Hammond G L, Nadal-Ginard B, Talner N S, Markert C L
Circulation. 1976 Apr;53(4):637-43. doi: 10.1161/01.cir.53.4.637.
Small myocardial specimens were obtained from 12 patients undergoing coronary reconstructive surgery and from 12 patients undergoing surgical correction for cyanotic congenital heart defects. The specimens were analyzed for LDH isozyme distribution. A control analysis was performed on myocardial specimens obtained at the time of surgical correction for acyanotic congenital heart defects in seven patients with normal coronary arteries. There was a 42% increase in the proportion of A subunits in the hearts of coronary patients as compared to controls. This represented a shift toward an anaerobic isozyme distribution. There was no change in the percentage of A units from the hearts of cyanotic patients as compared to acyanotic hearts of the same age. Cardiac muscle from patients with coronary vascular disease had an altered LDH subunit composition. Such an alteration was not present with chronic systemic hypoxia. These deficiencies may or may not be related to differing local metabolic responses to the two conditions. However, in the clinical situations, ischemic heart muscle may be oxygen deprived to the point of lactic acid production while hypoxic heart muscle usually is not. Consequently, these findings may represent a compensatory cellular mechanism which provides for continued energy production during chronic ischemia by enhancing glycolysis.
从12例接受冠状动脉重建手术的患者以及12例接受紫绀型先天性心脏缺陷手术矫正的患者身上获取了小块心肌标本。对这些标本进行了乳酸脱氢酶同工酶分布分析。对7例冠状动脉正常的非紫绀型先天性心脏缺陷患者在手术矫正时获取的心肌标本进行了对照分析。与对照组相比，冠状动脉疾病患者心脏中A亚基的比例增加了42%。这表明向无氧同工酶分布转变。与同龄非紫绀型心脏相比，紫绀型患者心脏中A亚基的百分比没有变化。患有冠状动脉疾病患者的心肌乳酸脱氢酶亚基组成发生了改变。慢性全身性缺氧时不存在这种改变。这些差异可能与也可能不与对这两种情况的不同局部代谢反应有关。然而，在临床情况下，缺血心肌可能会缺氧到产生乳酸的程度，而缺氧心肌通常不会。因此，这些发现可能代表了一种代偿性细胞机制，通过增强糖酵解在慢性缺血期间提供持续的能量产生。
