title: Feeding and fasting determine postischemic glucose utilization in isolated working rat hearts.
abstract: To assess the effects of endogenous substrate on glucose utilization after 15 min of ischemia, we perfused isolated working rat hearts from fed and fasted (16 h) animals with glucose and the positron-emitting glucose analogue 2-[18F]fluoro-2-deoxy-D-glucose (2-FDG). Hearts were perfused in a recirculating system with bicarbonate buffer containing glucose (10 mM) and 2-FDG (0.5 microCi/ml). Mechanical performance and 2-FDG uptake were measured on-line, and glucose and lactate metabolic rates were calculated. Fasting raised the glycogen content by 25% and the triglyceride content by 38%. Hearts in both groups recovered preischemic function. Rates of 2-FDG uptake during the preischemic period were the same in both groups. In contrast, during the postischemic period rates of 2-FDG uptake were significantly depressed in hearts of fed animals but were unchanged in hearts of fasted animals. Thus hearts of fasted animals took up more 2-FDG during the postischemic period than hearts of fed animals (P less than 0.005). The lumped constant (range, 0.38-0.40) was the same in both groups before and after ischemia. Glucose utilization was suppressed during the postischemic period in hearts of fed animals, whereas at the same time lactate utilization was significantly increased. We conclude that 1) 2-FDG accurately traces glucose utilization independent of the nutritional state or ischemic insult; 2) reversibly ischemic, viable myocardium exhibits vastly different rates of glucose utilization depending on the nutritional state of the animal before ischemia; 3) lactate derived from glycolysis suppresses utilization of exogenously supplied glucose in the early reperfusion period without affecting postischemic performance.
authors.affiliation: Department of Medicine, University of Texas Medical School, Houston 77030.
authors.forename: C A
authors.initials: CA
authors.lastname: Schneider
authors.forename: V T
authors.initials: VT
authors.lastname: Nguyêñ
authors.forename: H
authors.initials: H
authors.lastname: Taegtmeyer
mesh_terms: D000818:Animals; D003327:Coronary Disease / Q000378:metabolism* / Q000503:physiopathology; D003847:Deoxyglucose / Q000031:analogs & derivatives / Q000378:metabolism; D004435:Eating; D005215:Fasting; D019788:Fluorodeoxyglucose F18; D005947:Glucose / Q000378:metabolism*; D006321:Heart / Q000503:physiopathology; D066298:In Vitro Techniques; D007773:Lactates / Q000378:metabolism / Q000494:pharmacology; D019344:Lactic Acid; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D015424:Reperfusion; D014280:Triglycerides / Q000378:metabolism
chemical_list: D007773:Lactates; D014280:Triglycerides; D019788:Fluorodeoxyglucose F18; D019344:Lactic Acid; D003847:Deoxyglucose; D005947:Glucose