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Objective: To investigate the effects of hyperglycemia on axonal excitability in human diabetics. Diabetic nerve dysfunction is partly associated with the alt ered polyol pathway and Na+ K+ATPase activity, probably resulting in a decrea se in the transaxonal Na+gradient and reduced nodal Na+currents. Methods:Thres hold tracking was used to measure the relative refractory periods (RPs) of media n motor axons in 58 diabetic patients, 45 normal subjects, and 12 patients with non diabetic axonal neuropathy. In diabetic patients, the relationship of RPs w ith hemoglobin A1c (HbA1c) levels was analyzed. Results: The mean RP was similar for diabetics and normal controls as a group, but was longer in patients with n on diabetic neuropathy than in normal controls (P=0.02). Diabetic patients with good glycemic control (HbA1c levels < 7%) had longer RPs than patients with po orer glycemic control and normal controls (P=0.01). RP was longest at the HbA1c level of 6%, gradually decreasing and reaching a plateau at the HbA1c level of 8 9%. Conclusions: Hyperglycemia shortens RPs, possibly because metabolic abno rmalities lead to reduced nodal Na+currents, and thereby to a lower inactivatio n of Na+channels when generating an action potential. Significance: RP measurem ents could provide new insights into the ionic pathophysiology of human diabetic neuropathy.
Objective: To investigate the effects of hyperglycemia on axonal excitability in human diabetics. Diabetic nerve dysfunction is partly associated with the alt ered polyol pathway and Na + K + ATPase activity, probably resulting in a decrea se in the transaxonal Na + gradient and reduced nodal Na + currents. Methods: Thres hold tracking was used to measure the relative refractory periods (RPs) of media n motor axons in 58 diabetic patients, 45 normal subjects, and 12 patients with non diabetic axonal neuropathy. In diabetic patients, the relationship of RPs Results: The mean RP was similar for diabetics and normal controls as a group, but was longer in patients with n on diabetic neuropathy than in normal controls (P = 0.02). Diabetic patients with had glycemic control (HbA1c levels <7%) had longer RPs than patients with po orer glycemic control and normal controls (P = 0.01). RP was longest at the HbA1c level of 6%, slowly decreasing and reach ing a plateau at the HbA1c level of 8 9%. Conclusions: Hyperglycemia shortens RPs, possibly because metabolic abnomalities lead to reduced nodal Na + currents, and thereby to a lower inactivatio n of Na + channels when generating an action potential. Significance: RP measurem ents could provide new insights into the ionic pathophysiology of human diabetic neuropathy.