MAINTENANCE OF DMX NMR SPECTROMETERS

脂肪酸代谢通过？-氧化是主要来源 心肌细胞的能量。 的产生效率 脂肪酸氧化产生的能量使心脏能够完成其主要功能， 收缩功能 相反，脂肪酸氧化迅速 在心肌缺血状态下受到抑制， 慢性心肌功能障碍 为了确定 在体内的β-氧化，研究人员已经研究了两种不同的 方法。 一种方法是使用放射性标记的脂肪 酸能经受什么？氧化 进行测量以评估 生产？氧化产物，通过测量静脉 血液样品中的反应产物活性 制剂或临床上通过测量 心肌的活动。 虽然血液的测量 样本已被证明是一个可靠的评估？氧化速率， 心脏活动下降体内成像较少 由于将完整示踪剂连接回循环， 以及示踪剂在中间池中的保留。 第二 一种方法是使用脂肪酸类似物， ?-氧化 这些示踪剂基本上被捕获，因为它们 无法在氧化途径中进一步进行。 虽然投诉率 被捕获的示踪剂的吸收被提出作为一个指标， ?-氧化速率，进一步的工作表明，吸收这些 示踪剂与氧化速率无关。 最近，一种新的硫磺 取代的脂肪酸类似物（FTHA）已经开发， 18F-氟标记，其将允许用正电子进行定量成像 发射断层扫描 本研究的具体目的是 确定提取、反向扩散程度和细胞 FTHA和另一种捕获的脂肪酸类似物的沉积以及第一种捕获的脂肪酸类似物的沉积 在控制灌注大型动物中FTHA的通过动力学 制备和利用断层成像来确定体内 FTHA摄取随底物改变，充血， 缺血和再灌注。 脂肪酸经典测定法 在方案中将使用酸β-氧化速率。 研究 将建立FTHA示踪动力学评估的适用性 脂肪酸代谢，一个适用于实验的领域 缺血性心脏病患者的研究和临床管理 疾病或心肌病。

Fatty acid metabolism via ?-oxidation represents the major source of energy of the cardiac myocyte. The efficiency of production of energy from fatty acid oxidation allows the heart to perform its major contractile functions. Conversely, fatty acid oxidation is rapidly inhibited in states of myocardial ischemia and is impaired in states of chronic myocardial dysfunction. To determine the rates of beta-oxidation in vivo, investigators have studied two different approaches. One approach has been the use of radiolabelled fatty acids which undergo ?-oxidation. Measurements are performed to assess the production of ?-oxidation products, either by measuring venous blood samples for reaction product activity in experimental preparations or clinically by measuring the rate of disappearance of activity from the myocardium. Although the measurement of blood samples has proved to be a reliable assessment of ?-oxidation rates, the in vivo imaging of decline in cardiac activity has been less reliable due to the linkage of intact tracer back into the circulation and the retention of the tracer in intermediary pools. A second approach has been the use of fatty acid analogs, which block ?-oxidation. These tracers are essentially trapped since they are unable to proceed further in the oxidative pathway. Although the rate of uptake of the trapped tracers was proposed as an index of ?-oxidation rate, further work has demonstrated that uptake of these tracers is independent of oxidation rates. Recently, a new sulphur substituted fatty acid analog (FTHA) has been developed with a 18F-fluorine label which will allow quantitative imaging with positron emission tomography. The specific aims of this research are to determine the extraction, degree of back-diffusion, and cellular deposition of FTHA and another trapped fatty acid analog and the first pass kinetics of FTHA in a controlled-perfusion large animal preparation and to utilize tomographic imaging to determine in vivo the changes in FTHA uptake with substrate alteration, hyperemia, ischemia and reperfusion. Classical method of determination of fatty acid beta-oxidation rates will be used in the protocols. The research will establish the applicability of FTHA tracer kinetics to assessment of fatty acid metabolism, an area of applicable to experimental studies and the clinical management of patients with ischemic heart disease or cardiomyopathy.