Metabolic Factors Influencing Myocardial Recovery from Acidosis (CiC3)

摘要

The mechanisms involved in cardiac dysfunction during acidosis were explored inan isolated heart model. Metabolic acidosis was observed to cause marked functional and energy metabolic derangement consistent with a primary impairment of energy production. Synergism with hypoxia was also demonstrated in this model. The site of metabolic blockage during acidosis was observed to be at the level of oxidative metabolism and not glycolysis. Isolated cardiac mitochondrial studies, however, did not demonstrate any direct effect of acidosis on mitochondrial respiration or coupling. Studies with respiratory acidosis were complicated by the coexistence of relative hypoxia which affected the model deleteriously. Treatment of acidotic isolated hearts with the experimental buffer, Carbicarb, caused marked increases in intracellular pH as well as functional and metabolic improvements. Isotonic rather than hypertonic Carbicarb was found to be substantially more effective in this model. The superiority of isotonic to hypertonic Carbicarb may be related to the tendency of hypertonic but not isotonic Carbicarb to significantly increase RA 2.