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G Petersson

Publications and source records attributed to G Petersson.

36 records · Page 2Linked to original sources
PubMed1993

Role of peptidases and NK1 receptors in vascular extravasation induced by bradykinin in rat nasal mucosa.

We used Evans blue dye to assess the effects of bradykinin on vascular extravasation in nasal mucosa of pathogen-free F344 rats. There was a dose-dependent increase in Evans blue extravasation when bradykinin was delivered by topical instillation in the nose (doses, 25-100 nmol). Only the highest intravenous doses (2 and 5 mumol/kg) of bradykinin caused increased extravasation. When bradykinin was delivered by either route, its effect on extravasation was exaggerated by pharmacological inhibition of the enzymes neutral endopeptidase (NEP) and kininase II [angiotensin-converting enzyme (ACE)]. When bradykinin was instilled locally, the effect of NEP inhibition was predominant; when bradykinin was injected intravenously, the effect of ACE inhibition was predominant. The mechanism of extravasation also varied with the mode of bradykinin delivery: when bradykinin was instilled locally in the nose, the selective neurokinin 1 (NK1) receptor antagonist CP-96,345 markedly inhibited the response, whereas it had no effect on Evans blue extravasation when bradykinin was injected intravenously. We conclude that bradykinin causes dose-related increases in Evans blue dye extravasation in the nose and that these effects are exaggerated when NEP and ACE are inhibited. Topically instilled bradykinin causes vascular extravasation to a large extent via NK1 receptor stimulation, thus suggesting a major role for tachykinins released from sensory nerve endings.

Animals↗
PubMed1993

Neurogenic vasodilation in the rat nasal mucosa involves neurokinin1 tachykinin receptors.

We studied the role of different tachykinin receptors in mediating neurogenic vasodilation in the nasal mucosa of anesthetized pathogen-free rats. Three successive determinations of blood flow were made by injecting radionuclide-labeled microspheres suspended in 70% dextrose into the left ventricle. A selective agonist of the tachykinin NK1 receptor increased nasal blood flow, but neurokinin NK2- and NK3-selective agonists were without effect. The natural agonist of NK1 receptors, substance P (1 microgram/kg), increased nasal blood flow, an effect that was abolished by the selective NK1 receptor antagonist (+)-(2S,3S)-3-(2-methoxybenzylamino)-2-phenylpiperidine (CP-99,994). Capsaicin (25 micrograms/kg), a drug that releases tachykinins from sensory nerves, increased nasal blood flow, and this effect was significantly reduced by CP-99,994. We conclude that a significant component of neurogenic vasodilation in rat nasal mucosa is due to the stimulation of NK1 tachykinin receptors.

Animals↗
PubMed1993

Neurogenic plasma extravasation in the rat nasal mucosa is potentiated by peptidase inhibitors.

The increase in vascular permeability associated with neurogenic inflammation in the nasal mucosa is mediated by neuropeptides such as substance P released from sensory nerves. Substance P is degraded by the peptidases neutral endopeptidase-24.11 (NEP-24.11) and angiotensin converting enzyme (ACE). In the present study, we used capsaicin to produce neurogenic inflammation in the nasal mucosa of rats, and we examined the effect of inhibition of NEP-24.11 by phosphoramidon, inhibition of ACE by captopril or inhibition of both enzymes by giving both inhibitors. Using as tracers intravenous Evans blue dye to quantify the extravasation and Monastral blue pigment to localize the sites of leakage, we examined the magnitude and distribution of capsaicin-induced plasma extravasation in the nasoturbinates, maxilloturbinates, ethmoidal turbinates and septum. Capsaicin caused a dose-dependent increase in Evans blue extravasation in the naso- and maxilloturbinates but had only a slight effect in the septum. The leaky blood vessels responsible for this plasma extravasation, as manifested by Monastral blue labeling, were most numerous in the naso- and maxilloturbinates, particularly near the front and free borders. After phosphoramidon, the leakage of Monastral blue was more widespread and extended in a more caudal direction. The response to capsaicin was augmented by phosphoramidon alone but not by captopril alone. However, in the presence of phosphoramidon, captopril further augmented the capsaicin-induced extravasation. We conclude that neurogenic inflammation in the rat nasal mucosa is greatest in the naso- and maxilloturbinates and can be modulated by NEP-24.11 and, to a lesser extent, by ACE.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Butenes and butadiene in urban air.

Samples of urban air hydrocarbons were taken on specifically made adsorbent cartridges and analysed by gas chromatography after thermal desorption. The four isomeric butenes and 1,3-butadiene were favourably resolved and separated from the abundant alkanes on an aluminium oxide PLOT column. The concentrations of butadiene, reflecting outdoor urban exposure, were in the range of 0.5-5 micrograms/m3. An approximate 1:4 ratio was observed between butadiene and propene which both originate predominantly from vehicle exhaust. The four butenes made up approximately 50% of the propene concentration in exhaust-polluted air, with methylpropene greater than 1-butene greater than trans-2-butene greater than cis-2-butene. Petrol vapour contributed less than exhaust but about five times more to the 2-butenes than to methylpropene and 1-butene. The highest exposure levels of butadiene and butenes were consistently observed in the vicinity of exhaust pipes and petrol-fuelled vehicles.

Air Pollutants↗
PubMed1992

Photoionization assessment of C3-C5 alkadienes and alkenes in urban air.

Hydrocarbons from samples of traffic-polluted urban air were separated by gas chromatography on an aluminium oxide column and assessed simultaneously by photoionization detection (PID) and flame ionization detection (FID) after effluent splitting. The 10.2 eV photoionization detector selectively detects alkadienes and alkenes but not alkanes and alkynes in the C3-C5 region. The maximum PID/FID response ratio for alkadienes and alkenes is also obtained in this region. The analytical system as a whole is particularly favourable for the C3-C5 alkenes. Analytical data are given for propadiene, 1,3-butadiene, propene, butenes and pentenes.

Air Pollutants↗
PubMed1991

Exposure of commuters to volatile aromatic hydrocarbons from petrol exhaust.

Twenty-two volatile aromatic hydrocarbons were determined in the air of an automobile during commuting. Sampling was made on Tenax cartridges and laboratory determinations were carried out using thermal desorption combined with temperature-programmed capillary gas chromatography. Selected hydrocarbons representative of petrol exhaust were determined in the automobile and in an electric commuter train during eight parallel commuter trips. In the automobile, the concentrations of benzene were 35-70 micrograms/m3 and those of total aromatic hydrocarbons 200-400 micrograms/m3. The petrol exhaust levels were 5-10 times higher in the automobile than in the compartment of the commuter train.

Air Pollution↗
PubMed1990

Hazardous petrol hydrocarbons from refuelling with and without vapour recovery.

Hydrocarbons in air were determined at pioneering European service stations equipped with vapour recovery systems. Vapour recovery was found capable of eliminating 99% of exposure during refuelling and greater than 95% of emissions to air. Vapour recovery is now being rapidly introduced at Swedish service stations as a result of demands concerning environmental and health hazards. The analytical technique used permitted samples corresponding to a single refuelling procedure to be analyzed. Sampling on an adsorbent tube was followed in the laboratory by thermal desorption and capillary gas chromatography. All prominent hydrocarbons were well separated on a methylsilicone phase. These include benzene and the alkenes of special interest with respect to health hazards. The particular importance of alkenes with respect to the formation of ozone and other photooxidants is discussed. The four isomeric butenes and the six isomeric pentenes were determined and found to constitute approximately 10% by weight of the petrol vapour. The highly reactive 2-alkenes were more abundant than the 1-alkenes.

Air Pollutants↗
PubMed1990

Nasal mucosal permeability after methacholine, substance P, and capsaicin challenge in the rat.

Nasal permeability was studied in anaesthetized rats after topical challenge with methacholine (MC), substance P (SP), or capsaicin. The drugs were applied onto strips of filter paper. After drying, they were inserted into one side of the nasal cavity while the other side received strips without drugs. The filter paper strips were used not only to stimulate secretion but also to collect the resulting fluid. FITC-albumin was given i.v. and the amount appearing in the nasal fluid was captured on the strips and measured by fluorometry. The presence of FITC-albumin in nasal secretions reflects a leakage of plasma through the capillary endothelium and the nasal epithelium. MC, SP, and capsaicin stimulated the secretion of nasal fluid. SP and capsaicin, but not MC increased the concentration of FITC-albumin in the nasal fluid.

Animals↗
PubMed1989

Hyperosmolarity but not histamine evokes secretion of nasal fluid in the rat.

Histamine (dihydrochloride or free base), mannitol or sodium chloride applied topically to the nasal mucosa of anaesthetized rats stimulated the secretion of fluid in a dose-dependent manner. Compound 48/80 applied in the same way and histamine given s.c. failed to evoke secretion. The secretion evoked by topically applied histamine was resistant to pretreatment with H1 and H2 receptor antagonists i.p. Furthermore, the secretion evoked by histamine and sodium chloride was resistant to pretreatment with atropine i.p. or lidocaine topically. The secretion evoked by mannitol or by sodium chloride was not reduced by H1 receptor antagonists and was not significantly different from that obtained after challenge with histamine of equivalent osmolality. We conclude that the response to topically applied histamine reflects the hyperosmolarity of the compounds applied and not the effect of histamine on histamine receptors.

Animals↗
PubMed1989

Capsaicin evokes secretion of nasal fluid and depletes substance P and calcitonin gene-related peptide from the nasal mucosa in the rat.

1. The secretion of nasal fluid was studied in anaesthetized rats after topical application of capsaicin, and of calcitonin gene-related peptide (CGRP) alone or CGRP in combination with substance P (SP). The flow of nasal fluid was stimulated and the secretions collected by a filter paper technique. The concentrations of SP and CGRP in nasal biopsies were determined after topical or systemic administration of capsaicin. 2. Capsaicin (single dose administration) stimulated nasal secretion in a dose-dependent manner. The effect was inhibited by hexamethonium, lignocaine, or by the tachykinin antagonist (D-Pro2, D-Trp7,9)-SP, but not by atropine, or by a combination of the histamine H1-receptor antagonist chlorpheniramine and the H2-receptor antagonist ranitidine. 3. When applied cumulatively, capsaicin rapidly produced desensitization. The concentrations of SP and CGRP in the nasal mucosa were reduced by capsaicin 6 days after topical or s.c. administration but not 15 min after topical application of desensitizing doses. 4. CGRP did not stimulate the secretion of nasal fluid and did not alter SP-evoked nasal secretion. 5. The inhibition by hexamethonium of the capsaicin-evoked nasal secretion suggests the involvement of ganglionic reflexes. In addition, the inhibition of the response to capsaicin by (D-Pro2,D-Trp7,9)-SP and lidocaine and the depletion of SP and CGRP after capsaicin indicate the involvement of tachykinin-mediated axon reflexes.

Animals↗
PubMed1989

Substance P and nasal secretion in dog, rat, and man.

The effect of substance P (SP) on nasal secretion was studied in dog, rat, and man. Substance P was administered topically by the use of filter papers that had been soaked with an aqueous solution of SP and dried. The SP-containing filter paper strips were applied to the nasal mucosa for five minutes. The secretion was absorbed onto the filter papers. The strips were weighed before and after the experiment. Substance P induced atropine-resistant nasal secretion in a dose-dependent manner in anaesthetized dogs and rats. In man, SP failed to evoke nasal secretion in the doses applied. Systemic effects limited the dose that could be given to man. When exposed to nasal secretions SP was rapidly degraded. This may explain the failure of SP to evoke nasal secretion in man.

Animals↗
PubMed1986

Clinical history, skin prick test and RAST in the diagnosis of birch and timothy pollinosis.

The diagnostic efficacy of clinical history (CH), skin prick test (SPT) and RAST was estimated in relation to nasal and conjunctival provocation tests (NPT, CPT) in 69 patients with seasonal rhinoconjunctivitis. The extracts used were freeze-dried, and biologically standardized birch and timothy allergen preparations matched to the extracts on Phadebas RAST discs. Based on single determinations the sensitivity, specificity and predictive values were calculated. There were highly significant (P less than 0.001) correlations between all parameters: NPT, CPT, CH, SPT and RAST. For birch the combination of SPT and RAST made the PTs superfluous as both sensitivity and specificity then reached 100%. With timothy the sensitivity was 97% and with the addition of CH 100%. However, the specificity was only 79% through combining CH, SPT and RAST. The present study using the same standardized allergen preparation in all tests showed a good correlation between indirect test results and provocation tests.

Allergens↗
PubMedDate not supplied

Effect of recombinant neutral endopeptidase (EC 3.4.24.11) on neuropeptide-mediated nasal fluid secretion and plasma exudation in the rat.

The nasal mucosa harbors sensory nerves containing neuropeptides such as substance P (SP), which are released by capsaicin. The neuropeptides are degraded by peptidases, e.g., neutral endopeptidase (NEP) that is present in the nasal mucosa. We studied the effect of enzymatically active recombinant NEP (rNEP) on neuropeptide-evoked secretion of nasal fluid and plasma exudation in rats. rNEP administered intranasally (i.n.) reduced the capsaicin-evoked nasal fluid secretion but failed to reduce the secretion evoked by SP (exogenous) under the experimental conditions used. rNEP reduced the increase in nasal plasma exudation evoked by capsaicin (endogenous neuropeptides). Because rNEP reduced neuropeptide-mediated nasal fluid secretion and plasma exudation in the rat, we suggest that peptidase activity in the nasal mucosa will determine the magnitude of the response to locally released neuropeptides.

Administration, Topical↗