EVALUATION OF MYOCARDIAL-METABOLISM, WITH N-13-LABELED AND C-11-LABELED AMINO-ACIDS AND POSITRON COMPUTED-TOMOGRAPHY
- 1 January 1982
- journal article
- research article
- Vol. 23 (8) , 671-681
Abstract
To evaluate the utility of labeled L-amino acids (AA) for imaging regional myocardial AA metabolism [in dogs] by positron computed tomography (PCT), the myocardial uptake and clearance of alanine, glutamic acid, glutamin, asparagine, leucine tagged with 13N and of 11C tagged asparagine, and oxaloacetate (Oxal), were examined in 44 experiments at control during ischemia and after transaminase inhibition. The myocardial time activity curves recorded after intracoronary after intracoronary tracer injection had 2 clearance phases (an early and a late) for all 13N AA, and 3 (early, intermediate, late) for the 2 11C compounds, with significantly different clearance half-times (t1/2) of 18.7 .+-. 8.0 (SD) for the early phase, 141.7 .+-. 56.5 s for the intermediate, and 61.2 .+-. 43.5 min for the late phase. The residual fractions ranged from 0.07 to 0.23 in normal myocardium, and consistently increased with ischemia by 0.02-0.07 for 13N-labeled alanine, glutamic acid, asparagine and leucine but not for 13N glutamine and the 11C compounds. Transaminase inhibition shortened the t1/2 of the late phases of 13N-labeled alanine, glutamic acid, asparagine and leucine; had no effect on t1/2 of 13N glutamin and 11C Oxal; and resulted in a loss of C 13N CO2 production and of the intermediate phase for 11C asparagine. On the PCT images, 13N activity from labeled alanine and glutamic acid, was not decreased in an ischemic segment despite a significant flow reduction, as demonstrated by NH3 imaging and labeled microspheres. From the results, 3 compartment tracer kinetic model is proposed for the noninvasive quantifification of Krebs-cycle activity, protein synthesis and metabolic derangements related to ischemia.This publication has 2 references indexed in Scilit:
- ENERGY-METABOLISM DURING REPERFUSION FOLLOWING ISCHEMIA1980
- Alterations of myocardial amino acid metabolism in chronic ischemic heart disease.Journal of Clinical Investigation, 1976