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Peripheral nerve function during hyperglycemic clamping in healthy subjects
Author(s) -
Sindrup S. H.,
Ejlertsen B.,
Gjessing H.,
Frøland A.,
Sindrup E. H.
Publication year - 1988
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1988.tb03635.x
Subject(s) - hyperinsulinemia , nerve conduction velocity , medicine , motor nerve , endocrinology , latency (audio) , sensory nerve , peripheral , ulnar nerve , sensory system , median nerve , anesthesia , postprandial , sural nerve , diabetes mellitus , anatomy , neuroscience , biology , insulin resistance , engineering , elbow , electrical engineering
‐ The influence of hyperglycemia with physiological hyperinsulinemia on peripheral nerve function was studied in 10 non‐diabetic subjects. Blood glucose concentration was raised from 3.8 ± 0.2 mmol/l (mean ± SEM) to 17.1 ± 1.4 mmol/l (mean ± SEM) within 15 min and kept at this level for 120 min by intravenous glucose infusion. Sensory and motor nerve conduction velocity, and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min of hyperglycemia. Mean sensory nerve conduction velocity increased from 57.7 m/s to 59.5 m/s ( P < 0.005) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia mean sensory nerve conduction velocity was 59.6 m/s ( P < 0.05). An insiginificant increase was seen in motor nerve conduction velocity during hyperglycemia. Mean distal motor latency decreased from 3.1 ms to 3.0 ms ( P < 0.025) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia distal motor latency was 2.9 ms ( P < 0.05). We conclude that short term hyperglycemia with physiological hyperinsulinemia seems to increase sensory nerve conduction velocity and decrease motor latency.

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