Adrenergic nerve function in the anaesthetized rat after treatment with a-methyldopa.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to L Svensson.
Explore the source record for details and available documents.
Clinical and animal studies have suggested that consumption of ethanol is influenced by the central serotonergic (5-HT) transmission system. In the present study this hypothesis was tested by observing the effects of a selective 5-HT receptor agonist, 8-OH-DPAT, on ethanol preference in the rat. The rats had access to a 6% (v/v) ethanol solution and water during baseline and treatment periods. Based on the baseline recordings, 2 groups of rats were formed: A high preference group (ethanol intake greater than 50% of total fluid intake) and a low preference group (ethanol intake less than 30%). Both groups were treated SC with 0.125 mg/kg 8-OH-DPAT twice daily for 3 days. The treatment caused a significant reduction of ethanol consumption in the high preference group, but no change in the low preference group. The findings support the hypothesis that activation of the 5-HT system reduces ethanol intake. This effect was restricted to the high preferring rats, suggesting that 8-OH-DPAT interferes only with the positive reinforcing effect of ethanol.
An in vivo voltammetry technique was used to monitor the extracellular ascorbate (AA) concentration in the nucleus accumbens and striatum of unanesthetized, freely moving rats. A single injection of ethanol, 1.0 g/kg intraperitoneally (IP), induced a significant increase in extracellular AA concentration in both the nucleus accumbens and striatum. This effect was dose dependent within a dose range from 0.5-2.0 g/kg. 4-Methylpyrazole (50 mg/kg, IP), which inhibits alcoholdehydrogenase, could not prevent the increase in AA concentration, evoked by ethanol. Furthermore, systemic administration of acetaldehyde (20 mg/kg, IP), the main metabolite of ethanol, did not have any effect on the level of AA in the nucleus accumbens or striatum. These results show that ethanol can alter the brain extracellular AA levels and that this effect seems to be attributed to ethanol itself and not to acetaldehyde. Consequently, these results indicate that a role for AA in the action of ethanol in the brain should be considered.
A two-bottle, free-choice paradigm was used to investigate the influence of the serotonergic (5-HT) system on ethanol intake in genetically heterogeneous Wistar rats. Systemic administration of the 5-HT1A agonist ipsapirone (1.25-5.0 mg/kg) caused a dose-dependent decrease in ethanol preference and intake, while the 5-HT2 antagonist ritanserin (1.25-5.0 mg/kg) and the 5-HT3 antagonists ondansetron (0.01-1.0 mg/kg) and granisetron (0.5-1.0 mg/kg) failed to alter ethanol consumption. The effect of ipsapirone treatment on ethanol intake was more pronounced in high-preferring animals than in low-preferring. A closer look at the microstructure of the rat's drinking behaviour by means of a microcomputer-controlled data acquisition system showed that ipsapirone treatment caused a significant decrease in the number of licks recorded at the ethanol-containing bottle and a decrease in the time spent at this bottle. Furthermore, ipsapirone treatment caused a significant increase in the number of breaks in licking behaviour recorded at this bottle. The drinking behaviour at the water-containing bottle was not affected by the ipsapirone treatment. Neither was the rat's eating behaviour altered by this treatment. These findings support the hypothesis that the 5-HT system is involved in the regulation of ethanol intake, with special emphasis on the involvement of the 5-HT1A receptor subtype, and may indicate that central reward-mediating mechanisms are influenced.
After travelling in subSaharan Africa, an area known for sporadic cases of Marburg virus infection, a young Swedish man presented with a classical picture of severe viral haemorrhagic fever complicated by disseminated intravascular coagulation and septicaemia. Serum samples examined by electron microscopy revealed particles of a size compatible with filovirions. Indirect fluorescent antibody tests indicated transient seroconversion to Marburg virus. In lymphocyte transformation assays of cells isolated from the patient 11 months after the onset of acute disease, Marburg viral antigen was able to stimulate lymphocyte proliferation 3.9-fold; however, exhaustive attempts to isolate virus from acute phase blood cultured in vitro or in vivo from guinea pigs and monkeys failed. Data suggest that this patient may have been infected with a filovirus. This case demonstrates the difficulties that may occur in laboratory diagnosis of viral haemorrhagic fevers.
Chlamydia trachomatis was recovered from the fallopian tubes of ten women with acute salpingitis. The median age of the patients was 19 years. The duration of pelvic pain before consulting a physician ranged from three to 27 days (median, seven days). Half of the patients complained of irregular bleeding, and nine reported increased vaginal discharge. One patient had a rectal temperature of greater than 38 C, and one had an erythrocyte sedimentation rate of less than 15 mm/hr. At laparoscopy, mild inflammatory changes were seen in the tubes of three patients, five had moderately severe inflammation, and two had pelvic peritonitis. C. trachomatis could not be isolated from the cervix of two patients. Paired sera were available from eight patients, six of whom had a significant rise in titer of IgG antibodies to C. trachomatis. Two women had IgM antibodies. Two other women, who harbored Neisseria gonorrhoeae in the cervix, had antibodies to gonococcal pili; one had a significant decrease in titer. This latter patient was one of the patients with a stationary titer of antibodies to C trachomatis. One patient had a stationary titer of antibodies to Mycoplasma hominis. In general, chlamydial salpingitis seems to have relatively benign symptoms. Neither the failure to isolate C. trachomatis from the cervix nor a stationary titer of antibodies to the organism precludes a chlamydial etiology of acute salpingitis.
We investigated the influence of the apolipoprotein (ApoE) epsilon4 allele on the rate of brain atrophy in patients with clinical dementia and in subjects at risk for dementia. Eighty-one subjects, consecutively referred to a memory clinic due to symptoms of dementia, went through a comprehensive examination, including cerebral magnetic resonance imaging. After an initial investigation these subjects were divided into one of six diagnostic groups; Alzheimer's disease (AD, n = 23), objective cognitive impairment (OCI, n = 27), subjective cognitive impairment (SCI, n = 17), vascular dementia (VaD), frontotemporal dementia (FTD) and unspecified dementia (USD). The last three groups were joined into one diagnostic group designated 'other dementia' (OD, altogether n = 14). In order to study the progression of cognitive impairment as well as the rate of atrophy in different brain regions all subjects were reinvestigated after an average period of 16 months. Interest was focused on investigating if those subjects with one or two epsilon4 alleles differed in either dementia progression or rate of brain atrophy compared to those without the epsilon4 allele. We found that the ApoE epsilon4 carriers had a statistically significantly larger increase in ventricular volume as compared with the ApoE epsilon4 noncarriers. In all diagnostic groups the ApoE epsilon4 carriers showed a greater rate of ventricular volume increase, as compared to the noncarriers. However, this difference was statistically significant only for the OD subjects. No statistical significant changes over time were seen for whole brain volume or volume of the temporal lobes and the medial temporal lobes. The diagnostic groups differed in dementia progression with the AD subjects having the most pronounced reduction in MMSE scores as compared to subjects at risk for AD (OCI and SCI subjects). The presence of ApoE epsilon4 allele did not influence the change in MMSE in any of the diagnostic groups.
We have measured the plantar forefoot skin circulation by the uptake of sodium fluorescein (fluorescein flowmetry), 133Xe clearance and laser Doppler fluxmetry in 24 healthy subjects and correlated measurements under basal conditions and after provocation by alcohol intake and application of external heat. To assess the change in skin circulation between the initial measurement at rest and the second measurement after provocation, the coefficient of correlation (r) of the fluorescein flowmetry to the fast slope of the 133Xe elimination curve was 0.46 (p < 0.05), to the slow slope of the 133Xe elimination curve 0.66 (p < 0.001) and to laser Doppler fluxmetry 0.86 (p < 0.001). The coefficient of correlation (r) of the fluorescence appearance time to fluorescein flowmetry was 0.65 (p < 0.001), to the fast slope of the 133Xe elimination curve 0.14 (p = 0.42), to the slow slope of the 133Xe elimination curve 0.47 (p < 0.05) and to laser Doppler fluxmetry 0.63 (p < 0.001). The uptake of sodium fluorescein as measured by fluorescein fluxmetry correlates well with both 133Xe clearance and laser Doppler fluxmetry in assessing a change in skin circulation in healthy humans. The fluorescence appearance time also correlates to the slow slope of the 133Xe elimination curve and to laser Doppler fluxmetry though to a lesser extent.
The stability of the fat-soluble vitamins and thiamine, riboflavin, pyridoxine, ascorbate, and folic acid when administered as part of Intralipid 10% was evaluated. Intravenous pediatric vitamin formulations (Vitalipid N Infant and Soluvit Infant) containing the daily dose for term neonates were diluted with Intralipid to final volumes of 12.5 mL or 260 mL. The volumes were then delivered for 24 hours via dihexylethyl-phthalate-free in vitro infusion systems that simulated clinical conditions. The first vitamin-Intralipid admixture (12.5-mL volumes) was pumped (by syringe) during 24 hours through neonatal infusion sets placed in an incubator (37 +/- 1 degree C, bilirubin light). Aliquots were collected at the beginning of the experiment and after 24 hours of infusion. The second admixture (260-mL volumes) was pumped (by a peristaltic pump) through infusion sets during 24 hours and was exposed to periodic indirect sunlight and to continuous fluorescent light to stimulate the feeding of a child. Aliquots were collected at 0, 8, and 24 hours during administration of the admixtures. The vitamin concentrations were measured by high-performance liquid chromatography. The effect of the vitamins on the stability of the emulsion was also assessed by visual inspection, lipid globule size distribution, and pH change. Losses of vitamins vary from different experimental conditions and were for the fat-soluble vitamins essentially nil, except for phylloquinone, which was 5% to 17% below the initial level. Thiamine, pyridoxine, and folic acid were stable. Losses of riboflavin and ascorbate amounted to 10% to 20% and 9% to 52%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Left coronary artery ligations or sham operations were performed on pentobarbitone-anesthetized rats. The rats were sacrificed at various times after artery occlusion or sham operation and the creatine kinase (CK), potassium (K+), and noradrenaline (NA) content was determined in the left and right ventricular myocardium and in the interventricular septum. One group of rats was pretreated with the NA synthesis inhibitor alpha-methyl-p-tyrosine methyl ester (alpha-MT), another group with d,l-propranolol, and a third group with saline. The NA level of the ischemic left ventricle fell rapidly after the onset of ischemia. This early NA reduction was attenuated after alpha-MT treatment, probably due to reduced transmitter release. Both CK and K+ decreased in a time-dependent manner in the ischemic area of the heart. The early reduction of CK tended to be attenuated after alpha-MT as well as after propranolol. The results support the theory of a detrimental effect of locally released NA. However, in this model the injury produced by the extensive and nearly total ischemia seems so severe that the additional effect of myocardial adrenoceptor activation may well be only marginal.
Explore the source record for details and available documents.