Albutaihi Ibrahim A M, DeJongste Mike J L, Ter Horst Gert J
Faculty of Medical Sciences, Thoraxcenter, University Hospital of Groningen, Groningen, The Netherlands.
Neurosignals. 2004 Sep-Oct;13(5):207-26. doi: 10.1159/000079336.
The awareness in specific brain centers of angina pectoris most often results from ischemic episodes in the heart. These ischemic episodes induce the release of a collage of chemicals that activate chemosensitive and mechanoreceptive receptors in the heart, which in turn excite receptors of the sympathetic afferent pathways. Ascending pain signals from these fibers result in the activation of the brain centers which are involved in the perception and integration of cardiac pain. Cytochemical studies of the nervous system provide the opportunity to identify these areas at the cellular level. In the present investigation, cardiac nociception was studied in the brains and the spinal cords of rats, using Fos protein as a marker of neuronal activation, following the application of pain-inducing chemicals to the heart. Induction of myocardial pain in conscious rats was achieved by infusion of bradykinin (0.5 microg) or capsaicin (5 microg) into the pericardial sac. During pain stimulation, the rats demonstrated pain behavior, in conjunction with alterations in heart rate and blood pressure. The cerebral Fos expression pattern was studied 2 h after pain stimulation. In contrast to the control group, increased Fos expression was found following the use of both capsaicin and bradykinin in a variety of areas of the brain. Bradykinin, but not capsaicin, induced Fos expression in the upper thoracic and upper cervical spinal cord; these segments are the sites where cardiac sympathetic fibers terminate. This finding suggests that these two chemicals use two different pathways, and provides extra evidence for the role of the vagus nerve in the transmission of cardiac nociception. Different cerebral areas showed an increase in the c-fos activity following pericardial application of pain-inducing chemicals. The role of these cerebral areas in the integration of cardiac pain is discussed in relation to the identified pathways which transmit cardiac pain.
心绞痛在特定脑中枢产生的意识，大多源于心脏的缺血发作。这些缺血发作会促使一系列化学物质释放，激活心脏中的化学敏感和机械感受受体，进而刺激交感传入通路的受体。来自这些纤维的上行疼痛信号会激活参与心脏疼痛感知和整合的脑中枢。神经系统的细胞化学研究为在细胞水平识别这些区域提供了契机。在本研究中，在向大鼠心脏施加致痛化学物质后，以Fos蛋白作为神经元激活的标志物，对大鼠的脑和脊髓中的心脏伤害感受进行了研究。通过向心包腔内注入缓激肽（0.5微克）或辣椒素（5微克），在清醒大鼠中诱发心肌疼痛。在疼痛刺激期间，大鼠表现出疼痛行为，并伴有心率和血压的改变。在疼痛刺激2小时后研究大脑Fos表达模式。与对照组相比，使用辣椒素和缓激肽后，在大脑的多个区域均发现Fos表达增加。缓激肽而非辣椒素，诱导上胸段和上颈段脊髓中的Fos表达；这些节段是心脏交感纤维终止的部位。这一发现表明这两种化学物质使用两条不同的途径，并为迷走神经在心脏伤害感受传递中的作用提供了额外证据。在心包应用致痛化学物质后，不同的脑区显示c-fos活性增加。结合已确定的传递心脏疼痛的途径，讨论了这些脑区在心脏疼痛整合中的作用。
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