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Biomedical subjects

B M Eriksson

Publications and source records attributed to B M Eriksson.

47 records · Page 3Linked to original sources
PubMed1983

Muscle sympathetic activity and plasma noradrenaline in normotensive and hypertensive man.

Micro-electrode recordings of muscle sympathetic activity were made in the peroneal nerve of 20 normotensive subjects and 18 patients with essential hypertension resting in the recumbent posture. The level of sympathetic activity was quantitated as bursts/100 heart beats or bursts/min. On another occasion blood was sampled from an antecubital vein and analyzed for plasma noradrenaline using radioenzymatic technique. In both groups the level of sympathetic activity increased with age and taking age into account there was no significant difference in sympathetic activity between normotensive and hypertensive subjects. There was no significant difference in plasma levels of noradrenaline between the groups. Both for normotensive and for hypertensive subjects there was a positive correlation between a subject's level of sympathetic activity and his plasma concentration of noradrenaline, and the regression lines did not differ significantly between the groups. It is suggested (a) that outflow of transmitter from sympathetic terminals in muscles contributes significantly to plasma concentrations of noradrenaline at rest both in normotensive and hypertensive subjects: (b) that neither for muscle sympathetic activity nor for plasma noradrenaline do the resting levels differ between normotensive and hypertensive subjects.

Adult↗
PubMed1982

Determination of catecholamines in rat heart tissue and plasma samples by liquid chromatography with electrochemical detection.

Liquid chromatography with electrochemical detection is used for the determination of adrenaline, noradrenaline and dopamine in rat heart tissue, and the method has also been applied to the determination of basic levels of these compounds in blood plasma. The catecholamines are isolated from the biological sample by adsorption onto alumina and are then desorbed by elution with perchloric acid. The stability of the compounds during the different stages in the work-up process has been studied. A greatly simplified procedure for the preparation of alumina is presented. Both ion-pair reversed-phase and ion-exchange liquid chromatography have been used for the separation of the catecholamines. For plasma samples the method has been validated against radioenzymatic assay and the choice of method is discussed.

Aluminum Oxide↗
PubMed1981

Determination of tritiated digoxin and metabolites in urine by liquid chromatography.

A liquid chromatographic method for the determination of digoxin, digoxigenin, its mono- and bisdigitoxoside and dihydrodigoxin in urine is described. Doses of 100 muCi of [12 alpha-3H]digoxin and 0.5 mg (640 nmol) of digoxin were administered orally to eight healthy volunteers. The compounds were extracted from urine with methylene chloride containing 3% of heptafluorobutanol. After separation, fractions corresponding to digoxin and the metabolites were measured by liquid scintillation counting. Conjugates of the glycoside metabolites were determined indirectly after pre-treatment of the samples with beta-glucuronidase-arylsulphatase. The detection limit was 0.1 nmol/l. Metabolites amounting to 0.5% of digoxin were assayed with a relative standard deviation of 5%. The advantages of the method are a high recovery in the extraction step, short separation times and the possibility of separate assay of dihydrodigoxin.

Chromatography, High Pressure Liquid↗
PubMed1981

Effect of ischaemic on the adrenergic neurons of the rat heart: a fluorescence histochemical and biochemical study.

Left coronary artery ligation was performed in pentobarbitone anaesthetised rats. Following 1/2 and 2 1/2 h of coronary artery occlusion or sham-operation the right and left ventricular myocardium and the interventricular septum were analysed for tissue content of catecholamines. In control rats and in rats with coronary artery ligation for various time periods (1/2, 2 1/2 and 5 h), the Hillarp-Falck fluorescence histochemical technique was used to visualise the catecholamines of the ventricular myocardium. The tissue noradrenaline content of the left ventricle was markedly reduced after 2 1/2 h of ischaemia while noradrenaline levels in the other parts of the ventricles were unaffected. The adrenergic innervation of the normal rat ventricles is described for the purpose of comparing the normal innervation picture with the appearance after ischaemia. A reduced catecholamine fluorescence was found mainly in the centre of the left ventricular free wall 30 min after coronary artery occlusion. After 2 1/2 and 5 h large areas of the ischaemic myocardium were found to be completely devoid of fluorescent terminals. The border zone between the areas of fluorescence disappearance and normally innervated myocardial tissue was generally quite sharp and occasionally terminals with a diffuse appearance were found in this zone. It is concluded that coronary artery ligation caused a time-dependent loss of noradrenaline from the adrenergic nerve terminals in the ischaemic myocardium. Catecholamine thus released may activate myocardial adrenoceptors and hence be related to increased ischaemic damage and ventricular arrhythmias.

Adrenergic Fibers↗
PubMed1981

Plasma noradrenaline correlates to sympathetic muscle nerve activity in normotensive man.

Recordings of multiunit sympathetic activity were made in muscle branches of the peroneal nerve in 22 healthy subjects at rest in recumbent position. Nerve activity was quantitated in terms of burst incidence (number of pulse synchronous sympathetic bursts per 100 heart beats or per min). In a separate session, 4-45 months later, blood was drawn from an antecubital vein for noradrenaline analysis. Both sympathetic activity and plasma concentrations of noradrenaline varied widely between subjects and both parameters increased with age. There was a significant positive correlation between a subject's level of sympathetic activity and his plasma concentration of noradrenaline. It is suggested that overflow of transmitter from sympathetic terminals in muscles contributes significantly to plasma levels of noradrenaline at rest.

Adult↗
PubMed1980

Changes in plasma noradrenaline and adrenaline during isometric exercise.

1. Plasma noradrenaline and adrenaline were measured radioenzymatically in twelve hypertensive and four normotensive subjects before and during handgrip. In the resting arm (n=11), plasma noradrenaline increased by 17% (P<0.01) and plasma adrenaline by 27% (P<0.001). In the exercising arm, plasma adrenaline increased by 97% (P<0.005) but the mean increase of noradrenaline of 10% was not significant (P>0.1). 2. The noradrenaline response suggests a small and variable sympathetic adrenergic response; the significant difference (P<0.05) in adrenaline responses between resting and exercising arms may reflect local variation in tissue clearance.

Adult↗
PubMed1979

Determination of apomorphine in plasma and brain tissue by ion-pair extraction and liquid chromatography.

Apomorphine is extracted from plasma or tissue homogenate with ethyl acetate. After back-extraction into hydrochloric acid, the apomorphine is extracted as an ion pair with 3,5-di-tert.-butyl-2-hydroxybenzene sulphonate into a small volume of methylene chloride and the solution is injected into the chromatographic column. Apomorphine is separated on microporous silica with a mixture of aqueous perchloric acid, methanol and methylene chloride as the mobile phase. With absorbance measurement of the eluent at 254 nm the method permits the determination of 15 pmol of apomorphine in 1 ml of plasma or in a rat brain. The coefficient of variation was 4% at the 100 pmol level.

Animals↗
PubMedDate not supplied

Effects of chronic beta-adrenoceptor antagonism on plasma catecholamines and blood pressure in hypertension.

Plasma catecholamines were measured before and after treatment with beta-adrenoceptor antagonists in 17 hypertensive patients. Chronic treatment with beta-adrenoceptor antagonists caused substantial reductions in heart rate and intra-arterial blood pressure recorded continuously during ambulation. Before treatment, a quantitative relationship was observed between plasma norepinephrine and blood pressure and heart rate during a variety of activities; a similar relationship was also observed after chronic treatment five of six patients, suggesting that plasma norepinephrine remains an index of sympathetic activity despite the influence of beta-adrenoceptor antagonism. After treatment, plasma norepinephrine tended to be higher at any level of blood pressure, although not significantly so. Chronic treatment caused no significant change in mean resting plasma levels of norepinephrine and epinephrine. During exercise, plasma norepinephrine and epinephrine levels were significantly elevated above control after acute but not after chronic treatment. These observations do not support the hypothesis that beta-adrenoceptor antagonist drugs lower blood pressure in hypertensive man through a sympatholytic mechanism in he central nervous system or at peripheral presynaptic receptors.

Adolescent↗