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J Bruhn

Publications and source records attributed to J Bruhn.

27 records · Page 2Linked to original sources
PubMed2000

Electroencephalogram approximate entropy correctly classifies the occurrence of burst suppression pattern as increasing anesthetic drug effect.

BACKGROUND: Approximate entropy, a measure of signal complexity and regularity, quantifies electroencephalogram changes during anesthesia. With increasing doses of anesthetics, burst-suppression patterns occur. Because of the high-frequency bursts, spectrally based parameters such as median electroencephalogram frequency and spectral edge frequency 95 do not decrease, incorrectly suggesting lightening of anesthesia. The authors investigated whether the approximate entropy algorithm correctly classifies the occurrence of burst suppression as deepening of anesthesia. METHODS: Eleven female patients scheduled for elective major surgery were studied. After propofol induction, anesthesia was maintained with isoflurane only. Before surgery, the end-tidal isoflurane concentration was varied between 0.6 and 1.3 minimum alveolar concentration. The raw electroencephalogram was continuously recorded and sampled at 128 Hz. Approximate entropy, electroencephalogram median frequency, spectral edge frequency 95, burst-suppression ratio, and burst-compensated spectral edge frequency 95 were calculated offline from 8-s epochs. The relation between burst-suppression ratio and approximate entropy, electroencephalogram median frequency, spectral edge frequency 95, and burst-compensated spectral edge frequency 95 was analyzed using Pearson correlation coefficient. RESULTS: Higher isoflurane concentrations were associated with higher burst-suppression ratios. Electroencephalogram median frequency (r = 0.34) and spectral edge frequency 95 (r = 0.29) increased, approximate entropy (r = -0.94) and burst-compensated spectral edge frequency 95 (r = -0.88) decreased with increasing burst-suppression ratio. CONCLUSION: Electroencephalogram approximate entropy, but not electroencephalogram median frequency or spectral edge frequency 95 without burst compensation, correctly classifies the occurrence of burst-suppression pattern as increasing anesthetic drug effect.

Adult↗
PubMed2000

Free and bound leptin levels during human pregnancy.

Leptin is a hormone secreted from adipocytes and trophoblasts which might influence energy metabolism during gestation. In this study we evaluated the course of free and bound leptin levels in 22 healthy pregnant women and compared these values to those in non-pregnant women matched for body mass index (BMI) and age. Serum concentrations of both leptin components and plasma levels of estradiol, progesterone, insulin, non-esterified fatty acids and glucose were measured at each trimester. The BMI increased from the first to the second trimester (22.8 +/- 3.1 and 24.7 +/- 2.9, respectively; p < 0.05) and remained stable thereafter (third trimester 25.3 +/- 2.9 kg/m2). Free leptin and bound leptin did not differ between patients and controls in the first trimester of pregnancy. Free leptin levels increased from the first (122 (60)) to the second trimester (181 (60) pmol/l; p < 0.05) and remained constant (third trimester 181 (76) pmol/l; difference between second and third trimesters, NS). Bound leptin increased from the second (0.43 (0.16)) to the third trimester (0.57 (0.21) nmol/l; p < 0.05). Only bound leptin was higher in the patient group in the third trimester compared to controls (p < 0.01). Our findings of a shift in free leptin to bound leptin in late pregnancy may indicate different physiological roles for both components. Free leptin may reflect maternal fat stores, whereas bound leptin may regulate maternal metabolism via central effects on food intake and energy expenditure.

Adult↗
PubMed1992

Effect of human corticotropin-releasing hormone on gonadotropin secretion in cycling and postmenopausal women.

OBJECTIVE: To test the hypothesis that corticotropin-releasing hormone (CRH) is linked to stress-associated reproductive dysfunction in the human by determining if the administration of human corticotropin-releasing hormone (hCRH) results in an inhibition of gonadotropin secretion. DESIGN: Twenty-four-hour prospective study with frequent (every 10 minutes) blood sampling. SETTING: University Clinical Research Center. INTERVENTIONS: Sequential 8-hour infusions of normal saline, hCRH (1 to 5 micrograms/kg per hour), and hCRH plus naloxone (2 mg/h). SUBJECTS: Four normal cycling women and four postmenopausal women. MAIN OUTCOME MEASURES: Plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (PRL), and adrenal and ovarian steroids. RESULTS: In response to hCRH, a prompt and sustained rise in cortisol (F) was noted in both normal cycling women and postmenopausal women. No inhibition of LH or FSH was noted during either the hCRH or hCRH plus naloxone infusion in either group of women. Unexpectedly, elevations in the mean LH peak amplitude and the transverse mean LH concentration were noted in the postmenopausal women during the infusion of hCRH as compared with saline. The infusion of hCRH had no apparent effect on concentrations of PRL, FSH, and gonadal and adrenal steroids (except for F). CONCLUSIONS: Under these conditions, intravenously administered hCRH has no inhibitory effect on gonadotropin secretion in either premenopausal or postmenopausal women. The mechanism by which stress exerts its deleterious effect on reproductive function in the human remains unknown.

Adult↗