Hampton K K, Alani S M, Wilson J I, Price D E
Department of Medicine, General Infirmary, Leeds.
J Neurol Neurosurg Psychiatry. 1989 Nov;52(11):1303-5. doi: 10.1136/jnnp.52.11.1303.
Median nerve function was studied in twelve diabetic subjects, six subjects with chronic hypoxaemia and ten control subjects. Resistance to ischaemic conduction failure (RICF), a characteristic electrophysiological feature of diabetic neuropathy, was assessed by measuring the decline in median nerve action potential amplitude at minute intervals for up to 20 minutes while the arm was rendered ischaemic. Initial nerve conduction velocity and action potential amplitude was similar in all three groups. Following the onset of ischaemia the time to a 50% reduction in action potential amplitude was prolonged in both diabetic subjects and hypoxaemic subjects compared with controls. After 20 minutes of ischaemia no control subject had persisting nerve function, while function remained in 5 (80%) of hypoxaemic subjects and 10 (83%) of diabetic subjects. The time to a 50% reduction in action potential amplitude during ischaemia correlated with the blood oxygen saturation among the hypoxic subjects and haemoglobin Alc among diabetic subjects. These results are consistent with the hypothesis that hypoxia has a role in the pathogenesis of resistance to ischaemic conduction failure in diabetes.
对12名糖尿病患者、6名慢性低氧血症患者和10名对照受试者的正中神经功能进行了研究。通过在手臂缺血长达20分钟的时间内,每隔一分钟测量正中神经动作电位幅度的下降情况,来评估缺血性传导衰竭抵抗(RICF),这是糖尿病性神经病变的一种特征性电生理特征。三组受试者的初始神经传导速度和动作电位幅度相似。缺血开始后,与对照组相比,糖尿病患者和低氧血症患者动作电位幅度降低50%的时间延长。缺血20分钟后,没有对照受试者仍有持续的神经功能,而低氧血症患者中有5名(80%)和糖尿病患者中有10名(83%)仍有功能。缺血期间动作电位幅度降低50%的时间与低氧受试者的血氧饱和度以及糖尿病患者的糖化血红蛋白A1c相关。这些结果与以下假设一致,即缺氧在糖尿病缺血性传导衰竭抵抗的发病机制中起作用。