Serial evaluation of fatty acid metabolism in rats with myocardial infarction by pinhole SPECT

Background. Iodine 123-labeled 15-(p-iodophenyl)-3-(R,S)-methylpentadecanoi c acid (BMIPP) is mainly trapped in the myocardium as triglyceride, dependi ng on the adenosine triphosphate level. Ten percent to 20% of it is metabol ized through alpha -oxidation after beta -oxidation; however, the precise m echanism of the regulatory pathways of BMIPP is yet to be clarified. Methods and Results. A brief left coronary artery occlusion (10-30 minutes) was performed in 28 male Wistar-Kyoto rats. Dual single photon emission co mputed tomography images of BMIPP and thallium 201 were obtained 3 days and 24 days after the operation. The activities of 3-hydroxyacyl-coenzyme A de hydrogenase (HAD), citrate synthase (CS), and alpha -glycerol-phosphate deh ydrogenase (GPD) were then measured in both ischemic and nonischemic region s. BMIPP and TI-201 chloride severity scores were also evaluated convention ally. CS and HAD levels were significantly lower in the ischemic region tha n in the nonischemic region in the chronic group (CS, 102.9 +/- 28.1 vs 138 .7 +/- 33.7 mu mol/g/min, respectively, P = .0051; HAD, 54.7 +/- 20.1 vs 78 .6 +/- 18.7 mu mol/g/min, respectively, P = .0031). There was no difference in GPD between the ischemic and nonischemic regions. The BMIPP severity sc ore had closer inverse relations with HAD (acute, r = -0.82; chronic, r = - 0.80) and CS (acute, r = -0.87; chronic, r = -0.81), but not with GPD, than did TI-201 chloride severity score. Conclusions. BMIPP imaging correlates well with the activities of HAD and C S, suggesting that a decrease in BMIPP uptake reflects deterioration of bot h fatty acid metabolism and citrate cycle and shows information other than regional myocardial perfusion.