Release of fatty acid-binding protein from ischemic-reperfused rat heart and its prevention by mepacrine

In an attempt to resolve the issue of whether there is a loss of fatty acid binding protein (H-FABP) from heart during ischemia and reperfusion, and to further examine the role of this protein in ischemic-reperfusion injury, the amount of H-FABP of heart was monitored during ischemia and reperfusion. Excellent correlation was obtained between the loss of H-FABP from heart and its appearance in the perfusate buffer when examined by Western blot using the specific antibody to H-FABP. Further quantitation was achieved by densitometric scanning of the Western blot and rocket electrophoresis. Maximum release of H-FABP was observed within 20 min of reperfusion, the total release being 10% of the H-FABP content of the heart. Mepacrine, a membrane stabilizer and a phospholipase inhibitor, reduced the release of H-FABP from the heart and prevented the accumulation of nonesterified fatty acids in the tissue during ischemia and reperfusion. In view of the established role of H-FABP in the preservation of membrane phospholipids by either scavenging free radicals during ischemia and reperfusion or by modulating the enzymes of phospholipid synthesis, it seems likely that the loss of H-FABP may have some contribution towards the ischemic-reperfusion injury.