Quantitative assessment of prolonged metabolic abnormalities in reperfused canine myocardium.

Abstract

Background. Prolonged metabolic abnormalities have been demonstrated previously in postischemic myocardium, including relative increases in glucose uptake and abnormal fatty acid kinetics. However, quantitative metabolic information is limited, and the time course of changes in MVo2 in postischemic myocardium is unknown. To address these issues, chronically instrumented dogs were studied serially over 1 month after transient left anterior descending coronary artery (LAD) occlusion, using positron emission tomography.Methods and Results. Dynamic imaging protocols were used in conjunction with tracer kinetic models to quantify blood flow and metabolic rates. Myocardial sectors were defined as normal, predominantly reversibly injured, and infarct-containing, based on occlusion blood flow images and postmortem histochemistry. Myocardial blood flow and metabolism were homogeneous at baseline. During LAD occlusion for 3 hours, myocardial blood flow in reversibly injured and infarct-containing sectors (determined with 13NH3) was decreased to 46% and 23%, respectively, of blood flow in normal tissue.

Influence of .BETA.-Adrenoceptor Blockade on the Myocardial Accumulation of Fatty Acid Tracer and Its Intracellular Metabolism in the Heart After Ischemia-Reperfusion Injury

“…[2][3][4][5][6] Slow recovery of the tracer uptake after ischemic insult has been found in both clinical and experimental studies. [17][18][19] In the present study, the reduced tracer uptake by the IR seen in the early image after tracer injection was not present in the delayed image because of slow clearance of the tracer in the IR, a finding consistent with the previous study. 10 Beta-adrenoceptor blockers, including carvedilol, are frequently prescribed for patients with coronary heart disease and heart failure, so it is important to clarify their influence on the distribution and intracellular metabolism of FA tracers in the myocardium.…”

Time course of technetium-99m sestamibi myocardial distribution in dogs with a permanent or transient coronary occlusion

“…However, the relatively higher uptake of the tracer in the viable-ischaemic as compared to the necrotic zone following prolonged reperfusion can be attributed to a redistribution of 99mTc-sestamibi from extracardiac or normal myocardium concomitant with cell recovery as documented by fluorine-18 fluorodeoxyglucose SPET [37]. It is not due to a loss by the infarct to the benefit of the salvated myocardium, as suggested by the in vitro study of Crane et al [25] reporting a loss of 99mTc-sestamibi by myocardial mitochondrial suspensions, since the uptake by necrotic myocardium remains superior to blood flow.…”

125I-BMIPP and 18F-FDG uptake in a transgenic mouse model of stunned myocardium

“…In experimental models, myocardium subjected to repetitive stunning shows prolonged but reversible down-regulation of glucose uptake and oxidative metabolism despite restoration of the myocardial flow [12,13,14]. In contrast, however, regional glucose uptake in post-ischaemic myocardium has also been reported to be increased [6,7,8,9] or unchanged [10,11]. In the heart, glucose transport is mediated via insulin-sensitive glucose transporter proteins similar to those in skeletal muscle [53].…”

“…In post-ischaemic myocardial stunning, reported changes in glucose metabolism are not uniform and range from increased regional glucose uptake [6,7,8,9], through unaltered glucose uptake [10,11] to reduced glucose uptake [12,13,14]. Conflicting results have also been published on fatty acid metabolism in post-ischaemic myocardium [15,16,17,18].…”