Involvement of energetic metabolism in the effects of ischemic postconditioning on the ischemic-reperfused heart of fed and fasted rats

Abstract

The effects of ischemic-postconditioning (IPOC) on functional recovery and cell viability of ischemic-reperfused hearts from fed and fasted rats were studied in relation to triacylglycerol and glycogen mobilization, ATP content, glucose-6-phosphate dehydrogenase activity and reduced/oxidized glutathione (GSH/GSSG). Oxidative damage was estimated by measuring thiobarbituric acid reactive substances (TBARS). IPOC improved contractile recovery and cell viability in the fed but attenuated them 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. ATP was increased by IPOC in the fed hearts, but lowered in the fasted ones, which appeared to be associated with the rates of ATP synthesis in isolated mitochondria. In the fed hearts IPOC raised glucose-6-phosphate dehydrogenase activity and GSH/GSSG, and lowered TBARS. These results suggest that IPOC effects are associated with changes in the ATP supply, mobilization of energy sources and glutathione antioxidant ratio.

Impact of caloric restriction on myocardial ischaemia/reperfusion injury and new therapeutic options to mimic its effects

“…Ischaemic postconditioning improves contractile recovery and cell viability in fed, but attenuates them in fasted hearts. Furthermore, ATP content and ATP synthesis increases while oxidative stress decreases in hearts of fasted rats following ischaemic postconditioning (Marina Prendes et al ., ). The same group also reported improved functional recovery and increased resistance to MPTP opening after ischaemic postconditioning (Hermann et al ., ).…”

Metabolic Considerations in Direct Procurement and Perfusion Protocols with DCD Heart Transplantation

“…In several pre-clinical studies, differences in cardiac metabolism and recovery after ischemia have been investigated in hearts from fasted and fed rats. Fasting elevates serum fatty acids and myocardial fatty acid uptake, promoting a substrate shift towards greater fatty acid use [53]. This increase in fatty acid oxidation (FAO) elevates the glycogen content through the inhibition of the glycolytic pathway [31,[53][54][55].…”

“…Fasting elevates serum fatty acids and myocardial fatty acid uptake, promoting a substrate shift towards greater fatty acid use [53]. This increase in fatty acid oxidation (FAO) elevates the glycogen content through the inhibition of the glycolytic pathway [31,[53][54][55]. Fed rats, on the other hand, present higher glucose and insulin concentrations in the blood, and, therefore, shift cardiac metabolism towards greater glucose oxidation [56,57].…”

“…Fed rats, on the other hand, present higher glucose and insulin concentrations in the blood, and, therefore, shift cardiac metabolism towards greater glucose oxidation [56,57]. However, the findings are inconsistent; while some report an increased post-ischemic cardiac recovery in fasted compared to fed rats [31,[53][54][55][56], others claim the exact opposite [57,58]. In an isolated rat heart model of DCD, a brief pre-ischemic exposure to high levels of free fatty acids (1.2 mM palmitate) lowered post-ischemic functional recovery by 50% compared to glucose as the sole pre-ischemic energy substrate [39].…”