POSITRON-EMISSION-TOMOGRAPHY REVEALS CHANGES IN GLOBAL AND REGIONAL CEREBRAL BLOOD-FLOW DURING NOXIOUS-STIMULATION OF NORMAL AND INFLAMED ELBOW JOINTS IN ANESTHETIZED CATS

In cats the global (gCBF) as well as the regional cerebral blood flow (rCBF) and blood pressure were measured before, during, and after noxi ous inward and outward rotations of normal and inflamed elbow joints. The animals were anesthetized with halothane and immobilized by gallam ine triethiodide. The gCBF as well as the rCBF were measured using pos itron emission tomography (PET) with a camera specifically designed fo r use in small animals. Slow intravenous bolus injections of O-15-labe led water were followed by 3-min acquisition of regional radioactivity starting at the time of injection. In all experiments the gCBF as wel l as the blood pressure were increased by noxious inward-outward rotat ions of the normal and of the inflamed joint, whereas the blood pressu re and the rCBF remained unchanged during bolus injections under contr ol conditions (without any joint movement). Movements of the inflamed joint evoked significantly greater increases in blood pressure and gCB F than corresponding ones of the normal joint. These increases in gCBF were paralleled by increases in rCBF along the complete anterior to p osterior axis of the brain. Again, the increases in rCBF were larger, more extensive and more uniform following the stimulation of the infla med joint relative to the results obtained with stimulation of the nor mal joint. No significant laterality was seen, but when an atlas-based region of interest (ROI) analysis was carried out and when the indivi dual variations in rCBF were removed with two-way ANOVA, significant d ifferences were disclosed in rCBF between the stimulated condition and the resting condition in a large number of brain regions. In particul ar, noxious rotation of the normal (right) elbow joint induced a signi ficant increase in rCBF over the cerebral cortex and in the right thal amus and hippocampus. The same stimulation of the (left) inflamed join t induced a significant increase in rCBF throughout the brain; the big gest increase being over the right posterior cortex. It is concluded t hat under the conditions of the present experiments the generally acce pted autoregulation of the cerebral blood flow is not fully functionin g, and various factors that may be responsible for this failure (which obscures rCBF differences) are discussed. The more pronounced increas es in rCBF when moving inflamed joints instead of normal ones is thoug ht to be a direct consequence of the peripheral sensitization of the a rticular nociceptors and the consequent central hyperexcitability indu ced in the articular nociceptive pathways.