Rabinov M, Chen X Z, Rosenfeldt F L
Baker Medical Research Institute, Melbourne, Australia.
J Thorac Cardiovasc Surg. 1989 Jan;97(1):43-9.
The aim of this study was to test for metabolic differences in the response of hypertrophic and normal hearts to hypothermic cardioplegia. Hypertrophic dog hearts and normal control hearts were subjected to 6 hours of hypothermic cardioplegia with the St. Thomas' Hospital solution. Levels before arrest of subepicardial and subendocardial adenosine triphosphate, creatine phosphate, and lactate in eight hypertrophic hearts were the same as those levels in 12 normal hearts. In hypertrophic hearts, but not in normal hearts, the induction of arrest was slow and was associated with an 11% increase in adenosine triphosphate levels, a 59% decrease in creatine phosphate levels, and a 12-fold increase in lactate levels. Seven hypertrophic hearts and eight normal hearts were studied during 6 hours of arrest and showed no further differences in metabolic response. Reducing the myocardial temperature from 20 degrees C to 12 degrees C slowed the rate of depletion of adenosine triphosphate and the rate of accumulation of lactate in both groups. We conclude that in the nonfailing, severely hypertrophic heart, levels before arrest of high-energy phosphates and lactate are normal, but that marked biochemical changes may occur if the induction of arrest is prolonged because of underdosing with cardioplegic solution. Cooling from 20 degrees C to 12 degrees C improves myocardial preservation in both hypertrophic and normal hearts.
本研究的目的是测试肥厚型心脏和正常心脏对低温心脏停搏反应的代谢差异。将肥厚型犬心脏和正常对照心脏用圣托马斯医院溶液进行6小时的低温心脏停搏处理。8个肥厚型心脏在停搏前的心外膜下和心内膜下三磷酸腺苷、磷酸肌酸和乳酸水平与12个正常心脏的这些水平相同。在肥厚型心脏中，而非正常心脏中，停搏的诱导缓慢，且与三磷酸腺苷水平增加11%、磷酸肌酸水平降低59%以及乳酸水平增加12倍有关。在6小时的停搏期间对7个肥厚型心脏和8个正常心脏进行了研究，结果显示代谢反应无进一步差异。将两组的心肌温度从20℃降至12℃减缓了三磷酸腺苷的消耗速率和乳酸的积累速率。我们得出结论，在无衰竭的严重肥厚型心脏中，停搏前高能磷酸盐和乳酸水平正常，但如果因心脏停搏液剂量不足导致停搏诱导时间延长，则可能会发生显著的生化变化。从20℃降至12℃可改善肥厚型心脏和正常心脏的心肌保存。
