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

Abstract

Background. Iodine 123-labeled 15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (BMIPP) is mainly trapped in the myocardium as triglyceride, depending on the adenosine triphosphate level. Ten percent to 20% of it is metabolized through α-oxidation after β-oxidation; however, the precise mechanism 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 computed tomography images of BMIPP and thallium 201 were obtained 3 days and 24 days after the operation. The activities of 3-hydroxyacyl-coenzyme A dehydrogenase (HAD), citrate synthase (CS), and α-glycerol-phosphate dehydrogenase (GPD) were then measured in both ischemic and nonischemic regions. BMIPP and Tl-201 chloride severity scores were also evaluated conventionally. CS and HAD levels were significantly lower in the ischemic region than in the nonischemic region in the chronic group (CS, 102.9 ± 28.1 vs 138.7 ± 33.7 μmol/g/min, respectively, P = .0051; HAD, 54.7 ± 20.1 vs 78.6 ± 18.7 μmol/g/min, respectively, P = .0031). There was no difference in GPD between the ischemic and nonischemic regions. The BMIPP severity score 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 Tl-201 chloride severity score. Conclusions. BMIPP imaging correlates well with the activities of HAD and CS, suggesting that a decrease in BMIPP uptake reflects deterioration of both fatty acid metabolism and citrate cycle and shows information other than regional myocardial perfusion. (J Nucl Cardiol 2001;8:472-81.)