TRANSMURAL DISTRIBUTION OF 2-DEOXYGLUCOSE UPTAKE IN NORMAL AND POSTISCHEMIC CANINE MYOCARDIUM

This investigation was performed to determine (i) whether P-31 spatial ly localized P-31 NMR spectroscopy could be utilized to determine the transmural distribution of 2-deoxyglucose (2DG) uptake in the in vivo canine heart and (ii) whether transmural 2DG uptake would be affected by a preceding ischemic insult, 2DG was infused and the accumulation o f 2-deoxyglucose-6-phosphate (2DGP) was monitored (by means of spatial ly localized P-31 NMR) in control hearts, in pharmacologically hyperpe rfused hearts, and in hearts subjected to four (5 min) occlusions of t he left anterior descending coronary artery, Myocardial blood Bow was measured with radioactive microspheres, In control hearts, subendocard ial (ENDO) 2DGP contents were significantly higher than those in the s ubepicardium (EPI) being 3.8+/-0.3 and 2.2+/-0.2 mu mol/g, respectivel y; the ENDO/EPI ratio of 2DGP was 1.70+/-0.21. During hyperperfusion b lood flow increased approximately four-fold but 2DGP accumulation was not altered, ATP levels in post-ischemic myocardium were significantly decreased (ENDO more than EPI) and 2DGP accumulation in each layer wa s increased (p<0.01 vs control); however, the ENDO/EPI ratio of 2DGP w as not altered, 2DG infusion induced a marked elevation of blood insul in and norepinephrine levels, These data demonstrate that in the prese nce of high blood levels of 2DG and insulin: (i) 2DGP accumulation can be measured in the in vivo canine heart; (ii) in normal hearts 2DG up take is more pronounced in the inner layers of the left ventricular wa ll (this transmural 2DG uptake gradient is not due to subendocardial h ypoperfusion); and (iii) 2DG uptake is greater in the post-ischemic he art but the ENDO/EPI gradient of 2DG uptake is not altered indicating that the more severe ischemic insult in the subendocardium does not re sult in a disproportionate increase in 2DG uptake in that region of th e myocardium. Although 2DG uptake patterns in this model most probably reflect those of glucose (at comparable glucose and insulin levels), quantitative extrapolations with regard to the rate of glucose uptake are not possible from the present data.