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Biomedical subjects

P Bradding

Publications and source records attributed to P Bradding.

44 records · Page 3Linked to original sources
PubMed1992

Interleukin 4 is localized to and released by human mast cells.

Recent attention has focused on the T helper type 2 (Th2) lymphocyte as a source of interleukin 4 (IL-4) in allergic disease. However, Th2 cells themselves require a pulse of IL-4 to initiate this synthesis. Here we provide immunohistochemical evidence of IL-4 localization to human mast cells of the skin and respiratory tract, and demonstrate that immunoglobulin E-dependent stimulation of purified human lung mast cells leads to the rapid release of IL-4 into the extracellular environment. We propose that mast cell activation in an allergic response provides a rapid and local pulse of IL-4 into the local environment essential for the triggering of T lymphocytes into sustained IL-4 production and to initiate inflammatory cell accumulation and activation.

Culture Techniques↗
PubMed1991

A simultaneous, noninvasive comparison with sinus rhythm, of two activity sensing, rate adaptive pacemakers, in an elderly population.

We compared the rate response to low level work, arm exercise, step testing, and treadmill exercise between the Siemens Sensolog 703 S (Sg) and the Medtronic Activitrax (Ax) pacemakers, and simultaneous sinus rhythm (SR) in an elderly population. In ten subjects mean age 70.6 years, range 49-81 years, the pacemaker responses were noninvasively compared by strapping the units to the chest wall under constant and equal pressure applied by an adjustable belt. Pacemaker rates and SR were recorded simultaneously on a three-channel ECG recorder. The units were programmed in situ to give an increase in rate from 70 beats/min sitting, to 100 beats/min after walking at a normal pace for 30 seconds. Programming took three times longer for Sg (P less than 0.02). The response to standing and bending was poor for both units (Ax mean 75.7 beats/min, Sg mean 77.6 beats/min), when compared to SR (mean 90.3 beats/min). A 20-step test resulted in a greater rate response from Ax (mean 105.3 beats/min) than from Sg (mean 96.3 beats/min [P = 0.09]), though both were still less than SR (116.3). There were significant differences between the two pacemakers on treadmill testing, at peak rate achieved (Ax mean 112.5 beats/min; Sg mean 102.7 beats/min [P less than 0.005], SR mean 122.5 beats/min) and at end exercise (Ax mean 112.5 beats/min; Sg mean 92.9 beats/min [P less than 0.002], SR mean 121.3 beats/min). Arm exercise, however, resulted in a significantly greater response from Sg than Ax (105.1 and 88.5 beats/min, respectively; P less than 0.01, SR 98.7 beats/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Activities of Daily Living↗
PubMed1988

Bronchoconstrictor and antibronchoconstrictor properties of inhaled prostacyclin in asthma.

Prostacyclin (PGI2) is generated in appreciable amounts during allergic reactions in human lung tissue. To define its activity on human airways we have studied the effects of doubling concentrations of inhaled PGI2 and its hydrolysis product 6-oxoprostaglandin F1 alpha (6-oxo-PGF1 alpha) on specific airway conductance (sGaw), maximum expiratory flow at 30% vital capacity (Vmax30), forced expiratory volume in 1 s (FEV1), and static lung volumes in subjects with mild allergic asthma. In a second study the effect of inhaled PGI2 on bronchoconstriction provoked by increasing concentrations of inhaled prostaglandin (PG) D2 and methacholine was observed. Inhalation of PGI2 up to a concentration of 500 micrograms/ml had no significant effect on sGaw but produced a concentration-related decrease in FEV1 and Vmax30 in all subjects. In two of four subjects inhalation of PGI2 also increased residual volume and decreased vital capacity but had no effect on total lung capacity. PGI2, but not 6-oxo-PGF1 alpha, protected against bronchoconstriction provoked by either PGD2 or methacholine whether airway caliber was measured as sGaw, FEV1, or Vmax30. The apparent disparity between the bronchoconstrictor and antibronchoconstrictor effects of PGI2 might be explained by its potent vasodilator effect in causing airway narrowing through mucosal engorgement and reducing the spasmogenic effects of other inhaled mediators by increasing their clearance from the airways.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

The combined effects of two pairs of mediators, adenosine with methacholine and prostaglandin D2 with histamine, on airway calibre in asthma.

Mediators released from mast cells and secondary effector cells in the airways contribute to bronchoconstriction of allergic asthma. This study investigates methods for defining the effect of two inflammatory mediators on airway calibre in asthma. In an initial study on three asthmatic subjects, subconstrictor (subthreshold) concentrations of two mast cell derived mediators, histamine and prostaglandin (PG) D2, produced similar displacement to the left of a histamine concentration-specific airways conductance (sGaw) response curve. With both agonists enhancement of histamine-induced bronchoconstriction was greater at low histamine concentrations. Since potentiation of histamine-induced bronchoconstriction was independent of the class of subconstrictor agent given, it is likely to represent a physiological rather than a pharmacological interaction. During provoked asthma different constrictor mediators are likely to be released simultaneously into the airways. A method was therefore devised to investigate the combined effect of equiconstrictor concentrations of two mediators on airway calibre. Two pairs of inhaled bronchoconstrictor agonists were chosen for study: adenosine with methacholine and PGD2 with histamine. For each agonist, concentration-sGaw response curves were constructed, from which were derived the provocation concentrations of agonist causing a 25% fall in sGaw from baseline (PC25) and required to further this to 50% (PC50-25). On separate days, eight subjects received paired inhalations of methacholine-adenosine, methacholine-methacholine and adenosine-adenosine. The concentration used for the first inhalation was the PC25 value and for the second inhalation the PC50-25 value. Before, immediately after the first inhalation, and at regular intervals after the second inhalation, sGaw was followed for 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗