Ishikawa Y, Shimatsu A, Imura H, Tatsuoka Y, Fujitake J
Department of Internal Medicine, Kyoto University Faculty of Medicine.
Rinsho Shinkeigaku. 1992 Mar;32(3):281-6.
The effects of insulin-induced hypoglycemia on catecholamine secretion were investigated in patients with various neurological disorders affecting the autonomic nervous system. In control subjects, insulin-induced hypoglycemia resulted in marked increases in plasma epinephrine and norepinephrine levels. Heart rates were increased within 15 minutes after the insulin injection which were associated with slight elevation and depression of systolic and diastolic blood pressure, respectively. In patients with upper level spinal cord lesions (C1-T6) of various etiology, Shy-Drager syndrome and familial amyloidosis, insulin-induced hypoglycemia failed to increase plasma epinephrine and norepinephrine levels and resulted in falls in systolic and/or diastolic blood pressure 15 minutes after the injection. Heart rates were increased at 30-45 minutes after the injection. In patients with lower spinal cord lesions (T10-L1), neurosyphilis or brain stem tumor with orthostatic hypotension, the catecholamine responses were normal and blood pressure did not fall during insulin-induced hypoglycemia. In patients with Parkinson's disease and spinocerebellar degeneration with autonomic symptoms catecholamine responses were not impaired. These findings suggest that any lesion involving the sympathetic efferent systems of baroreflex such as the spinal descending pathway, sympathetic preganglionic neuron and peripheral nervous system causes both impairment of catecholamine secretion and a fall in blood pressure during hypoglycemia, and that lesions in sympatho-afferent system may not affect the secretion of catecholamine and neural control of blood pressure.
在患有各种影响自主神经系统的神经疾病的患者中,研究了胰岛素诱导的低血糖对儿茶酚胺分泌的影响。在对照受试者中,胰岛素诱导的低血糖导致血浆肾上腺素和去甲肾上腺素水平显著升高。胰岛素注射后15分钟内心率增加,分别与收缩压的轻微升高和舒张压的降低有关。在患有各种病因的上位脊髓损伤(C1-T6)、Shy-Drager综合征和家族性淀粉样变性的患者中,胰岛素诱导的低血糖未能增加血浆肾上腺素和去甲肾上腺素水平,并在注射后15分钟导致收缩压和/或舒张压下降。注射后30-45分钟心率增加。在患有下位脊髓损伤(T10-L1)、神经梅毒或伴有体位性低血压的脑干肿瘤的患者中,儿茶酚胺反应正常,胰岛素诱导的低血糖期间血压未下降。在患有帕金森病和伴有自主神经症状的脊髓小脑变性的患者中,儿茶酚胺反应未受损。这些发现表明,任何涉及压力反射交感传出系统的病变,如脊髓下行通路、交感神经节前神经元和周围神经系统,都会导致低血糖期间儿茶酚胺分泌受损和血压下降,而交感传入系统的病变可能不会影响儿茶酚胺的分泌和血压的神经控制。