory utilized mass spectrometry to measure myocardial oxygen (PO2) and carbon dioxide (PCO2) tensions in isolated feline hearts subjected to periods of global ischemia and reperfusion. Myocardial carbon dioxide tension was found to increase during ischemia, and its rate of increase was found to correlate inversely with subsequent recovery of myocardial function following reflow. The present study utilized phosphorus-31 nuclear magnetic resonance (NMR) to assess whether the severity of intracellular acidosis or the depletion of high energy phosphate stores would show a similar correlation with recovery of function. Hyperkalemic cardioplegia employed as a myocardial preservation technqiue in combination with hypothermia was compared with hypothermia alone as the control intervention. The experimental results demonstrated that intracellular pH fell to 6.09 +/- 0.13 with hypothermia alone and to 6.31 +/- 0.09 with cardioplegia plus hypothermia. Furthermore, myocardial ATP content fell to 22% +/- 2% of control with hypothermia alone, while falling to 36% +/- 4% of control with the combined therapy. Recovery of myocardial performance was found to correlate inversely with the severity of intracellular acidosis and depletion of ATP during ischemia. In contrast, no relationship was observed between preservation of phosphoryl-creatinine levels either during ischemia or after reflow and recovery of ventricular function. These results suggest that, similar to mass spectrometry, which allows monitoring of myocardial PCO2, 31P NMR permits the on-line monitoring of intracellular pH as well as high energy phosphate compounds, and thereby provides useful metabolic indices of the severity of ischemia. Since tight coupling was found between changes in these parameters and subsequent recovery of contractile performance, further development of 31P NMR for evaluation of techniques designed to minimize the severity of ischemic damage would seem indicated.
D000138:Acidosis / Q000378:metabolism; D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D003327:Coronary Disease / Q000378:metabolism*; D006324:Heart Arrest, Induced; D007036:Hypothermia, Induced; D009682:Magnetic Resonance Spectroscopy; D013058:Mass Spectrometry; D009206:Myocardium / Q000378:metabolism*; D009943:Organophosphorus Compounds / Q000378:metabolism; D010761:Phosphorus Radioisotopes; D011817:Rabbits
D009943:Organophosphorus Compounds; D010761:Phosphorus Radioisotopes; D002245:Carbon Dioxide