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Biomedical subjects

E Qvigstad

Publications and source records attributed to E Qvigstad.

At least 19 recordsLinked to original sources
PubMed2007

Skin conductance or entropy for detection of non-noxious stimulation during different clinical levels of sedation.

BACKGROUND: State entropy (SE) measures electroencephalographic signals, whereas response entropy (RE) also includes frontal electromyographic activity. In the presence of electromyographic activity, the RE index is larger than the SE index, the difference being denoted as RE-Delta (RE-Delta= RE - SE). Skin conductance (SC) may be expressed by a slow reacting variable, the mean SC level, the derivate of the mean SC level (D-SC), the number of SC fluctuations (NSCF) or the amplitude of the SC fluctuations (ASCF), which directly shows skin sympathetic nerve activity. The goal of this study was to evaluate whether these SC and entropy variables could differentiate between the responses obtained to load sound stimuli at different sedation levels before the induction of general anaesthesia. METHODS: Twenty women scheduled for gynaecological laparotomy were studied. The modified observer's assessment of alertness sedation (OAAS) was used to classify the patients' hypnotic levels. White sounds (98 dB) were given at OAAS level 5 without propofol, at OAAS levels 4-3 and 3-2 with propofol and at OAAS levels 3-2 and < 2 with propofol and remifentanil. RESULTS: RE and SE showed a steady decline from OAAS level 5 to level < 2 (P < 0.01). RE-Delta did not discriminate between any of the OAAS levels (P= NS). The mean SC level discriminated between OAAS levels 4-3 to < 2 (P < 0.01). D-SC discriminated between all the different OAAS levels (P < 0.01). NSCF discriminated between OAAS levels 5 to 3-2 (P < 0.05), but did not discriminate at OAAS level 3-2 between propofol alone or combined with remifentanil, or between OAAS level 3-2 and < 2. ASCF differentiated between OAAS levels 5 and 4 (P < 0.001) and OAAS levels 3-2 and < 2 (P < 0.05) only. CONCLUSION: RE, SE and D-SC showed a similar discrimination between sound responses at the different sedation levels.

Acoustic Stimulation↗
PubMed2007

Comparison of skin conductance with entropy during intubation, tetanic stimulation and emergence from general anaesthesia.

BACKGROUND: The number of skin conductance fluctuations (NSCF) expresses sympathetic skin nerve activity. The response entropy (RE) measures electromyographic and electroencephalographic activity in the forehead. The state entropy (SE) measures mainly electroencephalographic activity. When the suppression of frontal muscular activity is complete, RE is equal to SE. RE-Delta is defined as SE minus RE. The purposes of this study were to examine whether NSCF and RE-Delta correlate with signs of clinical stress during intubation and tetanic noxious stimulation and to elucidate how rapidly and accurately entropy and NSCF react during emergence from general anaesthesia. METHODS: Twenty women scheduled for gynaecological laparotomy were studied. During intubation in remifentanil and propofol general anaesthesia, NSCF and RE-Delta were correlated with the clinical stress score. After a wash-out period, two series of tetanic stimuli were given, the first with (R+) and the second without (R-) remifentanil infusion. The tetanic pre-stimuli periods were compared with the tetanic post-stimuli periods, and R+ was compared with R-. During emergence, the responses of entropy and skin conductance were related to the time of extubation. RESULTS: NSCF correlated well with the clinical stress score during intubation (r(2)= 0.73, P < 0.0005). RE-Delta showed a weaker correlation (r(2)= 0.33, P= 0.007). During tetanic stimuli, the NSCF pre-stimuli level was lower than the post-stimuli level (P < 0.001), and the NSCF R+ response was lower than the NSCF R- response (P= 0.002). RE-Delta did not show similar differences. During emergence, RE reacted before NSCF and SE (P= 0.003). CONCLUSION: NSCF was better than RE-Delta for the measurement of clinical stress during intubation, and was sensitive to tetanic stimuli at different opioid analgesic levels, by contrast with RE-Delta. Both modalities were able to predict emergence at the end of anaesthesia, but RE was more rapid.

Adult↗
PubMed2006

Effects of treatment with a 5-HT4 receptor antagonist in heart failure.

BACKGROUND AND PURPOSE: Positive inotropic responses (PIR) to 5-hydroxytryptamine (5-HT) are induced in the left ventricle (LV) in rats with congestive heart failure (CHF); this is associated with upregulation of the G(s)-coupled 5-HT(4) receptor. We investigated whether chronic 5-HT(4) receptor blockade improved cardiac function in CHF rats. EXPERIMENTAL APPROACH: Rats were given either the 5-HT(4) antagonist SB207266 (0.5 mg kg(-1) 24h(-1); MI(int)) or placebo (MI(pl)) through mini-osmotic pumps for 6 weeks subsequent to induction of post-infarction CHF. In vivo cardiac function and ex vivo responses to isoprenaline or 5-HT were evaluated using echocardiography and isolated LV papillary muscles, respectively. mRNA levels were investigated using real-time quantitative RT-PCR. KEY RESULTS: LV diastolic function improved, with 4.6% lower LV diastolic diameter and 24.2% lower mitral flow deceleration in MI(int) compared to MI(pl). SB207266 reduced LV systolic diameter by 6.1%, heart weight by 10.2% and lung weight by 13.1%. The changes in posterior wall thickening and shortening velocity, cardiac output, LV systolic pressure and (dP/dt)(max), parameters of LV systolic function, did not reach statistical significance. The PIR to isoprenaline (10 microM) increased by 36% and the response to 5-HT (10 microM) decreased by 57% in MI(int) compared to MI(pl). mRNA levels for ANP, 5-HT(4(b)) and 5-HT(2A) receptors, MHCbeta, and the MHCbeta/MHCalpha -ratio were not significantly changed in MI(int) compared to MI(pl). CONCLUSIONS AND IMPLICATIONS: Treatment with SB207266 to some extent improved in vivo cardiac function and ex vivo myocardial function, suggesting a possible beneficial effect of treatment with a 5-HT(4) receptor antagonist in CHF.

Adrenergic beta-Agonists↗
PubMed2006

Conventional-dose hormone therapy (HT) and tibolone, but not low-dose HT and raloxifene, increase markers of activated coagulation.

OBJECTIVES: Hormone therapy (HT) is associated with a modest, but significantly increased risk for arterial and venous thromboembolism. We have compared the effects of estrogen, tibolone, and raloxifene on relevant markers of coagulation activation and investigated whether there is a dose-response relationship of oral HT. METHODS: Randomized, open-label, comparative study of 202 healthy women who were assigned to receive treatment for 12 weeks with either low-dose hormone therapy containing 1 mg 17beta-estradiol + 0.5 mg norethisterone acetate (NETA) (n=50), conventional-dose HT containing 2 mg 17beta-estradiol and 1 mg NETA (n=50), 2.5 mg tibolone (n=51), or 60 mg raloxifene (n=51). RESULTS: The groups were comparable with regard to demographic characteristics and laboratory variables at baseline. D-dimer increased markedly in the conventional-dose HT group, but remained unchanged in the low-dose HT group. Tibolone was associated with a medium increase, whereas raloxifene was associated with a decrease in D-dimer levels. Changes in prothrombin fragment 1 + 2 showed a similar pattern for all four groups, whereas no significant differences in changes of thrombin-antithrombin complex were observed. CONCLUSIONS: Our data suggest that low-dose HT is associated with less activation of coagulation than conventional-dose HT. This finding may be of clinical importance since randomized clinical trials showing increased risk of thrombosis have utilized conventional-dose HT.

Antineoplastic Agents, Hormonal↗
PubMed2004

Nine weeks of bedtime diazoxide is well tolerated and improves beta-cell function in subjects with Type 2 diabetes.

AIMS: To test whether a bedtime dose of diazoxide can improve daytime beta-cell function without side-effects in Type 2 diabetes. METHODS: A double-blind randomized study was performed in 27 Type 2 diabetic subjects (17 male, 10 female) who were treated with bedtime insulin and metformin. Subjects received either bedtime diazoxide, 100 mg, or placebo for 9 weeks. Duplicate C-peptide glucagon tests were performed before and in the last days of intervention. RESULTS: No side-effects of diazoxide were detected. Treatment with diazoxide did not incur any increase in bedtime insulin. C-peptide responses to glucagon tended to increase: 0.15 +/- 0.06 nmol/l vs. -0.01 +/- 0.04 nmol/l for placebo, P < 0.06 for difference. Corresponding effects on insulin were 66.2 +/- 41.7 pmol/l for diazoxide vs. -84.2 +/- 51.5 for placebo, P < 0.03. Treatment with diazoxide decreased fasting glucagon levels by 41% vs. placebo, P < 0.03. Glycated haemoglobin (HbA1c) levels were not affected, whereas levels of blood glucose post breakfast were higher during diazoxide (1.34 +/- 0.43 mmol/l, P < 0.01 vs. placebo). CONCLUSIONS: Bedtime treatment with diazoxide in Type 2 diabetic subjects on bedtime insulin and metformin has no significant side-effects, does not increase bedtime insulin supplementation, tends to ameliorate beta-cell function but fails to improve metabolic control.

Blood Glucose↗
PubMed2004

Effects of a 3-day low-fat diet on metabolic control, insulin sensitivity, lipids and adipocyte hormones in Norwegian subjects with hypertriacylglycerolaemia and type 2 diabetes.

The metabolic and hormonal impact of rapid dietary changes in type 2 diabetes has not been clarified. The objective of this study was to test whether a short-term, low-fat diet affected metabolic control, insulin sensitivity, lipids and adipocyte hormones in patients with type 2 diabetes with hypertriacylglycerolaemia. Nineteen outpatient subjects (10 M, 9 F) with type 2 diabetes and triacylglycerols >2.2 mmol/L at screening were included in the study. Dietary intake was assessed by weighing during two periods of 3-day baseline diet followed by a 3-day low-fat dietary intervention. The two periods of baseline diet did not differ with respect to relevant variables during intervention. Subjects were advised to increase fibre-rich and low-fat foods and to decrease intake of visible fat in an isoenergetic manner. The percentage of energy from fat was reduced from 39 to 22 (p < 0.0001), median values. Daytime blood glucose did not change and fasting insulin and fasting glucose to insulin ratios were unaffected. Total cholesterol decreased from 6.3 to 6.2 mmol/L (p < 0.005), high-density lipoprotein cholesterol from 1.13 to 1.10 mmol/L (p < 0.048) and the ratio of n-6 to n-3 fatty acids in phospholipids from 2.5 to 1.9 (p < 0.003). Concentrations of leptin decreased from 12.1 to 9.9 ng/mL (p < 0.005) and adiponectin increased from 8.6 to 10.5 microg/mL (p < 0.024). The effect on leptin was confined to women. A low-fat diet intervention for 3 days in insulin-resistant type 2 diabetes affects lipid, adiponectin and leptin levels but fails to improve insulin sensitivity and metabolic control.

Adiponectin↗
PubMed2003

Increased contribution of alpha 1- vs. beta-adrenoceptor-mediated inotropic response in rats with congestive heart failure.

AIM: In failing myocardium the mechanical response to beta-adrenoceptor stimulation is attenuated. Alternative signalling systems might provide inotropic support when the beta-adrenoceptor system is dysfunctioning. Accordingly, the inotropic responses to alpha 1- and beta-adrenoceptor stimulation by the endogenous adrenoceptor agonist noradrenaline in non-failing and failing rat hearts were compared. METHODS: Chronic heart failure was induced in male Wistar rats by coronary artery ligation. Corresponding sham groups were prepared. After 6 weeks, papillary muscles from non-failing and failing hearts were isolated. Receptor binding studies were performed in the corresponding myocardium. The alpha 1-adrenoceptor-mediated inotropic response was not changed while the beta-adrenoceptor-mediated response was substantially reduced in failing compared with non-failing myocardium. RESULTS: No change in potency for the agonists was observed at the alpha 1-adrenoceptors, while an increased potency for the agonists at the beta-adrenoceptors was found during heart failure. The lusitropic response to beta-adrenoceptor stimulation was intact during heart failure. No over all change in affinity or number of either adrenoceptor type was observed in receptor binding studies. The alpha 1-adrenoceptor-mediated inotropic response became dominating compared with the beta-adrenoceptor-mediated one in failing rat myocardium in contrast to the dominating role of the latter in non-failing myocardium. The attenuation of the beta-adrenoceptor-mediated inotropic response in rat failing myocardium was not because of a reduced number of receptors. CONCLUSION: Increasing contractility through stimulation of alpha 1-adrenoceptors in situ by the endogenous agonist may be an alternative way of inotropic support during heart failure and even more so during beta-adrenoceptor blockade.

Adrenergic alpha-Agonists↗
PubMed2002

Effects of long-term fasting on insulin responses to fatty acids in man.

OBJECTIVE: To investigate whether the prolonged physiological elevation of nonesterified fatty acids (NEFA) seen in man during fasting associates with an altered acute insulin response to NEFA. SUBJECTS AND METHODS: Fourteen non-diabetic subjects, age 18-25 years, BMI 23.2 +/- 0.8 kg/m2 underwent hyperglycemic clamps (blood glucose 11 mM) for 120 min, during which either saline or Intralipid was administered in the last 60 min. Subjects were tested after an overnight as well as after a 58 h fast. RESULTS: After the overnight fast, insulin levels increased during Intralipid infusion, at min 120 reaching an increment of 33.0 +/- 8.5 microU/ml vs. 9.5 +/- 4.4 microU/ml during saline; p<0.05 for difference. Conversely, after the 58 h fast. Intralipid failed to promote a successive increase of insulin levels (increment during Intralipid at min 120: 0.5 +/- 5.8 microU/ml vs. -4.3 +/- 2.5 microU/ml during saline, NS). Insulin sensitivity as assessed by the amount of infused glucose and its ratio to insulin was enhanced by Intralipid after an overnight fast, but was decreased after a 58 h fast. CONCLUSION: Long-term elevated NEFA during fasting associates with diminished beta cell responsiveness to an acute elevation of fatty acids in conjunction with negative effects on insulin sensitivity.

Adolescent↗
PubMed2001

The effects of hormone replacement therapy (HRT) on hemostatic variables in women with previous venous thromboembolism--results from a randomized, double-blind, clinical trial.

In a recent randomized, double-blind, placebo-controlled trial of women with a history of venous thromboembolism (VTE), we found that hormone replacement therapy (HRT) was associated with an early excess risk of recurrent thrombosis. The aims of the present study were to characterize the effects of HRT on coagulation in these women to elucidate the mechanism(s) by which HRT increases the risk of thrombosis. The study comprised 140 women who were randomized to receive continuous treatment for 24 months with once daily 2 mg 17-beta-estradiol plus 1 mg norethisterone acetate (n = 71) or placebo (n = 69). HRT caused significant increases in prothrombin fragments 1+2, thrombin-antithrombin complex, and D-Dimer after 3 months, but these changes were less pronounced on prolonged treatment. The increases in markers of activated coagulation was higher in those women who subsequently developed recurrent thrombosis, but was similar in carriers and non-carriers of the factor V Leiden mutation. HRT had no effects on fibrinogen and factor VIII. Activated factor VII, but not factor VII antigen, decreased significantly on HRT as compared with placebo. The coagulation inhibitors antithrombin, protein C, and TFPI, but not protein S, all showed significant sustained decreases in the HRT group as compared with placebo. Antithrombin and protein C decreased by 8-12% on HRT, whereas TFPI activity decreased by 12-17% and TFPI free antigen by 29-30%. In multivariate analysis, only TFPI activity was a significant predictor for the increased activation of coagulation. We conclude that HRT was associated with early activation of coagulation, which corroborates the finding of an early risk of recurrent VTE. This activation may in part be explained by reduction in circulating anticoagulants.

Biomarkers↗
PubMed2000

Fatty acids and insulin secretion.

It has long been recognized that acute elevation of non-esterified fatty acids (NEFA) stimulates insulin secretion to a moderate extent both in vitro and in vivo. The effects of longer-term exposure to elevated fatty acids have, however, been investigated only recently. Our own studies in the rat have documented the time dependence of NEFA effects, with inhibition of glucose-induced insulin secretion being apparent after 6-24 h in vivo exposure to Intralipid or in vitro exposure to palmitate, oleate and octanoate. Evidence indicates that the inhibitory effects are coupled to fatty acid oxidation in B-cells, with ensuing reduction in glucose oxidation, in parallel with diminished activity of the pyruvate dehydrogenase enzyme. These findings were essentially confirmed in human pancreatic islets. In the db/db mouse, a model of type 2 diabetes with obesity, evidence was obtained for elevated NEFA playing a significant role in decreased glucose-induced insulin secretion. Evidence also indicates that elevated NEFA inhibit insulin biosynthesis and increase the proinsulin:insulin ratio of secretion. Results on experimentally induced elevations of NEFA in non-diabetic and diabetic humans are thus far inconclusive. Further studies are needed to ascertain the impact of elevated NEFA on insulin secretion in clinical settings.

Animals↗
PubMed2000

Increased risk of recurrent venous thromboembolism during hormone replacement therapy--results of the randomized, double-blind, placebo-controlled estrogen in venous thromboembolism trial (EVTET).

Recent observational studies suggest a 2-4 fold increased risk of venous thromboembolism (VTE) in women taking hormone replacement therapy (HRT). The present study was started before publication of these studies, and the aim was to determine if HRT alters the risk of VTE in high risk women. The study was a randomized. double-blind, and placebo-controlled clinical trial with a double-triangular sequential design. Females with previously verified VTE were randomized to 2 mg estradiol plus 1 mg norethisterone acetate, 1 tablet daily (n = 71) or placebo (n = 69). The primary outcome was recurrent deep venous thrombosis (DVT) or pulmonary embolism (PE). Between 1996 and 1998 a total of 140 women were included. The study was terminated prematurely based on the results of circumstantial evidence emerging during the trial. Eight women in the HRT group and one woman in the placebo group developed VTE. The incidence of VTE was 10.7% in the HRT group and 2.3% in the placebo group. In the HRT group, all events happened within 261 days after inclusion. The sequential design did not stop the study, but strongly indicated a difference between the two groups. Our data strongly suggests that women who have previously suffered a VTE have an increased risk of recurrence on HRT. This treatment should therefore be avoided in this patient group if possible. The results also support those of recent epidemiological studies, which also indicate increased risk of VTE in non-selected female populations during HRT.

Actuarial Analysis↗
PubMed1998

Nicotine concentration in the hair of nonsmoking mothers and size of offspring.

OBJECTIVES: The purpose of this study was to estimate the risk of small-for-gestational-age birth by levels of nicotine in the hair of mothers and offspring. METHODS: In a sample of 58 case subjects and 105 control subjects, hair nicotine concentrations were measured by gas chromatography and mass spectrometry. RESULTS: With women whose hair nicotine concentrations were in the lowest quartile as the reference group, the odds ratio (OR) for small-for-gestational-age birth was increased among women with concentrations in the upper and two middle quartiles (OR=4.2, 95% confidence interval [CI]=1.5, 11.5, and OR = 3.2, 95% CI=1.3, 8.0). When smoking mothers were excluded from the analysis, the corresponding odds ratios were 2.1 (95% CI=0.4, 10.1) and 3.4 (95 % CI= 1.3, 8.6). CONCLUSIONS: The results suggest that passive maternal smoking increases the risk of small-for-gestational-age births.

Case-Control Studies↗
PubMed1997

Weight gain during the first year of life in relation to maternal smoking and breast feeding in Norway.

OBJECTIVE: To assess the weight gain during the first year of life in relation to maternal smoking during pregnancy and the duration of breastfeeding. DESIGN: This was a one year cohort study. SETTING: The city of Oslo, Norway. PARTICIPANTS: Altogether 3020 children born in Oslo in 1992-93. Children were divided into three groups as follows: 2208 born to non-smoking mothers, 451 to mothers who were light smokers (< 10 cigarettes per day), and 261 to mothers who were heavy smokers (> or = 10 cigarettes per day). MAIN RESULTS: The mean birth weights were 3616 g, 3526 g, and 3382 g and 1 year body weights were 10,056 g (gain 6440 g per year), 10,141 g (6615 g), and 10,158 g (6776 g) in children of non-smoking and light and heavy smoking mothers respectively. Cox regression analysis showed that children of heavy smokers were 2.0 (95% confidence interval, 1.7, 2.3) times and children of light smokers 1.3 (1.2, 1.5) times more likely to have stopped breast feeding during their first year of life compared with children whose mothers were non-smokers. Linear regression analysis, adjusting for confounders, showed that weight gain was slower in breast fed children than in those who were not breast fed (-38 g (-50, -27) per month of breast feeding). Compared with children of non-smokers, the adjusted weight gain was 147 g (40, 255) per year greater in children of light smokers and 184 g (44, 324) per year in children of heavy smokers. CONCLUSION: Children catch up any losses in birth weight due to maternal smoking, but some of the catch up effect is caused by a shorter duration of breast feeding in children of smoking mothers.

Birth Weight↗
PubMed1996

[Maternal blood group 0 as a risk factor of neonatal hyperbilirubinemia requiring treatment].

The present prospective study indicates that children of mothers with blood group O run a double risk of hyperbilirubinemia requiring treatment as compared to children of mothers of blood group A, and 5-10 times increased risk of needing exchange transfusion. The most frequent cause of need for exchange transfusion was ABO-incompatibility between mother and child. A positive direct antiglobulin reaction in an ABO-incompatible child in need of treatment doubles the risk of exchange transfusion being required. Blood group O in the mother should be considered to be an independent risk factor for the child, and O-pregnant women should be ABO-grouped for this reason.

ABO Blood-Group System↗
PubMed1994

[Normal labor. Is it induced as a result of subtle intrauterine inflammatory reactions?].

The present study was conducted in order to test the hypothesis the elevated cytokine levels in amniotic fluid from normal deliveries may be generated by a subclinical inflammatory response in intrauterine tissue. Specimens were collected from 38 women with normal deliveries. The levels of tumour necrosis factor, IL1 and IL6 in amniotic fluid samples correlated with the extent of inflammatory cell infiltration in specimens of the foetal membranes, placenta and umbilical cord. Tumour necrosis factor, IL1 and IL6 are generally produced as part of the inflammatory reaction and stimulate synthesis of prostaglandin. Thus a subclinical, intrauterine inflammatory response may play a role in initiation of normal parturition at term.

Amniotic Fluid↗