Sakiyama Y, Sato A, Senda M, Ishiwata K, Toyama H, Schmidt R F
Department of the Autonomic Nervous System, Tokyo Metropolitan Institute of Gerontology, Japan.
Exp Brain Res. 1998 Feb;118(4):439-46. doi: 10.1007/s002210050300.
In cats the global (gCBF) as well as the regional cerebral blood flow (rCBF) and blood pressure were measured before, during, and after noxious inward and outward rotations of normal and inflamed elbow joints. The animals were anesthetized with halothane and immobilized by gallamine triethiodide. The gCBF as well as the rCBF were measured using positron emission tomography (PET) with a camera specifically designed for use in small animals. Slow intravenous bolus injections of 15O-labeled water were followed by 3-min acquisition of regional radioactivity starting at the time of injection. In all experiments the gCBF as well as the blood pressure were increased by noxious inward-outward rotations of the normal and of the inflamed joint, whereas the blood pressure and the rCBF remained unchanged during bolus injections under control conditions (without any joint movement). Movements of the inflamed joint evoked significantly greater increases in blood pressure and gCBF than corresponding ones of the normal joint. These increases in gCBF were paralleled by increases in rCBF along the complete anterior to posterior axis of the brain. Again, the increases in rCBF were larger, more extensive and more uniform following the stimulation of the inflamed joint relative to the results obtained with stimulation of the normal joint. No significant laterality was seen, but when an atlas-based region of interest (ROI) analysis was carried out and when the individual variations in rCBF were removed with two-way ANOVA, significant differences were disclosed in rCBF between the stimulated condition and the resting condition in a large number of brain regions. In particular, noxious rotation of the normal (right) elbow joint induced a significant increase in rCBF over the cerebral cortex and in the right thalamus and hippocampus. The same stimulation of the (left) inflamed joint induced a significant increase in rCBF throughout the brain; the biggest increase being over the right posterior cortex. It is concluded that under the conditions of the present experiments the generally accepted autoregulation of the cerebral blood flow is not fully functioning, and various factors that may be responsible for this failure (which obscures rCBF differences) are discussed. The more pronounced increases in rCBF when moving inflamed joints instead of normal ones is thought to be a direct consequence of the peripheral sensitization of the articular nociceptors and the consequent central hyperexcitability induced in the articular nociceptive pathways.
在猫身上，测量了正常和发炎肘关节进行有害的内旋和外旋之前、期间及之后的全脑脑血流量（gCBF）、局部脑血流量（rCBF）以及血压。动物用氟烷麻醉，并用三碘季铵酚使其固定。使用专门为小动物设计的相机，通过正电子发射断层扫描（PET）测量gCBF和rCBF。缓慢静脉推注15O标记的水，然后从注射时开始采集3分钟的局部放射性。在所有实验中，正常和发炎关节的有害内旋和外旋均会使gCBF以及血压升高，而在对照条件下（无任何关节运动）推注期间，血压和rCBF保持不变。发炎关节的运动引起的血压和gCBF升高明显大于正常关节相应运动引起的升高。这些gCBF的升高与沿脑的整个前后轴的rCBF升高平行。同样，相对于正常关节刺激所获得的结果，发炎关节刺激后rCBF的升高更大、更广泛且更均匀。未观察到明显的侧别差异，但当进行基于图谱的感兴趣区域（ROI）分析并使用双向方差分析消除rCBF的个体差异时，在大量脑区的刺激状态和静息状态之间的rCBF中发现了显著差异。特别是，正常（右侧）肘关节的有害旋转导致大脑皮层、右侧丘脑和海马体的rCBF显著增加。对（左侧）发炎关节进行相同刺激会导致整个大脑的rCBF显著增加；最大的增加发生在右侧后皮层。得出的结论是，在本实验条件下，普遍接受的脑血流自动调节功能未完全发挥作用，并讨论了可能导致这种功能障碍（掩盖rCBF差异）的各种因素。与正常关节相比，发炎关节运动时rCBF更明显的增加被认为是关节伤害感受器外周敏化以及关节伤害感受通路中随之而来的中枢性过度兴奋的直接结果。
