INVOLVEMENT OF ENERGETIC METABOLISM IN THE EFFECTS OF ISCHEMIC POSTCONDITIONING ON THE ISCHEMIC-REPERFUSED HEART OF FED AND FASTED RAT

, M G MARINA PRENDES1, R HERMANN1, M E TORRESIN1, C SBARBATI1, P SOUTO2, S TALLIS2, E A SAVINO1 AND A VARELA1.; ENRIQUE A SAVINO

JOURNAL OF PHYSIOLOGICAL SCIENCES

SPRINGER TOKYO

Año: 2011 vol. 61 p. 303 - 312

1880-6546

The effects of fasting and ischemic postconditioning (IPOC) on functional recovery of Langendorff-perfused rat hearts exposed to ischemia-reperfusion were studied in relation to triacylglycerol and glycogen mobilization, ATP content, glucose-6-phosphate-dehydrogenase activity and reduced/oxidized glutathion (GSH/GSSG). Tissue damage was estimated by measuring creatine-kinase release and thiobarbituric-acid-reactive-substances (TBARS). Fasting improved contractile recovery, while IPOC improved recovery in the fed but attenuated it in the fasted hearts. In both groups ischemia lowered glycogen. IPOC further reduced it. Triacylglycerol remained unchanged during ischemia-reperfusion in both groups, but triacylglycerol mobilization was activated by IPOC in the fasted group. Fasting lowered creatine-kinase release, and IPOC caused the same effect in the fed but the opposite in the fasted. ATP content was increased by IPOC in the fed group, but lowered in the fasted, which appeared to be associated with the rates of ATP synthesis in isolated mitochondria from each group. Fasting and IPOC raised glucose-6-phosphate-dehydrogenase activity and GSH/GSSG, and lowered TBARS.