Right ventricular sensitivity to metabolic injury during cardiopulmonary bypass.
To determine intrinsic right ventricular susceptibility to metabolic injury, we examined the effect of ischemia and reperfusion during cardiopulmonary bypass on right and left ventricular myocardial adenine nucleotide metabolism in the absence of ventricular work load as a determinant of energy production and utilization. Dogs were subjected either to 30 minutes of normothermic or hypothermic myocardial ischemia and reperfusion or to 60 minutes of potassium-arrested normothermic ischemia; serial ventricular biopsy specimens were assayed for adenosine triphosphate, adenosine diphosphate, adenosine monophosphate, nucleoside, and base content. In each group the depletion rates of right and left ventricular nucleotides with ischemia did not differ. Mitochondrial ability to rephosphorylate the nucleotide pool during and after ischemia also did not differ in the two ventricles, and there were no detectable differences in the catabolism of nucleotide precursors and loss of total purine content with reperfusion. These observations indicate that right ventricular myocardium is as equally sensitive to ischemic and reperfusion injury as left ventricular myocardium, and metabolic recovery from injury is equally prolonged.
D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D003326:Coronary Circulation; D004285:Dogs; D004734:Energy Metabolism; D006324:Heart Arrest, Induced; D007036:Hypothermia, Induced; D008929:Mitochondria, Heart / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D010766:Phosphorylation; D011687:Purines / Q000378:metabolism; D013997:Time Factors
D000227:Adenine Nucleotides; D011687:Purines; C030985:purine