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目的用18F-FDG PET/CT技术,研究帕金森病猫模型额、顶叶皮质内脑组织糖代谢变化规律,从而证实该区域的功能变化情况,为深入的机制研究提供可靠的实验依据。方法选用健康雄性家猫,腹腔注射MPTP(5 mg/kg,qd×5 d)制作PD模型。实验共分1个对照组和4个模型组,每组4只。经行为学观察和H E染色验证后,对照组与实验组动物经静脉注射18F-FDG,进行PET/CT脑断层显像,通过观察18F-FDG浓聚程度确定感兴趣区(ROI),并测定该区内标准吸收值(SUV)进行半定量分析。结果PD模型首次注药后第2天时,双侧额、顶叶皮质内脑组织18F-FDG浓聚程度及SUV值均保持正常(P>0.05);第5天时双侧额叶出现明显减低(P<0.05),双侧顶叶仍保持正常;第8天时双侧额叶进一步降低(P<0.01),双侧顶叶出现明显升高(P<0.05);第11天时双侧额叶维持在第8天时水平,双侧顶叶恢复到正常。对照组与实验组内额、顶叶皮质左、右侧相比18F-FDG浓聚程度及SUV值无明显差别(P>0.05)。结论帕金森病大脑额叶皮质脑组织葡萄糖代谢降低,提示该区存在功能障碍,并随时间逐步加重,达到一定程度后趋于稳定;而顶叶皮质脑组织葡萄糖代谢升高,提示该区存在功能亢进,这可能是对额叶皮质功能低下的一种代偿,但时间短暂,呈一过性。
OBJECTIVE: To study the changes of brain function and glucose metabolism in forehead cortex and parietal cortex of 18 cats with 18F-FDG PET / CT in order to confirm the functional changes in this region and provide a reliable experimental basis for the further study of the mechanism. Methods Healthy male domestic cats were selected and intraperitoneally injected with MPTP (5 mg / kg, qd × 5 d) to make PD model. The experiment is divided into 1 control group and 4 model groups, 4 in each group. After behavioral observation and HE staining, the animals in the control group and experimental group were subjected to PET / CT scintigraphy by intravenous injection of 18F-FDG, and the ROI was determined by observing the concentration of 18F-FDG. SUVs were semi-quantitatively analyzed. Results The concentration of 18F-FDG and the value of SUV in bilateral frontal and parietal cortex were all kept normal (P> 0.05) on the second day after the first injection of PD. On the fifth day, the bilateral frontal lobe was significantly reduced (P <0.05), bilateral parietal lobe remained normal; on the 8th day, bilateral frontal lobe was further decreased (P <0.01), bilateral parietal lobe was significantly increased (P <0.05); on the 11th day, bilateral frontal lobe was maintained On day 8, both parietal lobes returned to normal. There was no significant difference in the concentration of 18F-FDG and SUV in the left and right sides of the medial forehead and parietal cortex between the control group and the experimental group (P> 0.05). Conclusions Decreased glucose metabolism in the frontal cortex brain of Parkinson’s disease suggests that there is dysfunction in this area and gradually aggravates with time, reaching a certain level and then tends to be stable. Glucose metabolism in the parietal cortex brain tissue is elevated, suggesting that there exists Hyperthyroidism, which may be a compensatory function of the frontal cortex, but a short time, was transient.