Search PubMed⌕ Search

Biomedical subjects

P Lundborg

Publications and source records attributed to P Lundborg.

At least 109 records · Page 6Linked to original sources
PubMed1977

The exchangeable splenic platelet pool in response to selective adrenergic beta-i-receptor blockade.

The aim of the present work was to investigate the effect of selective beta-I-blockade on the exchangeable splenic platelet pool (ESPP). Therefore, 50 mg of metoprolol (a selective beta-I-receptor blocking agent) was given by mouth to three groups of subjects: (1) 15 healthy volunteers, (2) five asplenic subjects, and (3) 10 patients with different myeloproliferative disorders (MPD) with and without splenomegaly. The platelet count was determined 90, 150, 210, 270 and 330 min after the ingestion of the drug. In the group of healthy controls a significant increase (P less than 0.005) in the platelet count occurred and amounted to about 10% over baseline. The average peak value was reached at 150 min and the elevation in platelet count was maintained more than 4 h. An increase in the platelet count was also induced in patients with MPD, but the mean for the peak value only reached borderline significance (0.10 greater than P greater than 0.05). In the group of asplenic subjects no change in the platelet count occurred. It is concluded that acute oral administration of metoprolol causes a significant release of platelets from the ESPP. This platelet release is, however, no enhanced if the ESPP is enlarged.

Adolescent↗
PubMed1977

Metoprolol and the peripheral platelet count.

An acute oral administration of 50 mg metoprolol (a selective beta-1-receptor antagonist) to 18 healthy volunteers induced a significant increase in the peripheral platelet concentration lasting more than 4 h. It is suggested that this increment in the platelet count originates from the exchangeable splenic platelet pool. The mechanism by which metoprolol exerts its effect remains to be established.

Administration, Oral↗
PubMed1977

Effect of hypoxia on monoamine synthesis in brains of developing rats.

Tyrosine and tryptophan hydroxylase activity was studied in the postnatal rat brain in vivo by measuring the accumulation of dihydroxyphenylalanine and 5-hydroxytryptophan, respectively after inhibition of L-aromatic amino acid decarboxylase with NSD 1015. With increasing age there was a significant increase in the amount of dopa and 5-HTP accumulated in the brain after administration of NSD 1015. After 30 min in a 12% oxygen environment there were significant reductions of tyrosine hydroxylase and tryptophan hydroxylase activity at 1,14 and 28 but not 4 days of postnatal age. Further, the decrease in 5-HTP accumulation was significantly more marked at 14 and 28 days than at 1 day of age. Thus, the oxygen-dependent synthesis of the neurotransmitter 5-hydroxytryptamine seems to be less vulnerable in the early postnatal rat brain.

5-Hydroxytryptophan↗
PubMed1977

Bioavailability of quinidine in slow-release form. A comparison between two preparations containing quinidine bisulphate as the active constituent.

Two different slow-release preparations of quinidine bisulphate (A and B) have been tested. The in vitro dissolution rate of preparation B was substantially lower in intestinal than in gastric juice, whereas the release rate of quinidine from preparation A was virtually unaffected by the pH of the dissolution medium. After a single dose of two tablets of each of the preparations to 6 healthy volunteers, corresponding to 386 mg (B) and 320 mg of quinidine base (A), the maximum plasma concentration was attained after about 4.5 h. The peak concentration was 5.2 +/- 0.5 mumol/l for preparation A and 4.1 +/- 0.4 mumol/l for B. A similar difference was found in the area under the plasma concentration curve (AUC), which was 68 +/- 10 mumol-h/l and 54 +/- 5 mumol-h/l, respectively. Taking into consideration that preparation B contained 20.6% more active drug per tablet these values indicate that the extent of bioavailability is about 50% higher for tablet A than for tablet B.

Administration, Oral↗
PubMed1976

Ontogenetic development of locomotor activity and rate of tyrosine hydroxylation.

A combined biochemical and behavioral study was performed postnatally on albino rats. An almost linear increase in total motor activity was observed from 1 to 15 days of age followed by a pronounced decrease in motor activity between days 15 and 18. The in vivo rate of tyrosine hydroxylase activity in whole brain was estimated by means of measuring accumulation of L-3,4-dihydroxyphenylalanine (Dopa) after administration of an inhibitor of aromatic amino acid decarboxylase NSD 1015. Additionally, Dopa accumulation was studied in regional brain areas in 10 and 14-day-old animals. A slight gradual increase in the amount of Dopa accumulation in whole brain was observed from 1 to 10 days of age, followed by a pronounced increase between 10 and 14 days. Regional studies revealed that the increase in Dopa accumulation was primarily located to striatum. The data suggest an involvement of central catecholamine neurons possibly dopaminergic, terminating in striatum. The decrease in motor activity observed after 15 days of age is interpreted as involvement of maturing inhibitory pathways of noncatecholaminergic origin.

Animals↗
PubMed1976

Plasma levels and effect on heart rate and blood pressure of metoprolol after acute oral administration in 12 geriatric patients.

Metoprolol, a cardioselective beta-blocking agent, has been given orally to 12 geriatric patients with moderate hypertension. Drug levels of metoprolol as well as the effect of the drug on resting heart rate and BP were studied. Metoprolol was given in a dose of 20 mg, and 8 of the 12 patients also received a 50 mg dose. After the 20 mg dose the peak drug plasma concentration varied between 5 and 80 ng/ml (mean 33), and after the 50 mg dose between 14 and 212 ng/ml (mean 111). This variation is much greater than that seen in earlier studies on healthy volunteers and on a group of non-geriatric hypertensive patients. Plasma half-life of metoprolol averaged about 3.5 hours after both the 20 mg and the 50 mg dose; this does not differe from the plasma half-life in earlier studies in younger age groups. The variability observed in the study might be explained multifactorially, e.g. by different body weight, absorption and/or first-pass effect of the drug.

Administration, Oral↗
PubMed1976

The peripheral platelet count in response to intravenous infusion of isoprenaline.

5 healthy male volunteers received i.v. infusions of isoprenaline in doses of 0.03, 0.06 and 0.09 mug X kg-1 X min-1 over a period of 6 min. A statistically significant decrease in the peripheral platelet count was obtained, but no dose-response-curve for isoprenaline was observed. It is suggested that while an i.v. infusion of epinephrine causes a release of platelets from the exchangeable splenic platelet pool, isoprenaline might have the opposite effect on the spleen, thereby causing a decrease of platelets in the peripheral blood.

Adult↗
PubMed1975

Antagonism by d-amphetamine of learning deficits in rats induced by exposure to antipsychotic drugs during early postnatal life.

The acquisition of a conditioned avoidance response (CAR) was investigated in rats of nursing mothers given pimozide 0.5 mg/kg on days 1, 2, 3, 4, 5, 6, and 7 after delivery. Four weeks after birth, the male litter-mates were tested for CAR acquisition in a two-way avoidance situation or for correct CAR acquisition in a brightness discrimination situation. Offspring of mothers treated with pimozide were markedly inferior in the CAR acquisition in both behavioural situations as compared to those of mothers given glucose. The administration of d-amphetamine 15 min prior to the training session specifically counteracted the behavioural impairment obtained in the offspring of pimozide-treated mothers. The results obtained in the present investigation lend further support to the contention that the behavioural deficits in offspring of nursing mothers treated with neuroleptic agents are due to a developmental disturbance in central catecholamine neurones.

Animals↗