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Biomedical subjects

K Strandberg

Publications and source records attributed to K Strandberg.

At least 37 records · Page 2Linked to original sources
PubMed1977

Thromboxane A2: effects on airway and vascular smooth muscle.

Thromboxane A2, an unstable compound derived from prostaglandin G2, was generated by incubation of arachidonic acid with a suspension of human platelets. The activity of thromboxane A2 relative to that of prostaglandin H2 in causing contractions of a number of smooth muscle organs were as follows: rabbit aorta, 7-20; human umbilical artery, 9-60; and guinea pig trachea, 2-12. Intravenous injection of thromboxane A2 into anaesthetized quinea pigs was followed by a pronounced increase in the tracheal insufflation pressure, potency compared to prostaglandin H2, 31-45.

Animals↗
PubMed1977

Prostaglandin release by slow reacting substance from guinea pig and human lung tissue.

Slow reacting substance (SRS) injected into the pulmonary artery released prostaglandins E (PGE) and F2alpha (PGF2alpha) and the 15-keto-13, 14-dihydro PG metabolites from non-sensitized and ovalbumin sensitized, isolated, perfused guinea pig lungs. PGs were also released from lungs incubated with SRS. Sensitized lungs released more PGs in both types of preparations. Indomethacin inhibited the effect of SRS. Passively sensitized human lung fragments, in parallel to guinea pig lung, released PGE, PGF2alpha and the metabolites when incubated with SRS or antigen. In in vivo experiments, SRS and arachidonic acid given intravenously increased the airway insufflation pressure in anesthetized quinea pigs. These effects, but not the action of injected PGF2alpha and histamine, were abolished by indomethacin. The results indicate that one of the modes of SRS action is by release of PGs, and are consistent with the hypothesis that PGs are predominantly "secondary" mediators (in the temporal sense) of the antigen-antibody reaction.

Airway Resistance↗
PubMed1977

Potentiation of itch and flare responses in human skin by prostaglandins E2 and H2 and a prostaglandin endoperoxide analog.

The itch and erythematous responses induced by intradermal injection of prostaglandin E2 (PGE2), the unstable prostaglandin endoperoxide PGH2 (t1/2 approximately 5 min at 37 degrees C) and the stable endoperoxide analog (15S)-hydroxy-9alpha, 11alpha-(epoxymethano)prosta-5,13-dienoic acid (EPA) were studied in volunteers. The compounds were given alone or in combination with histamine. All the compounds produced flare reaction in the skin; the order of potency was PGE2 greater than PGH2 greater than EPA. PGE2 and PGH2 evoked a sensation of itch in about half of the subjects whereas the same doses of EPA gave no itch response. In combination with histamine all compounds elicited itch of longer duration and flare of larger area than could be accounted for by simple additive effects of any released histamine. The results indicate that the PGs and PG intermediates formed in skin may potentiate the pruritogenic and flare-inducing effects of inflammagens in man.

Adolescent↗
PubMed1977

Release of histamine and formation of prostaglandins in human lung tissue and rat mast cells.

Release of histamine and prostaglandins (PGs) from human lung tissue and rat mast cells was investigated. Passively sensitized lung fragments released PGE, PGF2alpha and the 15-ketodihydro metabolites into the media with time alone. Antigen challenge liberated 20% tissue histamine and there was a twofold increase in PGs. Twice as much PGF2alpha as PGE was found. beta-Adrenergic agonists inhibited the anaphylactic release of mediators and this action was blocked by propranolol. Both PGF2alpha and PGE were consistently found in the mast cell media, demonstrating that mast cells can synthesize PGs. Anaphylaxis induced a marked liberation of histamine but not of PGs. The results indicate that the release of histamine may precede the major release of PGs and suggest that the bulk of PGs may derive from cells in the proximity of the mast cells.

Adrenergic Agonists↗
PubMed1977

Prostaglandin E2 in blister fluid of bullous diseases and experimental suction blisters.

Prostaglandin(PG)-like activity in the fluid of spontaneous and suction blisters was measured by bioassay on isolated guinea-pig colon after acidic lipid extraction. The fluid from spontaneous blisters in 15 patients with various bullous dermatoses, such as pemphigoid, porphyria cutanea tarda, erythema multiforme, contact dermatitis, X-ray dermatitis, all contained measurable amounts of activity, varying from 0.4 to 54 ng/ml, expressed as PGE2-activity. From 4 patients with pemphigoid, samples of fluid were collected, adequate to permit of analysis regarding the identity of the spasmogenic material. In silicic acid column chromatography, thin-layer chromatography, and in reversed phase partition chromatography, the major part of the biological activity co-chromatographed with 3H-PGE2. In one patient part of the activity coincided with PGF2alpha. The PG-like activity of experimental suction blisters was found to be significantly higher in patients with dermatitis herpetiformis than in control and psoriasis patients. The appearance of PGs in blister fluid is compatible with a role as chemical mediator involved in blister formation.

Adult↗
PubMed1977

Pruritogenic activity of prostaglandin E2.

The itch and erythematous responses induced by intradermal injection of histamine and PGE2 were studied in human skin. Both compounds produced a sensation of itch. The histamine-elicited flare reached a maximum in 3 min and had disappeared after 1 hours. PGE2 induced a similar flare reaction initially, but it was gradually replaced by a smaller, dusky and well delimited erythema. The itch and the flare-like erythema induced by either histamine or PGE2 were alleviated when the subjects were pretreated with the antihistaminic drug chlorcyclizine, thus indicating that at least part of the PGE2 response may be mediated via histamine release. However, when given combined in a mixture, histamine and PGE2 elicited itch of longer duration and flare of larger area than could be accounted for by simple additive histamine effects. Thus, PGE2 seems to potentiate the itch and flare responses induced by histamine in human skin.

Adolescent↗
PubMed1976

Composition of phospholipids and phospholipid fatty acids in rat mast cells.

The composition of phospholipids and phospholipid fatty acids in isolated rat serous fluid mast cells was analyzed by thin layer chromatography, gas-liquid chromatography and mass spectrometry. The phospholipids constituted about 50% of the mast cell lipids and phosphatidylethanolamine, phosphatidylserine, phosphatidylinositol, phosphatidylcholine were identified. The phosphatidylethanolamine fraction contained aldehydes and the highest proportion of unsaturated fatty acids. Sphingomyelin contained predominantly saturated fatty acids whereas the ratio unsaturated fatty acids: saturated fatty acids for the other phospholipids was more close to 1.

Animals↗
PubMed1976

Formation and action of prostaglandin endoperoxides in the isolated human umbilical artery.

The effects on the isolated human umbilical artery (HUA) of the recently isolated endoperoxide intermediates in prostaglandin (PG) biosynthesis, PGG2 and PGH2, were studied. Both endoperoxides were potent contractors of the artery strips, the threshold concentrations being 3 (1-4) ng/ml for PGG2 and 1 (1-12) ng/ml for PGH2, as compared with 200 (40-400) ng/ml for PGE2. The hemiacetal derivative of 8-(1-hydroxy-3-oxopropyl)-9,12L-dihydroxy-5,10-heptadecadienoic acid (thromboxane B2), a metabolite of PGG2, appeared in the bath medium indicating PG and thromboxane generation in the isolated HUA. The formation of thromboxane B2 was inhibited by indomethacin (8-40 mug/ml) and by eicosa-5,8,11,14-tetraynoic acid (ETA) (25 mug/ml), ETA also inhibited the contractile responses to both endoperoxides. The results support the view that local generation of PGs might be involved in the closure of the HUA at birth.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1976

Tracheobronchial clearance and beta-adrenoceptor stimulation in patients with chronic bronchitis.

The effect of a beta-adrenoceptor stimulating agent, terbutaline, on mucociliary transport in the lungs was studied in 10 patients with chronic bronchitis. Mucociliary transport was studied by having the patients inhale 6mum teflon particles tagged with 99mTc and by external measurement of the radioactivity in the lungs in the supine position. Terbutaline 0.25 mg and vehicle respectively were given subcutaneously in a cross-over double-blind study. On the average, clearance was slow in the examinations where the patients were given vehicle. Terbutaline produced a marked increase in mucociliary transport in four patients, a smaller increase in one and no effect in the others. Three out of the four patients who showed a marked inrease in clearance had less ventilatory impairment than the other seven patients. This may indicate that the mucociliary transport mechanism is less severely damaged in relatively early stages of the disease than in later stages. On the average FEV1.0 deteriorated significantly during the clearance measurements when vehicle was given, but did not change significantly when terbutaline was given.

Adult↗
PubMed1976

Tracheobronchial clearance in bronchial asthma: response to beta-adrenoceptor stimulation.

Tracheobronchial clearance was studied in 12 patients with bronchial asthma. They inhaled a test aerosol of 6 mum teflon particles tagged with 99mTc, after which external measurement of the radioactivity in the lungs was made for 2 h in the supine position. Clearance was determined after subcutaneous administration of 0.25 mg of the beta-adrenoceptor stimulating compound terbutaline and vehicle, respectively, in a crossover, double-blind study. The average clearance in the asthmatics did not differ significantly from that of healthy non-smokers. Terbutaline significantly enhanced clearance in the asthmatics, though considerably less than reported for healthy subjects. Alternative explanations for this weak effect of terbutaline in the asthmatics might be that the mucociliary transport system was affected by the asthma disease, or that earlier treatment with beta-adrenoceptor stimulating compounds or other drugs had produced increased tolerance and/or carry-over effects. Ventilatory function measured as FEV1.0 deteriorated significantly during the clearance measurement when vehicle was given, but not when terbutaline was given. Terbutaline thus counteracted the unfavourable effect of the supine position on ventilation.

Adult↗
PubMed1976

Involvement of endoperoxides and thromboxanes in anaphylactic reactions.

Our recent work on prostaglandin endoperoxides in the lung has shown that: 1. The endoperoxides were 5 to 10 times more potent than PGF2alpha in an in vitro preparation of respiratory smooth muscle, i.e., the guinea pig trachea. 2. The endoperoxides were 5 to 10 times more potent than PGF2alpha in causing an increase in tracheal insufflation pressure in the anaesthetized, artificially ventilated guinea pig. 3. Endoperoxides formed from exogenous arachidonic acid in homogenates of guinea pig lung and in intact guinea pig lung were converted to a large extent into metabolites different from the classical prostaglandins, i.e., thromboxane B2 (8-(1-hydroxy-3-oxopropyl)-9-12L-dihydroxy-5,10-heptadecadienoic acid) and HHT (12L-hydroxy-5,8,10-heptadecatrienoic acid). 4. Injection of antigen into sensitized guinea pig lungs caused a significant release of the endoperoxide metabolite, thromboxane B2. PGF2alpha has previously been implicated to be involved in anaphylaxis (14). The findings described above show that the prostaglandin endoperoxides are important not only as precursors of PGF2alpha but also through their own effects on airway smooth muscle. Furthermore, the release of thromboxane B2 indicates that its immediate precursor, the biologically active thromboxane A2 is also formed in this system (15). This compound, which has a half-life of 30 to 40 sec causes platelet aggregation and contraction of the isolated rabbit aorta (15). Work is in progress to study the respiratory effects of thromboxane A2 and its possible role in anaphylactic reactions.

Anaphylaxis↗