Biomedical subjects

S H Sindrup

Publications and source records attributed to S H Sindrup.

57 records · Page 4Linked to original sources

PubMed1989

Peripheral nerve function during hyperglycemic clamping in insulin-dependent diabetic patients.

The influence of hyperglycemia on peripheral nerve function was studied in 9 patients with long-term insulin-dependent diabetes. Blood glucose concentration was raised 13.5 +/- 0.5 mmol/l (mean +/- SEM) within 15 min and kept approximately 15 mmol/l over basal level for 120 min by intravenous glucose infusion. Hyperglycemia was accompanied by increased plasma osmolality. Sensory and motor nerve conduction and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min hyperglycemia. Distal (5th finger - wrist) and proximal (wrist - elbow) sensory nerve conduction showed an insignificant increase as hyperglycemia was induced. During hyperglycemia mean distal sensory conduction decreased from 53.1 m/s to 50.4 m/s (P less than 0.05) and mean proximal sensory conduction decreased from 56.0 m/s to 54.2 m/s (P less than 0.01). A mean of distal and proximal sensory conduction increased (53.5 m/s vs 54.6 m/s) (P less than 0.05) as hyperglycemia was induced and decreased (54.6 m/s vs 52.3 m/s) (P less than 0.01) during clamping. Motor nerve conduction decreased insignificantly throughout the study. Mean distal motor latency decreased from 3.1 ms to 2.8 ms (P less than 0.005) immediately after induction of hyperglycemia. During hyperglycemia it increased from 2.8 ms to 3.1 ms (P less than 0.001). We conclude that acute induction of hyperglycemia in long-term diabetics seems to increase sensory conduction and decrease distal motor latency, while 120 min hyperglycemia seems to decrease sensory conduction and increase distal motor latency.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

[Clinical chemical parameters for metabolic control of patients with diabetes mellitus].

Fructosamine and various measures of blood glucose were compared to glycosylated hemoglobin as indices of glycaemic control in 148 patients with insulin treated diabetes. Fructosamine correlated fairly well with glycosylated hemoglobin (r = 0.67), but around 40 per cent of the patients with glycosylated hemoglobin below upper reference limit had a fructosamine value over upper reference limit and vice versa. The possibility to predict the level of glycosylated hemoglobin from fasting blood glucose, postprandial blood glucose, and self-measured blood glucose was poor. The difference in self-measured blood glucose from patients with high versus low levels of glycosylated hemoglobin was very modest (0.5-2.0 mmol/l). It is concluded that it is reasonable to measure both glycosylated hemoglobin and fructosamine to evaluate glycaemic control in insulin treated diabetic patients. Fasting blood glucose, postprandial blood glucose, and self-measured blood glucose only seem to reflect glycaemic control to a minor degree.

Adult↗

PubMed1988

Peripheral nerve function during hyperglycemic clamping in healthy subjects.

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 less than 0.005) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia mean sensory nerve conduction velocity was 59.6 m/s (P less than 0.05). An insignificant increase was seen in motor nerve conduction velocity during hyperglycemia. Mean distal motor latency decreased from 3.1 ms to 3.0 ms (P less than 0.025) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia distal motor latency was 2.9 ms (P less than 0.05). We conclude that short term hyperglycemia with physiological hyperinsulinemia seems to increase sensory nerve conduction velocity and decrease motor latency.

Adult↗