fructose/infarction

OBJECTIVE Fructose-1,6-diphosphate (FDP) appears to improve early post-myocardial infarction hemodynamics and limit early myocardial infarct size in previous canine studies. However, these studies did not account for the effect of collateral blood flow on infarct size. Our objective was to determine

In the current study, effects of acute short term administration of fructose on cardiac arrhythmias and myocardial infarction size following ischemia/reperfusion were investigated in isolated rat heart. The hearts were subjected to 30 min zero flow global ischemia followed by 120 min reperfusion. In

Fructose 1,6-diphosphate has been reported to reduce ischemic damage following coronary artery occlusion. To further evaluate fructose 1,6-diphosphate, we studied its effect on myocardial infarct size in open-chest, anesthetized dogs. Twenty min following left anterior descending coronary artery

OBJECTIVE We tested the hypothesis that fructose-1,6-bisphosphate, when administered 10 minutes before the end of 2 hours of reversible middle cerebral artery occlusion, reduces ischemia-reperfusion injury and infarct volume measured after a 3-day survival period in rats. METHODS After 1 hour and 50

Purpose: In the present study, postconditioning effect of fructose against ischemia/reperfusion (I/R)-induced arrhythmias and infarct size were investigated in isolated rat heart. Methods: The isolated hearts were divided into 7 groups, mounted on a Langendorff apparatus at constant pressure then

Acute hemodynamic and electrocardiographic effects of fructose-1,6-diphosphate (FDP), an agent that is supposed to restore anaerobic glycolytic flux in the ischemic myocardium, were studied in 40 patients with acute myocardial infarction who were grouped into 4 subsets: subset 1, normal (15 mm Hg or

BACKGROUND Fructose intake has been increased steadily during the past two decades. Fructose, like other reducing sugars can react with proteins, which may account for aging and myocardial infarction. Fructose participates in glycation (fructation) and AGE formation some 10 times faster than

The experiments on rats indicated that fructose-1,6-diphosphate substantially decreased the sizes of a necrotic zone, elevated myocardial ATP levels, reduced the edematization of lung tissue, shortened the duration of early postocclusive arrhythmias, and increased the latent period for their

In vitro and in vivo studies suggest that fructose-1,6-diphosphate (FDP), an intermediary glycolytic pathway metabolite, ameliorates ischemic tissue injury through increased high-energy phosphate levels and may therefore have cardioprotective properties in patients undergoing coronary artery bypass

BACKGROUND Fructose-1,6-diphosphate (FDP) is a metabolite in the glycolytic pathway created from glucose. Exogenously administered FDP increases the yield of ATP from anaerobic glycolysis. FDP reduces ischaemic tissue area in experimentally-induced cerebral and myocardial infarction and improves

Infusion of fructose 1,6-diphosphate, (FDP), the rate-limiting substrate in anaerobic metabolism, decreases infarction in the ischemic heart. This study evaluates the effect of FDP (5% in H2O), glucose (D5W), or normal saline (N/S) infusions and species-specific blood (SSB) exchange transfusions on

OBJECTIVE To explore the protective mechanism of fructose-1, 6-diphosphate (FDP) on ischemic brain injury. METHODS A model of permanent focal cerebral ischemia was performed in rats by intraluminal filament occlusion of middle cerebral artery. TTC staining, immunohistochemistry, Western blotting,

Acute myocardial infarction can result from thrombosis of a coronary artery. The purpose of this study was to evaluate the ability of fructose-1,6-diphosphate (FDP; Esafosfina) to reduce myocardial necrosis during acute thrombosis of a coronary artery. A canine model of acute myocardial infarction