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Biomedical subjects

C Larsson

Publications and source records attributed to C Larsson.

At least 361 records · Page 20Linked to original sources
PubMed1981

Chronic nicotine exposure in rat: a behavioural and biochemical study of tolerance.

Rats received nicotine (50 mg nicotine base/1) in their drinking fluid for 28 days. The daily consumption of nicotine was about 4 mg/kg per day. Controls received plain water. Body weight, food consumption and fluid intake were registered during the whole treatment period and up to 31 days after withdrawal of nicotine. A significant lower body weight was noted in rats, treated with nicotine, in comparison with control rats during the whole treatment period. After withdrawal of nicotine the body weight returned to normal. Only slight effects were seen on the food intake (at the beginning of the nicotine treatment). The fluid intake, on the other hand, was significantly lower in the nicotine group during the whole period of treatment and a reduced intake persisted 28 days after withdrawal of nicotine. Tolerance to nicotine was measured in rats 24 hours after withdrawal of nicotine, using two behavioural tests. No tolerance to nicotine was found after 31 days of withdrawal of nicotine. The number of nicotine-like binding sites was found to be reduced in the midbrain 24 hours after withdrawal of nicotine, while no significant change was found in the cortex and hippocampus.

Animals↗
PubMed1981

Prostaglandin involvement in contractions evoked in rabbit detrusor by field stimulation and by adenosine 5'-triphosphate.

Previous reports suggest that in rabbit urinary bladder both noncholinergic nonadrenergic excitatory responses and the contraction produced by adenosine 5'-triphosphate (ATP) are antagonized by indomethacin. We have attempted by further indirect testing on isolated detrusor strips to determine what role prostaglandins (PGs) might play in these processes. The second part of the biphasic contractile response to ATP was reduced to about 30% of control by PG synthesis inhibitors but the initial phase of the ATP response and te contraction produced by the beta, gamma-methylene analogue of ATP were unaffected. At concentrations that did not affect the response to acetylcholine but greatly suppressed the response to arachidonic acid, indomethacin antagonized the contraction evoked by field stimulation by about 30% at 1-2 Hz (largely noncholinergic and nonadrenergic). SC 19220, a putative PG receptor blocker, also produced about 25% reduction in the response to field stimulation but with only about 50% reduction in the response to arachidonic acid, PGE2, or PGF2alpha, SC 19220 also antagonized the frequency-response curve in atropine-treated strips. These findings lead us to suggest that beside maintaining tone and spontaneous activity in the bladder PGs mediate the slow tonic phase of the ATP response and may contribute to facilitatory modulation of noncholinergic nonadrenergic excitatory transmission.

Adenosine Diphosphate↗
PubMed1980

Interactive computer system for monitoring multiphasic health screening.

In an on-going population screening investigation at the Department of Preventive Medicine in Malmö, an interactive computer system has been developed for monitoring: (i) the electron and invitation of the health screening population; (ii) on-line registration and representation of demographic informations, test results and questionnaires; (iii) generation of the patient files and other listings; (iv) systems for diagnostic and statistical processing and representation. Ten thousand health screening investigations have now been monitored by the system, which is described in this report.

Computers↗
PubMed1980

Hereditary ovalocytosis and splenic rupture.

A family with hereditary ovalocytosis (HO) is described. The probands, 2 brothers, had splenic rupture after modest trauma as preenting symptoms. 7 members of the family had HO. The sister of the pobands had a moderately enlarged spleen. The other members proved normal on routine clinical examination.

Erythrocytes, Abnormal↗
PubMed1980

Studies of muscarinic and nicotinic binding sites in brain.

Binding properties for the muscarinic antagonist quinuclidinyl benzilate (QNB), the nicotinic antagonist tubocurarine and nicotine to crude synaptosomal fractions from mouse and rat brain have been studied. Marked regional differences in number of binding sites for labelled QNB (3H-QNB) were found with a high concentration in the striatum, cortex and a low concentration in the cerebellum. The specific binding sites for labelled tubocurarine (3H-tubocurarine) showed less regional variation. An increased number of muscarinic binding sites (with no change in receptor affinity) was found in rats following long-term treatment with barbital.

Animals↗
PubMed1979

Effects of glycidate on carbon dioxide fixation with isolated spinach chloroplasts.

Glycidate (2,3-epoxypropionate) stimulated CO(2) fixation in isolated spinach chloroplasts up to 100%. In the presence of glycidate the initial lag phase was abolished and the chloroplasts exported mainly 3-phosphoglycerate instead of dihydroxyacetone phosphate.Glycolate formation was not inhibited by glycidate, which is in agreement with the observation that preactivated ribulose-1,5-bisphosphate oxygenase is not inhibited by this compound. Furthermore, glycidate had no effect on electron transport (NADP reduction) and photophosphorylation, nor was a change in the coupling ratio observed.

Journal Article↗
PubMed1979

Inhibition of the contractile action of bradykinin on isolated smooth muscle preparations by derivatives of low molecular weight peptides.

The carbonyl terminal tripeptide sequence of bradykinin (Pro-Phe-Arg) is molecularly manipulated to obtain agents with potent antagonistic activity towards the smooth muscle contractile activity of bradykinin. Screening of various peptide derivatives revealed that heptyl amides or esters of H-D-Pro-Phe-Arg, and H-D-Phe-Phe-Arg possessed relatively stronger antibradykinin activity on the isolated smooth muscle preparation. The parent tripeptides, H-D-Pro-Phe-Arg-OH, and H-D-Phe-Phe-Arg-OH, and their amino acid components, i.e. D-Proline, D-Phenylalanine, L-Phenylalanine and Arginine, did not possess any antibradykinin activity in concentrations of up to 10(-4) M. When the heptyl derivatives of these peptides were incubated with either heparinized or citrated whole blood or plasma, the antibradykinin activity was not lost. Incubation of these peptide derivatives with either carboxypeptidase A or B did not result in any loss of the pharmacological effect. However, pancreatic protease extract produced a significant loss of the anti-oxytocic action on the isolated rat uterus preparation. H-D-Pro-Phe-Arg-NH-lauryl derivative also blocked the action of bradykinin and this effect sustained for a longer period of time comparative to the blockade with H-D-Pro-Phe-Arg-NH-heptyl derivative. In concentrations of 10(-7) M and 10(-8) M and 1 min incubation, which blocked the contractile action of bradykinin (1 nmole) on the isolated guinea pig ileum, these peptide derivatives did not block the action of acetylcholine, histamine, and serotonin. However, in concentrations of about 10(-6) M and higher with 5 min. incubation histamin is also blocked. On the isolated rat uterus preparation the contractile action of acetylcholine, angiotensin, oxytocin and vasopressin was blocked at concentrations of 10(-6) M. These findings warrant a differential pharmacological evaluation and in vivo testing of these peptide derivatives to investigate their therapeutic potential.

Acetylcholine↗
PubMed1978

Indomethacin and diclofenac sodium increase sodium and water excretion after extracellular volume expansion in the rabbit.

The renal effects of an acute extracellular fluid volume expansion (50 ml Ringer/kg body weight/60 min) were studied in aldosterone-treated (100 microgram/kg), anesthetized rabbits with and without pretreatment with either indomethacin (3.0 mg/kg) or diclofenac sodium (3.0 mg/kg), two different inhibitors of renal prostaglandin (PG) biosynthesis. In controls (n = 7), the volume expansion increased urine flow from 1.5 +/- 0.24 to 6.1 +/- 0.5 (S.E.) ml/min/100 g kidney weight and sodium excretion from 0.15 +/- 0.03 to 0.99 +/- 0.10 mmol/min/100 g. PAH and inulin clearance increased by 42 and 58%, respectively, while plasma renin activity and urinary excretion of PGF2 alpha-like immunoreactivity were reduced (P less than 0.05). In animals pretreated with indomethacin (n = 6) or diclofenac sodium (n = 6), the diuresis and the natriuresis following volume expansion were significantly increased about two-fold over controls, whereas PAH and inulin clearance, plasma renin activity and hematocrit did not differ from controls. Both drugs were found to reduce urinary excretion of PGF2 alpha-like immunoreactivity by 75--95% througout the experiment. The results indicate that diclofenac sodium, indomethacin and extracellular volume expansion enhance sodium and water excretion partly by suppression of a PG sensitive reabsorption process in the kidney.

Animals↗
PubMed1978

Natural history and life expectancy in severe alpha1-antitrypsin deficiency, Pi Z.

Clinical data from 246 adult Swedish individuals with severe alpha1-antitrypsin deficiency, Pi Z, diagnosed in 1963--77, were analyzed. Primary emphysema was present in 109 cases. Of 75 Pi Z patients with other types of chronic obstructive pulmonary disease (COPD), all but 7 showed signs of emphysema. Median age at onset of dyspnoea in Pi Z smokers was 40 years, compared to 53 in non-smokers (p less than 0.001). Of the Pi Z individuals over the age of 50, 19% had a diagnosis of liver cirrhosis and 15% signs of glomerular renal damage. Of 91 deceased patients, 56 died from COPD and 12 from liver disease. A greatly reduced survival was demonstrated in Pi Z individuals, regardless of sex. Smoking Pi Z individuals had a significantly lower life expectancy than Pi Z non-smokers (p less than 0.01).

Adult↗
PubMed1978

Intermediate alpha1-antitrypsin deficiency, Pi M-.

A 50-year-old man was found to have 40% of the normal serum alpha1-antitrypsin concentration but subsequent electrofocusing showed a pattern indistinguishable from the ordinary M pattern. This finding and family studies suggested that he was a carrier of a null (-) allele. Heavy smoking and this Pi M- phenotype in interaction probably were responsible for the development of emphysema, documented by an extensive investigation of lung function. Two non-smoking offspring carrying the null allele had normal lung function. Normal karyotypes were found in all the Pi M- subjects.

Adolescent↗
PubMed1978

The renal prostaglandin system: localization and some biological effects.

The renal prostaglandins (PGs) are formed mainly in the endoplasmatic reticulum from locally available precursor, arachidonic acid (C20:4). Although the main PG formation occurs in the papilla, significant amounts of PGs are also formed in the cortex. PGs are not stored, but at once released to the cytosol and metabolized by soluble enzymes, 15-OH-PG-dehydrogenase (PGDA), delta13-PG-reductase and PGE-9-keto-reductase. PG metabolism by the PGDH pathway occurs predominantly in cortex. C20:4 can be used to study the biological effects of the renal PG system. C20:4 given to rabbits increases renal biosynthesis of PGs, renal blood flow, predominantly in the juxtamedullary cortex, and plasma renin activity. These effects are inhibited by PG synthesis inhibitors like indomethacin.

Animals↗
PubMed1977

Smoking and intermediate alpha1-antitrypsin deficiency and lung function in middle-aged men.

Lung function was evaluated in a representative population sample of 50-year-0ld men living in one Swedish city. Twenty-four smoking and 15 non-smoking men heterozygous for alpha1-antitrypsin deficiency--that is, with the protease-inhibitor (Pi1 phenotype MZ--were carefully matched for weight and smoking habit with Pi M controls. The pulmonary function of non-smoking Pi MZ subjects did not differ from that of non-smoking Pi M controls. In contrast, smoking heterozygotes showed a significant loss of elastic recoil, enlarged residual volumes, and increased closing capacity but no signs of obstructive ventilatory impairment. Most smoking Pi MZ individuals reported mild exertional dyspnoea.

Homozygote↗
PubMed1977

Increase of free arachidonic acid by furosemide in man as the cause of prostaglandin and renin release.

Arachidonic acid (C20 :4) plasma renin activity (PRA), PGF2alpha, and sodium excretion were determined before and after furosemide in men. C20 : 4 and PRA increase (p less than 0.005) within 10 min after furosemide, PRA then decreased again whereas C20 : 4 levels remained elevated. Maximal exretion of PGF2alpha and sodium occurred 30-60 min after furosemide. Indomethacin prevented the rise of C20 : 4, PRA and PGF2alpha after furosemide, leaving sodium excretion unaltered. The release of C20 : 4 is assumed to be the primary mechanism of furosemide to increase PG biosynthesis and renin release.

Adult↗