Myocardial LDH isozyme distribution in the ischemic and hypoxic heart.
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.
D000293:Adolescent; D000328:Adult; D002648:Child; D003327:Coronary Disease / Q000201:enzymology* / Q000378:metabolism; D006019:Glycolysis; D006330:Heart Defects, Congenital / Q000201:enzymology* / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000201:enzymology; D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase / Q000378:metabolism*; D007773:Lactates / Q000378:metabolism; D008875:Middle Aged; D009206:Myocardium / Q000201:enzymology* / Q000378:metabolism
D007527:Isoenzymes; D007773:Lactates; D007770:L-Lactate Dehydrogenase