Postischemic recovery of heart metabolism and function: role of mitochondrial fatty acid transfer

Postischemic recovery of contractile function is better in hearts from fast ed rats than in hearts from fed rats. In this study, we examined whether fe eding-induced inhibition of palmitate oxidation at the level of carnitine p almitoyl transferase I is involved in the mechanism underlying impaired rec overy of contractile function. Hearts isolated from fasted or fed rats were submitted to no-flow ischemia followed by reperfusion with buffer containi ng 8 mM glucose and either 0.4 mM palmitate or 0.8 nM octanoate. During rep erfusion, oxidation of palmitate was higher after fasting than after feedin g, whereas oxidation of octanoate was not influenced by the nutritional sta te. In the presence of palmitate, recovery of left ventricular developed pr essure was better in hearts from fasted rats. Substitution of octanoate for palmitate during reperfusion enhanced recovery of left ventricular develop ed pressure in hearts from fed rats. However, the chain length of the fatty acid did not influence diastolic contracture. The results suggest that nut ritional variation of mitochondrial fatty acid transfer may influence posti schemic recovery of contractile function.