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18F-fluorodeoxyglucose accumulation in the heart, brain and skeletal muscle of rats; the influence of time after injection, depressed lipid metabolism and glucose-insulin

机译:18 F-氟脱氧葡萄糖在大鼠心脏,大脑和骨骼肌中的蓄积;注射时间,脂质代谢下降和葡萄糖-胰岛素的影响

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BACKGROUND: to study the effect of lipid depressing drugs on 18 FDG myocardial concentration. The changes of 18 FDG uptake in myocardium, brain and skeletal muscle of rats were compared as influenced by acipimox, tyloxapol and glucose with insulin. MATERIAL AND METHODS: 5.55 MBq of 18 FDG were administered to Wistar rats. Control rats were killed 15, 30, 45 and 60 minutes following intravenous injection and the radioactivity concentration (cpm/g of tissue) in relation to injected cpm was determined in a well crystal adjusted to 511 KeV in order to check the time of maximal 18 FDG tissue uptake. The radioactivity in myocardium, skeletal muscle and brain in intact animals was compared with that of rats treated with tyloxapol (tritton WR 1339, 125 mg intravenously immediately before 18 FDG injection), acipimox (nicotinic acid derivative, 25 mg by stomach cannula 15 minutes before 18 FDG), or glucose with insulin (intravenous injection of 0.04 g and 0.04 UI immediately before 18 FDG). The animals were killed 45 minutes following 18 FDG injection. RESULTS: Tyloxapol and acipimox significantly elevated myocardial 18 FDG concentration (tyloxapol +37% and acipimox +48%), but the increase in 18 FDG concentration after glucose and insulin was slight and insignificant. The changes in skeletal muscle after lipid depressing agents were quite contrasting; the decrease in 18 FDG concentration was -74% after tyloxapol and -44% following acipimox administration. The accumulation of 18 FDG in brain was not influenced markedly by the drugs used or by glucose with insulin. CONCLUSION: The highest 18 FDG uptake in myocardium could be achieved by depressing the lipid metabolism and not by administration of glucose with insulin only. A marked increase in glucose accumulation in myocardium is not possible without previous shift from the utilisation of fatty acids. This finding is fully in agreement with present knowledge about energetic metabolism of myocardium.
机译:背景:研究降脂药物对18 FDG心肌浓度的影响。比较了阿西莫克斯,泰洛沙泊和葡萄糖与胰岛素对大鼠心肌,脑和骨骼肌中18 FDG摄取的变化。材料与方法:对Wistar大鼠给予5.55 MBq的18 FDG。在静脉内注射后15、30、45和60分钟处死对照大鼠,并在调节至511KeV的孔晶体中测定相对于注射cpm的放射性浓度(cpm / g组织),以检查最大18小时的时间。 FDG组织摄取。比较了完整动物的心肌,骨骼肌和脑的放射性,与用替洛沙泊(tritton WR 1339,在注射18 FDG之前即刻静脉注射125 mg),acipimox(烟酸衍生物,在15分钟前通过胃套管注射25 mg)治疗的大鼠的放射性进行了比较。 18 FDG)或葡萄糖加胰岛素(在18 FDG之前静脉注射0.04 g和0.04 UI)。在注射18剂FDG后45分钟处死动物。结果:泰洛沙泊和阿昔莫司显着提高了心肌的18 FDG浓度(泰洛沙泊+ 37%和阿昔莫司+ 48%),但是葡萄糖和胰岛素作用后18 FDG浓度的增加微乎其微。降脂药后骨骼肌的变化是相当相反的。替洛沙泊后18 FDG浓度下降为-74%,阿西莫司给药后下降-44%。所用药物或葡萄糖加胰岛素对大脑中18 FDG的积累没有显着影响。结论:心肌中FDG的最高摄取18可以通过抑制脂质代谢而不是仅通过胰岛素给予葡萄糖来实现。如果不先改变脂肪酸的利用,心肌中葡萄糖积累的显着增加是不可能的。该发现与关于心肌的能量代谢的当前知识完全一致。

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