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Biomedical subjects

M Ericson

Publications and source records attributed to M Ericson.

At least 37 records · Page 2Linked to original sources

Endurance time, pain and resumption in passive loading of the elbow joint.

This study investigated reactions in passively loaded, fully extended elbow joints in 13 men. Pain reactions during and after loading were studied, as were endurance time, T(end), and resumption time, Tr. The loading moment on the elbow joint, Mn, varied between 7 and 100% of maximum elbow moment. Discomfort/ pain was estimated with Borg's CR-10 scale. T(end) decreased with increasing load level. The opposite was found for the resumption time: the higher the load, held until T(end), the shorter the Tr. The pain limiting the working capability originated mainly from muscle tissue and not from the joint itself. It is concluded that the relation between load and endurance time for passively loaded, fully extended elbow joints resembles that for muscular loading in more 'normal' postures. Equations for estimation of endurance and resumption times (in minutes) for fully extended joints are proposed: T(end) = 20.6e(-6.04Mn) and Tr = 0.0167e(8.84/(1.46+0.346Mn)), respectively.

Adolescent↗

Heart rate variability in infants with apparent life-threatening events.

UNLABELLED: Heart rate variability (HRV) is often used as an index of sympatho-vagal balance. A decreased HRV has been observed in patients with central hypoventilation and in infants who have later succumbed to sudden infant death syndrome (SIDS). The aim of the present study was to investigate whether HRV is altered in infants with apparent life-threatening events (ALTE), a group with an increased risk of SIDS. Fifty infants with ALTE were compared with 50 age- and sex-matched controls. ECG was recorded overnight in all infants. Two sequences of RR intervals free of artefacts were selected from each sleep state and spectral analysis of RR variability was performed. The mean and SD of RR and the low (LFPow) and high (HFPow) frequency power were analysed. In active sleep (AS) the LF/HF ratio was lower in ALTE infants, but no differences were seen in either the LFPow or the HFPow. In quiet sleep (QS), however, ALTE infants had higher SD-RR (p = 0.006), greater HFPow (p = 0.02) and VLFPow (very low frequency power, p = 0.02) than the control infants. The same results were seen when the two sleep states were combined for analysis, ALTE infants had higher SD-RR (p = 0.004), HFPow (p = 0.006) and VLFPow (p = 0.04). CONCLUSION: The different HRV pattern in ALTE infants compared to healthy controls suggests an altered autonomic control.

Analysis of Variance↗

Involvement of the medial geniculate body in prepulse inhibition of acoustic startle.

Prepulse inhibition of acoustic startle is the normal reduction in startle response to an intense auditory stimulus when this stimulus is immediately preceded by a weaker prestimulus. Previous studies have shown that several neuroanatomical structures and pathways in the brain are involved in the modulation of prepulse inhibition. In the present study, the functional importance of the medial geniculate body (MG) in the modulation of prepulse inhibition was investigated. To this end, in vivo brain microdialysis probes were used to infuse drugs locally into the MG of awake, freely moving rats simultaneously with startle response and prepulse inhibition measurements in the same animals. Intrageniculate infusion of the sodium channel blocker, tetrodotoxin, significantly reduced prepulse inhibition without affecting baseline startle amplitude. A similar effect was obtained after intrageniculate infusion of the GABA(B) receptor agonist, baclofen. In addition, intrageniculate infusion of muscimol, an agonist at the GABA(A) receptor complex, reduced prepulse inhibition, although this effect was obtained at a higher concentration of the drug compared to that of baclofen. These studies suggest that the MG is involved in the modulation of prepulse inhibition and that auditory signals relayed via the MG may be subjected to inhibitory control at this level, involving GABA neurotransmission.

Acoustic Stimulation↗

Peribulbar innervation and substance P expression following nonpermanent injury to the human scalp hair follicle.

The hair pluck procedure alters the anatomy of the anagen hair bulb. Hemorrhage can occur in the mesenchymal sheath and breaks at the proximal epithelium, above or around the upper third of the dermal papilla, have been reported. We hypothesized that innervation, as identified with protein gene product 9.5 (PGP 9.5), and expression of the neuropeptide Substance P (SP) within the dermal papilla would also be altered following plucking. We focused on studying SP as this neuropeptide has been associated with several cellular responses, including anagen hair growth in the C57BL/6 mouse model. Four millimeter punch biopsies were obtained from the occipital scalp of two healthy adults. Hair was then plucked and additional biopsies were obtained immediately, and at 1 d, 1 wk, and 1 mo after plucking. Each set was processed for immunohistochemical analyses and in-focus optical sections of the dermal papilla were captured by laser scanning confocal microscopy and later reconstructed into single images. Following injury, SP was expressed in a disorganized pattern below the dermal papilla. There was also a significant reduction in labeled neuronal cells, and SP expression was enhanced within peribulbar blood vessels at 1 d and 1 wk. By 1 mo, peribulbar nerves, vessels, and SP expression were similar to baseline observations. It remains to be ascertained whether PGP 9.5, also known as unbiquitin hydrolase, and SP are involved in the proliferation of new matrix cells in the human scalp hair follicle following injury.

Adult↗

Bovine growth hormone transgenic mice display alterations in locomotor activity and brain monoamine neurochemistry.

Recent clinical and experimental data indicate a role for GH in mechanisms related to anhedonia/hedonia, psychic energy, and reward. In the present study we have investigated whether bovine GH (bGH) transgenic mice and nontransgenic controls differ in spontaneous locomotor activity, a behavioral response related to brain dopamine (DA) and reward mechanisms, as well as in locomotor activity response to drugs of abuse known to interfere with brain DA systems. The animals were tested for locomotor activity once a week for 4 weeks. When first exposed to the test apparatus, bGH transgenic animals displayed significantly more locomotor activity than controls during the entire registration period (1 h). One week later, after acute pretreatment with saline, the two groups did not differ in locomotor activity, whereas at the third test occasion, bGH mice were significantly more stimulated by d-amphetamine (1 mg/kg, ip) than controls. At the fourth test, a tendency for a larger locomotor stimulatory effect of ethanol (2.5 g/kg, ip) was observed in bGH transgenic mice. bGH mice displayed increased tissue levels of serotonin and 5-hydroxyindoleacetic acid in several brain regions, decreased DA levels in the brain stem, and decreased levels of the DA metabolite 3,4-dihydroxyphenylacetic acid in the mesencephalon and diencephalon, compared with controls. In conclusion, bGH mice display more spontaneous locomotor activity than nontransgenic controls in a novel environment and possibly also a disturbed habituation process. The finding that bGH mice were also more sensitive to d-amphetamine-induced locomotor activity may suggest that the behavioral differences observed are related to differences in brain DA systems, indicating a hyperresponsiveness of these systems in bGH transgenic mice. These findings may constitute a neurochemical basis for the reported psychic effects of GH in humans.

3,4-Dihydroxyphenylacetic Acid↗

Voluntary ethanol intake in the rat and the associated accumbal dopamine overflow are blocked by ventral tegmental mecamylamine.

The mesocorticolimbic dopamine system is believed to be involved in mediating the positive reinforcing effects of drugs of abuse, including ethanol. The nicotinic acetylcholine receptor antagonist mecamylamine perfused via reversed microdialysis in the ventral tegmental area antagonizes the increase of accumbal extracellular dopamine levels after systemic ethanol, and, after systemic injection, lowers ethanol intake in the rat. In the present study the effect of ventral tegmental mecamylamine on ethanol intake and preference, as well as on extracellular accumbal dopamine levels, was investigated in the same animal. To this end, in vivo microdialysis using a double probe approach (one in the nucleus accumbens and one in the ventral tegmental area) was combined with an ethanol preference model invoking a free choice between a bottle of water and a bottle of ethanol 6% (v/v) solution. Wistar rats drinking more than 60% of their total daily fluid intake from the ethanol solution (ethanol high-preferring animals) were selected during a screening period and used for the experiments. The animals received vehicle or mecamylamine (100 microM) in the ventral tegmental area and were then presented with a choice between water and ethanol in a limited access paradigm to which they previously had been adapted. On the next day the rats that received vehicle day 1 now received mecamylamine, and vice versa. When treated with vehicle, ethanol intake and preference were unaltered, as compared to baseline behavior, and accumbal dopamine levels increased significantly to approximately 130% of the pre-drug baseline level. When receiving mecamylamine, ethanol intake and preference were reduced markedly and dopamine levels were unaltered, as compared to pre-drug baseline levels. The present results further indicate that nicotinic acetylcholine receptors in the ventral tegmental area are involved in the positive reinforcing effects of ethanol. Thus, mecamylamine or other antagonists specifically aimed at ventral tegmental nicotinic acetylcholine receptors could represent a new pharmacological treatment principle against alcohol abuse, the efficacy of which should be explored in high-scale alcohol consumers or alcoholics.

Alcohol Drinking↗

The role of catecholamines in desmopressin induced locomotor stimulation.

Central and peripheral administration of DDAVP increase locomotor activity in rats in doses that alter brain dopamine neurochemistry. In order to delineate the role of catecholamines in this behavioural effect of DDAVP, the effects of different catecholamine manipulating agents on DDAVP-induced locomotor stimulation were studied in rats. The catecholamine depleting agent reserpine (5 mg/kg), administered alone or together with the catecholamine synthesis inhibitor alpha-methyltyrosine (250 mg/kg), completely prevented the locomotor stimulatory effect of DDAVP. The dopamine D1 receptor antagonist Sch-23390 (0.01 and 0.03 mg/kg) significantly antagonized the DDAVP-induced locomotor stimulation when administered in the higher dose, that also produced a significant reduction of locomotor activity per se, whereas the dopamine D2 receptor antagonist raclopride (0.08 and 0.16 mg/kg) had no significant effect. The two dopamine blockers administered together produced a significant, dose-dependent reduction of DDAVP-induced locomotor stimulation, while controls were not significantly affected. Also the alpha-adrenoceptor antagonist phenoxybenzamine decreased the DDAVP-induced locomotor stimulation in a dose (20 mg/kg) that did not influence locomotor activity in controls, and, finally, administration of Sch-23390, raclopride and phenoxybenzamine antagonised the DDAVP-induced effect in a dose combination that failed to influence locomotor activity per se. In vivo microdialysis experiments in awake, freely moving rats indicated that DDAVP increases dopamine overflow in the nucleus accumbens, a brain area of importance for initiation of locomotor activity, by approximately 25%, as compared to baseline levels. Taken together, these results indicate that the central stimulatory action of DDAVP involves granula-mediated dopamine release and subsequent activation of dopamine D1 and D2 receptors, and that alpha-adrenoceptors possibly also are involved.

Adrenergic alpha-Antagonists↗

Nefazodone attenuates the behavioral and neurochemical effects of ethanol.

This study evaluated the influence of nefazodone, a combined 5-HT2A receptor antagonist and 5-HT reuptake inhibitor, on the behavioral and neurochemical effects of ethanol in nonselected male Wistar rats. In microdialysis experiments, ethanol (2.5 g/kg, i.p.) increased extracellular accumbal dopamine levels by 36% (p = 0.0073) compared to baseline levels, and elevated the maximal DOPAC and HVA levels by 26% (p = 0.0093) and 52% (p = 0.0010), respectively, Nefazodone (50 mg/kg, s.c.) per se increased accumbal dopamine levels by 28% (p = 0.0199) but, when injected 40 min before ethanol, reduced the ethanol-induced elevation of accumbal dopamine overflow (p = 0.0132) and decreased the ethanol-induced HVA levels (p = 0.0159). In an ethanol(6% v/v)/water free-choice paradigm, nefazodone (50 mg/kg, s.c.) decreased ethanol intake by 51% (p = 0.0251) and preference by 22% (p = 0.0251) in high- but not low-preferring rats from a nonselected Wistar strain. These results show that nefazodone modulates the mesolimbic dopamine system in a dopamine activity-dependent manner, and influences the neurochemical and behavioral effects of ethanol in the rat.

3,4-Dihydroxyphenylacetic Acid↗

Heart rate variability in patients with epilepsy.

Autonomic function was studied by the use of spectral analysis of heart-rate variability in patients with epilepsy in relation to type of epilepsy and anti-epileptic drug therapy. A total of 21 patients with juvenile myoclonic epilepsy (JME) and 21 with temporal lobe epilepsy (TLE) were included; 18 patients were treated with carbamazepine (CBZ), 16 with valproate (VPA) and seven with phenytoin (PHT). One healthy drug free control, matched for age and sex, was selected for each patient. Patients and controls underwent an ambulatory 24 h EKG. Heart-rate variability was analyzed in time and frequency domains. Patients with TLE had significantly lower S.D. of the RR-intervals, lower low frequency power and a lower low frequency/high frequency power ratio than their controls. A lower low frequency/high frequency power ratio was the only significant difference between the JME patient group and their controls. Treatment, however, may have had a considerable influence on the heart rate variability in the epilepsy patients. Patients on CBZ had significantly lower S.D. of RR-intervals, low frequency power and a low frequency/ high frequency power ratio than did their matched healthy drug free controls. The ratio of low frequency/high frequency power was also lower in patients on VPA compared with their controls, but apart from that no differences could be demonstrated between this treatment group and the controls. In conclusion, patients with epilepsy appear to have an altered autonomic control of the heart, with a reduction in some heart-rate variability measures, suggesting a decreased sympathetic tone, which may be related to the drug therapy or the epilepsy as such. Further studies are warranted to explore these changes and their possible relevance for sudden death in epilepsy.

Adult↗

Do arthralgias occur after bilio-intestinal bypass for morbid obesity.

BACKGROUND: Intestinal bypass operations are used occasionally for treating morbid obesity if other methods are unsuitable. Jejuno-ileal bypass (JIB) operations are considered to be a cause of occasional joint pain related disorders. However, bilio-intestinal bypass (BIB) is intended to avoid the blind loop syndrome. This study compared joint pain disorders in an operated BIB group, an obese nonoperated control group, and a lean reference group. METHODS: Using a questionnaire in a cross-sectional study, pain disorders were investigated in age-, sex- and weight-matched groups of operated, obese and lean subjects. The operated group had previously had a BIB and was matched using the preoperative BMI (body mass index, kg/m2). RESULTS: Mean time since operation was 12.4 years (SD 3.4) and the BIB group had lost 15.2 kg/m2 compared with the obese control group. These two groups had a high frequency of pain disorders of similar distribution, differing significantly from the lean reference group. No evidence of major differences in the type of pain disorders could be seen in the two groups. CONCLUSION: Pain disorder was an integral part of an obese syndrome, and was not affected significantly by weight reduction after BIB. The study appears to support the view that approximately 4% of patients develop arthritis vasculitis syndrome after BIB.

Adult↗

Heart rate variability is related to leucocyte count in men and to blood lipoproteins in women in a healthy population of 35-year-old subjects.

OBJECTIVES: To investigate if, in a healthy randomly-selected population of 35-year-old men and women, there already is a relation between decreased heart rate variability and conventional risk factors for cardiovascular disease. BACKGROUND: Analysis of heart rate variability (HRV) has been used for estimating tonic autonomic activity. HRV is reduced in patients with various cardiovascular diseases. If a decreased HRV is a late phenomenon in the progression of cardiovascular disease, or if it parallels or even precedes manifest disease is unknown. DESIGN: Spectral analysis of HRV was made from 24-hour ambulatory electrocardiograms in a randomised population of healthy 35-year-old men (n = 63) and women (n = 70). The different spectral indices of HRV were analysed against gender, leucocyte count (previously described as an independent risk factor for cardiovascular disease), blood lipoproteins, smoking, heredity, body mass index (BMI) and systolic blood pressure. SETTING: A research centre of general medicine and a university hospital. RESULTS: Mean heart rate was lower, total power (TP), very low frequency power (VLF) and low frequency power (LF) were higher in men than in women. In women TP, VLF and LF were negatively correlated to BMI, smoking, triglycerides and positively correlated to HDL cholesterol. TP and VLF were also negatively correlated to risk factor score. High frequency power (HF), a marker of parasympathetic activity, was positively related to HDL cholesterol. In men, at daytime, TP, VLF, LF and HF were negatively correlated to leucocyte count. TP, VLF and LF were also negatively correlated to triglycerides and VLF also to risk factor score. CONCLUSIONS: There are correlations between HRV and known risk factors for cardiovascular disease already in a healthy 35-year-old population. A novel observation is the relationship in men between leucocyte count and heart rate variability.

Adult↗

Accumbal dopamine overflow after ethanol: localization of the antagonizing effect of mecamylamine.

It has been suggested that ethanol exerts its mesolimbic dopamine activating effects and its reinforcing effects via interaction with central nicotinic acetylcholine receptors, thus providing a basis for the often observed covariation between ethanol and nicotine consumption. We have previously demonstrated that the central nicotinic acetylcholine receptor antagonist mecamylamine totally counteracts the ethanol-induced elevation of extracellular dopamine in the nucleus accumbens, as measured by in vivo microdialysis. A contribution of peripheral nicotinic receptor blockade could, however, not be excluded. In the present study, mecamylamine (1.0 mg/kg, i.p.) again totally counteracted the ethanol-induced dopamine overflow, as measured by in vivo microdialysis, while the quarternary nicotinic receptor antagonist hexamethonium (10 mg/kg, i.p.) did not. Furthermore, the increase in accumbal dopamine overflow after systemic ethanol (2.5 g/kg, i.p.) was counteracted by local perfusion of mecamylamine (50 microM) in the ipsilateral ventral tegmental area, but not by mecamylamine perfusion in the nucleus accumbens. Ethanol-induced accumbal dopamine overflow was also counteracted by perfusion of hexamethonium (250 microM) in the ventral tegmental area. These results provide further evidence that ethanol-induced activation of the mesolimbic dopamine system is mediated via stimulation of central nicotinic acetylcholine receptors, and that the receptor population within the ventral tegmental area may be the most important in this regard. It is suggested that antagonists of central nicotinic acetylcholine receptors may be useful in the treatment of alcoholism.

Animals↗

Changes in arrhythmia profile and heart rate variability during abrupt withdrawal of antiepileptic drugs. Implications for sudden death.

Sudden unexpected death (SUD) has been associated with low or undetectable concentrations of antiepileptic drugs in patients with epilepsy suggesting that a sudden fall in plasma levels of these drugs might be a critical factor for the occurrence of SUD. We studied the changes in arrhythmia profile and heart-rate variability, during abrupt withdrawal of carbamazepine and phenytoin treatment in 10 patients with side effects on these drugs. Continuous ECG recording and daily measurements of drug plasma concentrations were performed from the last day of steady-state treatment and the following 4 days. Three patients had a 10-fold increase in ventricular premature beats. In addition, there was a significant reduction in heart-rate variability, assessed over 24 hours, in both the time (SDNN index, P = 0.03) and frequency domains from days 1-5. In the frequency domain analysis there was a significant reduction in total power (P = 0.01), very-low-frequency power (P = 0.004) and in low-frequency (LF) power (P = 0.01). Similar reductions in heart-rate variability and increases in ventricular automaticity have been associated with increased mortality in other patient groups. Two factors that might contribute to the increased rate of SUD in patients with epilepsy have thus been identified.

Adult↗

Heart rate variability in healthy subjects is related to age and gender.

The effects of age and gender on heart rate variability as measured by spectral and time domain analysis of 24 h ECG recordings were evaluated in 101 healthy subjects, 49 men and 52 women (20-69 years of age). In the frequency domain, total power, very low-frequency power, low-frequency power and high-frequency power were negatively correlated to age (P < 0.001 for all variables). Total power decreased by 30% between 20-29 and 60-69 years of age. In the time domain, SDNN-index, the mean of the standard deviations of all normal R-R intervals for all 5 min segments of a 24 h ECG recording, was negatively correlated to age (P < 0.001). Total power, very low-frequency power, low-frequency power and the low-frequency/high-frequency ratio were lower in women (P < 0.05, P < 0.05, P < 0.01 and P < 0.01), although the absolute differences were much smaller than for age. There was a pronounced circadian variation; at night total power increased in all age groups (P < 0.01). The results show that age, and to a lesser degree gender, are important determinants of heart rate variability in healthy subjects. Heart rate variability is a valuable tool for risk stratification in cardiovascular disease, but the physiological effects of ageing, with diminishing heart rate variability in older age groups, must also be taken into account.

Adult↗

Heart rate variability as a means of assessing prognosis after acute myocardial infarction. A 3-year follow-up study.

AIMS: The present study evaluated the prognostic value of heart rate variability after acute myocardial infarction in comparison with other known risk factors. The cut-off points that maximized the hazards ratio were also explored. PATIENTS AND METHODS: Heart rate variability was assessed with 24 h ambulatory electrocardiography in 74 patients with acute myocardial infarction, 4 +/- 2 days after hospital admission and in 24 healthy controls. Patients were followed for 36 +/- 15 months. RESULTS: During follow-up, 18 patients died, nine suffered a non-fatal infarction and 20 underwent revascularization procedures. Heart rate variability was higher in survivors than in non-survivors (P = 0.005). This difference was found at higher statistical levels when comparing non-survivors vs controls (P = 0.0002). A similar statistically significant difference was also found between survivors vs controls (P = 0.04). Patients suffering non-fatal infarction and cardiac events (defined as death, non-fatal infarction or revascularization) had a lower heart rate variability than those without (P = 0.03 and P = 0.03, respectively). With multivariate regression analysis, decreased heart rate variability independently predicted mortality and death or non-fatal infarction. The presence of a left ventricular ejection fraction < 40% and a history of systemic hypertension were, however, stronger predictors. The cut-off points that maximized the hazards ratio using the Cox model differed from those reported by others. CONCLUSION: Decreased heart rate variability independently predicted poor prognosis after myocardial infarction. However, the cut-off points that should be used in clinical practice are still a matter for further investigation.

Adult↗