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Biomedical subjects

C G Persson

Publications and source records attributed to C G Persson.

241 records · Page 14Linked to original sources
PubMed1970

Adrenoceptors in the cat choledochoduodenal junction studied in situ.

1. The effects of adrenaline, noradrenaline, isoprenaline and terbutaline (PINN), 1-(3,5-dihydroxyphenyl)-2(t-butylamino)-ethanol, on the sphincter of Oddi were studied in anaesthetized cats. Both adrenaline and noradrenaline (1-4 mug/kg) increased resistance to flow through the sphincter. This effect was blocked by dibenamine (0.5-2.5 mg/kg) and by phenoxybenzamine (0.5-1.0 mg/kg).2. Isoprenaline (0.5-5.0 mug/kg) as well as terbutaline (0.5-10.0 mug/kg) inhibited the spontaneous sphincter activity and decreased flow resistance. In these doses, isoprenaline provoked marked tachycardia and relaxation of the duodenum, whereas the cardial and intestinal effects of terbutaline were minimal. The effects were blocked by propranolol (0.5-1.0 mg/kg).3. The results confirm earlier observations of the presence of alpha-adrenoceptors active in contraction of the sphincter musculature and of beta-adrenoceptors active in its relaxation. It is suggested that the beta-adrenoceptors belong to the beta(2) type according to Lands' classification.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Positive inotropic and chronotropic effects and coronary vasodilation in vitro by two antiasthmatic xanthines with different abilities to antagonize adenosine.

The direct actions and the ability to antagonize adenosine of theophylline (1,3-dimethylxanthine) and enprofylline (3-propylxanthine) were examined in isolated guinea pig heart preparations. Enprofylline was approximately six times as potent as theophylline in reducing coronary perfusion pressure, and between three and five times more potent in increasing rate and force of contraction in isolated perfused hearts, spontaneously beating right atrias, and electrically stimulated left atrias. Adenosine reduced the coronary perfusion pressure and had negative inotropic and chronotropic actions. Theophylline (5-75 microM) concentration-dependently antagonized the coronary vasodilation and the negative chronotropic and inotropic actions of adenosine, whereas enprofylline (2.5-75 microM) did not antagonize adenosine. Since adenosine may be a protective autacoid in the heart under select stress conditions, the possibility that adenosine nonblocking xanthines, like enprofylline, may offer therapeutic advantages over theophylline should be investigated.

Adenosine↗
PubMedDate not supplied

Adrenoceptor and cholinoceptor mediated effects in the isolated urethra of cat and guinea-pig.

1. Preparations of isolated bladder-urethral junction from cats and guinea-pigs were suspended in Krebs solution (37 degrees C) which was bubbled with carbogen. The urethral lumen was perfused at a very low rate (1-3 ml/h) with Krebs solution. Resistance to flow and changes in longitudinal tension (initial setting 0-5 g) were recorded. In additional experiments, tension changes in urethral circular muscle preparations were registered. 2. The urethral preparations had a basal resistance to flow within the range 5-20 cm H2O. They had a spontaneous contractile activity that was unaffected by atropine 0-1 mug/ml, phenoxybenzamine 0-1 mug/ml, and tetrodotoxin 0-1-0-5 mug/ml, suggesting it was of myogenic origin. 3. The basal characteristics and the drug-induced changes in the perfused urethras were independent of whether the longitudinal tension was recorded isometrically or isotonically, or whether the perfusion was made retrograde or antegrade. Passive changes in longitudinal tension between 0-5 and 2-0 g did not affect the resistance to flow through the urethra. 4. Adrenaline and noradrenaline, 0-01-1 mug/ml, increased longitudinal tension and resistance to flow in the perfused preparations. The effects, which were sustained and concentration-related, were blocked or reversed into inhibition in the presence of phenoxybenzamine, 0-1 mug/ml. This finding suggests that the stimulatory effects were mediated via alpha-receptors. 5. Isoprenaline, 0-001-0-005 mug/ml, relaxed and inhibited the activity in the cat urethral smooth muscle and decreased the resistance to flow both under basal conditions and when the urethra was contracted by noradrenaline or acetylcholine. The inhibitory effects were blocked by propranolol, 0-1 mug/ml, suggesting that they were mediated via beta-receptors. In guinea-pig preparations, no effect of isoprenaline was observed. 6. Acetylcholine, 0-02-0-5 mug/ml, increased the longitudinal tension and the resistance to flow through the urethras. The latter effect was less pronounced than that produced by noradrenaline, especially in the guinea-pig preparations. Noradrenaline was also more effective than ecetylcholine in contracting the circular muscle of the urethra. The effect of acetylcholine was blocked by atropine, 0-1 mug/ml, suggesting that the contractions were mediated through muscarinic cholinoceptors.

Acetylcholine↗
PubMedDate not supplied

Nasal mucosal endorgan hyperresponsiveness.

Nonspecific hyperresponsiveness of the upper and lower airways is a well-known characteristic of different inflammatory airway diseases but the underlying mechanisms have not yet been satisfactorily explained. In attempts to elucidate the relation of hyperresponsiveness to disease pathophysiology we have particularly examined the possibility that different airway endorgans may alter their function in allergic airway disease. The nose, in contrast to the bronchi, is an accessible part of the airways where in vivo studies of airway mucosal processes can be carried out in humans under controlled conditions. Different endorgans can be defined in the airway mucosa: subepithelial microvessels, epithelium, glands, and sensory nerves. Techniques may be applied further in the nose to determine selectively the responses/function of these endorgans. Topical challenge with methacholine will induce a glandular secretory response, and topical capsaicin activates sensory c-fibers and induces nasal smart. Topical histamine induces extravasation of plasma from the subepithelial microvessels. The plasma exudate first floods the lamina propria and then moves up between epithelial cells into the airway lumen. This occurs without any changes in the ultrastructure or barrier function of the epithelium. We have therefore forwarded the view of mucosal exudation of bulk plasma as a physiological airway tissue response with primarily a defense function. Since the exudation is specific to inflammation, we have also suggested mucosal exudation as a major inflammatory response among airway endorgan functions. Using a "nasal pool" device for concomitant provocation with histamine and lavage of the nasal mucosa we have assessed exudative responses by analyzing the levels of plasma proteins (e.g., albumin alpha 2-macroglobulin) in the returned lavage fluids. A secretory hyperresponsiveness occurs in both experimental and seasonal allergic rhinitis. This type of nasal hyperreactivity may develop already 30 minutes after allergen challenge. It is attenuated by topical steroids and oral antihistamines. We have demonstrated that exudative hyperresponsiveness develops in both seasonal allergic rhinitis and common cold, indicating significant changes of this important microvascular response in these diseases. An attractive hypothesis to explain airway hyperresponsiveness has been increased mucosal absorption permeability due to epithelial damage, possibly secondary to the release of eosinophil products. However, neither nonspecific nor specific endorgan hyperresponsiveness in allergic airways may be explained by epithelial fragility or damage since nasal absorption permeability (measured with 51CR-EDTA and dDAVP) was decreased or unchanged in our studies of allergic and virus-induced rhinitis, respectively. Thus, the absorption barrier of the airway mucosa may become functionally tighter in chronic eosinophilic inflammation.

Blood Vessels↗