Insulin receptors have been identified in limbic brain structures, but their functional relevance is still unclear. In order to characterize some of their effects, we evaluated auditory evoked brain potentials (AEP) in a vigilance task, behavioral measures of memory (recall of words) and selective attention (Stroop test) during infusion of insulin. The hormone was infused at two different rates (1.5 mU/kg × min, ‘low insulin’, and 15 mU/kg × min, ‘high insulin’), inducing respectively serum levels of 543 ± 34 and 24,029 ± 1,595 pmol/l. This experimental design allowed to compare cognitive parameters under two conditions presenting markedly different insulin levels, but with minimal incidence on blood glucose concentrations since these were kept constant by glucose infusion. A ‘no insulin treatment’ group was not included in order to avoid leaving patients infused with glucose without insulin treatment. Measures were taken during a baseline phase preceding insulin infusion and every 90 min during the 360 min of insulin infusion. Compared with ‘low insulin’, ‘high insulin’ induced a slow negative potential shift in the AEP over the frontal cortex (average amplitude, high insulin: 0.27 ± 0.48 µV; low insulin: 1.87 ± 0.48 µV, p < 0.005), which was paralleled by enhanced memory performance (words recalled, high insulin: 22.04 ± 0.93; low insulin: 19.29 ± 0.92, p < 0.05). Also, during ‘high insulin’ subjects displayed enhanced performance on the Stroop test (p < 0.05) and expressed less difficulty in thinking than during ‘low insulin’ (p < 0.03). Results indicate an improving effect of insulin on cognitive function, and may provide a frame for further investigations of neurobehavioral effects of insulin in patients with lowered or enhanced brain insulin, i.e., patients with Alzheimer’s disease or diabetes mellitus.

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Ibuprofen pharmacokinetics showed a large interindividual variation in premature infants during treatment for patent ductus arteriosus, and significant changes may occur between day 3 and day 5 after birth in those infants with a closing ductus. These findings may have implications for the treatment schedule with ibuprofen in patients with patent ductus arteriosus.

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Abbreviations: AEBP, auditory-evoked brain potential; ANCOVA, analysis of covariance; Cz, central electrode location; EEG, electroencephalogram; EOG, electrooculogram; Fz, frontal electrode location; prior-hypo group, subjects who received a 2.5-h antecedent hypoglycemic clamp on the preceding day; Pz, parietal electrode location.A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. Adaptation of Cognitive Function to Hypoglycemia in Healthy Men O R I G I N A L A R T I C L EOBJECTIVE -Antecedent hypoglycemia reduces hypoglycemic counterregulation and symptoms, thereby provoking the hypoglycemia unawareness syndrome. The effects of antecedent hypoglycemia on hypoglycemia-induced cognitive dysfunction are less well established.RESEARCH DESIGN AND METHODS -To determine whether antecedent hypoglycemia also reduces hypoglycemic cognitive dysfunction, we performed stepwise hypoglycemic clamp experiments (4.1, 3.6, 3.1, and 2.6 mmol/l) during a 6-h period in 30 young healthy men. A total of 15 subjects additionally received a 2.5-h antecedent hypoglycemic clamp (3.1 mmol/l) on the preceding day (prior-hypo group), whereas the other 15 subjects did not (control group). Cognitive function was assessed by auditory-evoked brain potentials (AEBPs) and reaction time during a vigilance task and short-term memory recall. Tests were performed during the stepwise hypoglycemic clamp at baseline and at each hypoglycemic plateau.RESULTS -In both groups, performance on all measures of cognitive function deteriorated during stepwise hypoglycemia (all P Ͻ 0.01). However, after antecedent hypoglycemia, the hypoglycemia-induced decrease in the amplitude of the P3 of the AEBP was distinctly reduced compared with the control condition (P Ͻ 0.05). Also, short-term memory performance was less impaired in the prior-hypo group than in the control group (P Ͻ 0.005), and a minor hypoglycemic impairment of reaction time (P Ͻ 0.05) was evident in the prior-hypo group.CONCLUSIONS -Data provide evidence that a single episode of mild antecedent hypoglycemia (3.1 mmol/l) attenuates several aspects of cognitive dysfunction during subsequent hypoglycemia 18-24 h later. Diabetes C l i n i c a l C a r e / E d u c a t i o n / N u t r i t i o n 1060DIABETES CARE, VOLUME 23, NUMBER 8, AUGUST 2000Hypoglycemia and cognitive function formed in 30 subjects randomly allocated to 2 groups. One group additionally underwent an antecedent hypoglycemic clamp that lasted 2.5 h on the day preceding the stepwise hypoglycemia (priorhypo group), whereas the other 15 subjects did not undergo the clamp study (control group). A moderate antecedent hypoglycemic level of ϳ3.1 mmol/l was chosen because, under this condition, antecedent hypoglycemia per se is not expected to induce acute cognitive disturbances that may interfere with the effects of subsequent hypoglycemia (27-30).On the day of the antecedent hypoglycemic clamp study, the subjects in the prior-hypo group reported to the medical researc...