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Biomedical subjects

M J Matheson

Publications and source records attributed to M J Matheson.

11 recordsLinked to original sources
PubMed2003

Low lung volume alters contractile properties of airway smooth muscle in sheep.

Breathing at volumes lower than functional residual capacity (FRC) can induce changes in nonasthmatic airways consistent with the behaviour of asthmatic airways. This study investigated the chronic effect of breathing at volumes lower than FRC on the contractility of airway smooth muscle and myosin light chain kinase (MLCK) content and activity. Sheep of three age groups (neonate, adolescent and adult) had their FRC reduced by approximately 25%, for 4 weeks using a leather corset. Contractile responses to carbachol were then recorded in isolated tracheal strips and bronchial rings. MLCK content and activity were assessed by immunoblotting. The rate of stress generation increased in the bronchial smooth muscle of both adult and adolescent but not neonatal corseted sheep: adolescent corseted versus control, 65.0 +/- 4.1 versus 103.4 +/- 7.0 s (to reach 50% maximum stress), respectively; and adult corseted versus control, 57.0 +/- 6.4 versus 93.4 +/- 8.2 s, respectively. This was not due to increases in either bronchial or tracheal smooth muscle amount or MLCK content and activity. The present results indicate that chronic breathing at low lung volumes increases the rate of stress generation in airway smooth muscle.

Animals↗
PubMed1997

Tachykinins do not cause plasma leakage in the rabbit trachea.

The aim of this study was to determine if neuropeptides mediate increases in airway microvascular leakage in the rabbit. New Zealand white rabbits were anaesthetised and challenged with either capsaicin (50 mg/kg s.c. or i.p.) or substance P (10(-3) or 10(-4) nebulised or 1 microgram/kg i.v.) or vagally stimulated with a range of pulse trains (5-15 Hz, 5-15 V, 0.2-2 msec). Microvascular leakage was assessed using the Evans blue dye technique. A further two groups of rabbits were challenged with nebulised metabisulphite (100 mg) or phosphate buffered saline to serve as positive and negative controls. Challenge with capsaicin, substance P or vagal stimulation did not significantly increase tracheal or bronchial Evans blue concentrations above negative control levels. We conclude that neuropeptides do not mediate increases in microvascular leakage in the major airways of the rabbit.

Animals↗
PubMed1997

Role of platelet activating factor, leukotrienes and polymorphs in the FMLP induced increase in microvascular leakage in rabbit trachea.

This study was designed to determine the time course of N-formyl-methionyl-leucyl-phenylalanine (FMLP) induced microvascular leakage in the airways of anaesthetized, tracheostomized New Zealand white rabbits. We have previously shown that FMLP increases microvascular leakage in the rabbit trachea at 30 min post challenge. A further aim was to determine the mechanisms underlying this response. Microvascular leakage was assessed using the albumin binding dye, Evans blue which was injected intravenously (50 mg/kg) immediately prior to FMLP challenge (10 mg nebulised for 2 min) or the control (dimethylsulphoxide/saline). Microvascular leakage was assessed in the trachea and bronchi at 15 min, 22.5 min, 45 min and 120 minutes with n = 6 for each group. The only significant difference between control and FMLP challenged groups was at 45 min in the bronchi (FMLP 77.6 +/- 12.2, control 33.4 +/- 5.7, P < 0.05). To determine the mechanism underlying FMLP-induced increases in microvascular leakage rabbits were treated with one of the following: (i) nitrogen mustard (1.75 mg/kg intravenously), which depletes circulating polymorphs (n = 6); (ii) the platelet activating factor (PAF) receptor antagonist WEB 2086 (10 mg/kg; n = 5); (iii) the Cys-LTR1 receptor antagonist ICI198615 (nebulised 10(-4) mol/L), or challenged with the thromboxane agonist U46619. Tracheal Evans blue concentration was assessed at 30 min after FMLP challenge and compared with the appropriate control. Treatment with WEB 2086 significantly (P < 0.05) reduced tracheal microvascular leakage (FMLP 76.3 +/- 13.1 WEB 2086/FMLP 31.4 +/- 3.7 micrograms/g trachea) as did ICI198615 (FMLP 69.8 +/- 11.5 ICI198615/FMLP 30.0 +/- 5.7). In conclusion FMLP induced an increase in tracheal microvascular leakage which was significant in the bronchi at 45 min and this increase was mediated by platelet activating factor and the sulphidopeptide leukotrienes C4 and D4.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

Use of the Sensormedics MCT Accelerator in sputum induction.

Airway inflammation can be studied by obtaining sputum induced by inhalation of 3% saline. The Sensormedics MCT accelerator is an oral asymmetrical high frequency oscillator which safely enhances clearance of airway secretions. The aim of this study was to determine if use of the MCT Accelerator enhances sputum production in non-asthmatic non-atopic, atopic and asthmatic subjects. Fifteen subjects were studied over 3 days. On day 1 skin prick testing to common aeroallergens and methacholine bronchial reactivity were performed. On days 2 and 3, separated by 7 days, sputum was induced by inhalation of 3% saline alone for 30 mins or via the nebulizer port of the MCT Accelerator. The cellular profile and volume of sputum were analysed. The use of the MCT Accelerator did not alter the cellular profile of the induced sputum nor was there an increase in volume. In conclusion the induction of sputum by inhalation of 3% saline was not altered by use of the MCT Accelerator.

Asthma↗
PubMed1995

The protective effect of indomethacin on photocarcinogenesis in hairless mice.

Orally administered indomethacin at 10-600 micrograms per mouse per day has been shown to inhibit UV radiation-induced erythema dose responsively. At the higher doses tested (200-600 micrograms) there was evidence of drug toxicity. Indomethacin administered orally at 20 micrograms per mouse daily during photocarcinogenesis induction both increased the probability of remaining tumour free and reduced the average tumour multiplicity. When indomethacin was administered only during the UV irradiation period (initiation), a reduction in tumour multiplicity and in the progression of tumours to malignant squamous cell carcinomas was observed; when administered only during the post-irradiation promotion period, there was a significant increase in the probability of remaining tumour free. Thus both tumour initiation and promotion by UV radiation appear to be indomethacin-sensitive, possibly affected by different mechanisms.

Animals↗
PubMed1993

Inhaled FMLP increases microvascular permeability in the rabbit trachea.

This study was designed to determine the effect of inhaled N-formyl-methionyl-leucyl-phenylalanine (FMLP) on microvascular permeability in the rabbit trachea and to determine if the effect could be modified by cholinergic antagonism, neutral endopeptidase (NEP) inhibition, opioid receptor antagonism, or an opioid agonist. New Zealand White rabbits were anesthetized and pretreated intravenously with one of the following: saline, dimethyl sulfoxide (DMSO) (both controls), thiorphan, phosphoramidon (both NEP inhibitors), thiorphan and naloxone, morphine, or atropine. All rabbits were then given intravenous Evans blue before inhalation of nebulized DMSO (control) or FMLP. Extravascular tracheal Evans blue concentration was subsequently determined spectrophotometrically. FMLP caused a highly significant increase in microvascular permeability (92.6 +/- 7.1 micrograms/g of trachea, control 20.4' +/- 3.4). The effect of FMLP was significantly modified by cholinergic blockade (61.1 +/- 6.9) and by NEP inhibition (thiorphan 38.8 +/- 5.6, phosphoramidon 52.6 +/- 4.2). This effect of NEP inhibition could be reversed by concurrent treatment with the opioid receptor antagonist naloxone (95.9 +/- 34.6). Morphine had no significant effect. We concluded that FMLP increases microvascular permeability, which may in part explain the effect of FMLP on airway resistance in the rabbit. Inhibiting NEP decreases the response possibly through an effect on endogenous opioids. The response appears to be partially vagally mediated.

Administration, Inhalation↗
PubMed1991

The effect of the antihistamine cimetidine on ultraviolet-radiation-induced tumorigenesis in the hairless mouse.

This experiment investigated the effect on ultraviolet (UV) radiation-induced tumorigenesis of feeding the histamine type 2 receptor antagonist, cimetidine, to Skh:HR mice. Cimetidine was fed to one group during a 70 day period of chronic UVR (5 days/week for 10 weeks), to a second group from the end of this period to the end of the experiment at 286 days and a third group was fed a control diet only throughout the experiment. Feeding mice cimetidine during the 70 day period of irradiation protected them against the later development of skin tumours.

Animals↗
PubMed1976

Incorporation of mitochondrial membrane proteins into liposomes containing acidic phospholipids.

Cytochrome oxidase, QH2-cytochrome c reductase, and the oligomycin-sensitive adenosine triphosphatase were incorporated into liposomes by a new procedure which yielded unidirectional orientation of the proteins. Cytochrome oxidase was reconstituted in the mitochrondrial orientation and the adenosine triphosphatase in the submitochondrial orientation. Reconstitutions were achieved by incubating the proteins at room temperature with liposomes which contained phosphatidylcholine, phosphatidylethanolamine, and an acidic phospholipid (cardiolipin, phosphatidylinositol, or phosphatidylserine). The incorporation occurred without added detergent or sonication. This incorporation procedure may serve as a model for the insertion of proteins in vivo.

Adenosine Triphosphatases↗