Dionne Raymond A, Mueller Gregory P, Young Ronald F, Greenberg Richard P, Hargreaves Kenneth M, Gracely Richard, Dubner Ronald
Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20205 U.S.A.
Pain. 1984 Dec;20(4):313-321. doi: 10.1016/0304-3959(84)90109-X.
Levels of beta-endorphin immunoreactivity in cerebrospinal fluid were measured in 12 chronic pain patients undergoing the surgical implantation of an electrode into the periventricular gray matter. Cerebrospinal fluid fractions were collected following placement of a cannula into the third ventricle, following injection of metrizamide contrast medium into the ventricles, following implantation of the electrode, and following electrical stimulation. A second set of samples was collected on a non-surgical day before and after stimulation. Levels of beta-endorphin immunoreactivity increased significantly from baseline levels to post-electrode implantation in one group of patients, but no significant change was seen following the onset of stimulation. Immunoreactivity increased significantly following metrizamide injection in a second group and was still elevated, in comparison to baseline, following electrode placement, but no increase was seen following the onset of stimulation. Levels of immunoreactive beta-endorphin did not increase in either group after stimulation on a post-surgical day, despite consistent reports of pain relief. Addition of metrizamide or a related contrast medium, iothalamate meglumine (Conray) to the beta-endorphin radioimmunoassay revealed that both compounds interfered with antigen-antibody binding and also quenched the gamma radiation emitted by iodinated peptide ligands. Due to these combined effects, the contrast media alone produced results similar to those of the beta-endorphin standard. Moreover, similar observations were made when contrast media were incorporated into radioimmunoassays for met-enkephalin, dynorphin and cholecystokinin octapeptide. These findings indicate that increased levels of beta-endorphin in cerebrospinal fluid are not directly associated with patient report of pain relief following periventricular gray stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
对12名接受将电极手术植入脑室周围灰质的慢性疼痛患者，测量其脑脊液中β-内啡肽免疫反应性水平。在将套管置入第三脑室后、向脑室注射甲泛葡胺造影剂后、电极植入后以及电刺激后，收集脑脊液样本。在非手术日刺激前后收集第二组样本。一组患者中，β-内啡肽免疫反应性水平从基线水平到电极植入后显著升高，但刺激开始后未见显著变化。第二组中，甲泛葡胺注射后免疫反应性显著升高，与基线相比，电极置入后仍升高，但刺激开始后未见升高。术后日刺激后两组中免疫反应性β-内啡肽水平均未升高，尽管患者一致报告疼痛缓解。在β-内啡肽放射免疫测定中加入甲泛葡胺或相关造影剂碘他拉葡胺（康瑞）显示，这两种化合物均干扰抗原抗体结合，还淬灭碘化肽配体发出的γ射线。由于这些综合作用，仅造影剂产生的结果与β-内啡肽标准品相似。此外，将造影剂纳入甲硫氨酸脑啡肽、强啡肽和胆囊收缩素八肽的放射免疫测定时也有类似观察结果。这些发现表明，脑脊液中β-内啡肽水平升高与脑室周围灰质刺激后患者疼痛缓解的报告无直接关联。（摘要截短于250词）
