Biomedical subjects

N G Carroll

Publications and source records attributed to N G Carroll.

6 recordsLinked to original sources

PubMed2006

Do bronchial biopsies represent mast cell density in airways? A stereological study.

Endobronchial biopsy specimens may not adequately represent inflammatory cell counts throughout the airway wall. The present study aimed to compare mast cell density in biopsies and airway sections using both stereological and nonstereological methods. Post mortem biopsies and adjacent transverse sections were obtained from a mean of five proximal airways per case in 10 subjects who had died of nonrespiratory causes. Tryptase-positive mast cells were measured stereologically in 30-mum sections and nonstereologically in 5-microm sections using an optical disector (cells x mm(-3)) and cell profiles (cells x mm(-2)), respectively. Reference areas included the inner and total airway wall and to 100 microm below the basement membrane. Case means, based on four or more biopsy sites, significantly correlated with those on transverse sections for counts over the inner airway wall only, using both stereological and nonstereological methods. Cells x mm(-3) and cells x mm(-2) were significantly correlated within all reference areas. When endobronchial biopsies are obtained from at least four proximal airways per case, inter-subject comparisons of mean mast cell density in the inner airway wall are as well represented by counts on biopsies as they are on transverse sections. This is the case using either three-dimensional, stereological or two-dimensional, nonstereological methods.

Adolescent↗

PubMed2002

Increased mast cells and neutrophils in submucosal mucous glands and mucus plugging in patients with asthma.

BACKGROUND: Mucus plugging of the airways is invariably seen in cases of fatal asthma, mucus production is associated with asthma attacks, and the area of submucosal glands is increased in asthma. Mediators secreted from mast cells and neutrophils can stimulate mucous gland secretion. A study was undertaken to count the mast cells and neutrophils in submucosal glands and to relate cell numbers to the presence of mucus in the airway lumen. METHODS: Cartilaginous airways obtained at necropsy from cases of fatal asthma (n=8), non-fatal asthma (n=8), and control cases (n=8) were examined. Contiguous transverse sections were stained for mast cell tryptase and neutrophil elastase, and with Periodic Acid Schiff solution to identify mucus. Mucous gland area, lumen area, and the percentage of the relaxed lumen area occupied by mucus (mucus occupying ratio, MOR) were measured. Mast cells (intact and degranulated) and neutrophils per area of submucosal gland were calculated. RESULTS: Compared with controls, the cases of fatal asthma had increased mucous gland area, MOR, percentage of degranulated mast cells, and numbers of neutrophils in the submucosal glands (p<0.05). In cases of non-fatal asthma the MOR and the numbers of mast cells and neutrophils in the submucosal glands were increased (p<0.05). When all cases were pooled together, the MOR correlated with the total number of mast cells (r=0.55, p=0.005) and with the number of degranulated mast cells in the submucosal glands (r=0.51, p=0.013), but not with the number of neutrophils (r=0.21, p=0.121). CONCLUSION: These results show that mucous gland area, MOR, and mucous gland inflammation are increased in asthma and that degranulation of mast cells may contribute to secretion of mucus into the lumen in cases of fatal asthma.

Adult↗

PubMed2002

Distribution and degranulation of airway mast cells in normal and asthmatic subjects.

It was hypothesized that the distribution and activation of mast cells across the airway wall may reflect their function in asthma. The density of mast cells (intact and degranulated) within airway compartments in cartilaginous and membranous airways, obtained from autopsies on patients with fatal asthma, nonfatal asthma, and nonasthmatic control cases have been examined. In cartilaginous airways, the mean+/-SE density of mast cells in control cases was 27+/-9 cells x mm(-2). It was similar in nonfatal asthma (24+/-2 cells x mm(-2)) but reduced (p<0.05) in fatal asthma cases (16+/-2 cells x mm(-2)). In membranous airways, the density of mast cells in control cases was 155+/-21 cells x mm(-2) and was higher (p<0.05) in cases of nonfatal (270+/-51 cells x mm(-2)) and fatal asthma (219+/-26 cells x mm(-2)). Mast-cell density was greatest on the smooth muscle and mucous glands in cartilaginous airways and on the smooth muscle and outer airway wall in membranous airways. The percentage of degranulated mast cells was higher (p<0.05) in cases of asthma, related to disease severity, and was higher in cartilaginous than membranous airways. Degranulation was greatest on the smooth muscle in fatal asthma cases. Mast-cell distribution and degranulation varies between cartilaginous and membranous airways and across the airway wall. Degranulation of mast cells is related to asthma severity. The increased degranulation in proximal airways may reflect stimulation via the inhaled route.

Adolescent↗

PubMed2000

The airway longitudinal elastic fiber network and mucosal folding in patients with asthma.

A submucosal network of elastic fibers in a collagen and myofibroblast matrix form discrete longitudinal bundles (LB) in the bronchial tree. The LB may affect airway function by altering the mechanical properties of the airway wall or by changing the folding behavior of the airway mucosa. The area and number of LB were quantified from 12 cases each of fatal asthma (FA), nonfatal asthma (NF), and nonasthmatic (NA) control cases on elastic-trichrome stained airways. The effects of group, sex, age, and smoking were examined using multiple linear regression. The area fraction of LB increased (p < 0.05) approximately twofold in cases of FA compared with NA control cases in both large and small airways. The areas of LB were increased in smokers, older subjects, and men (p < 0.05). The number of mucosal folds was related to the number of longitudinal bundles in asthmatics and nonasthmatics and was not different between groups. Collagen and myofibroblasts were increased (p < 0.05) in LB of FA and NF cases compared with NA control cases. The increased size and altered composition of LB in asthma may influence airway function; however, excessive airway narrowing in asthma is not due to altered numbers of mucosal folds.

Adult↗

PubMed1997

Bronchial blood vessel dimensions in asthma.

The extent to which the bronchial vasculature contributes to airway wall thickening in large and small airways in patients with asthma is unknown. The aim of this study was to quantify the number and the area occupied by blood vessels in the airway submucosa of patients with and without asthma. We used the monoclonal antibody Factor VIII to measure the blood vessels between the airway basement membrane and the outer border of the smooth muscle. In large cartilaginous airways in patients with fatal asthma, the number and area of large blood vessels were increased and the number and area of small blood vessels were decreased, compared with that in patients with nonfatal asthma and control subjects. However, the total number of blood vessels and the total area occupied by blood vessels per square millimeter in the airway submucosa were similar in patients with fatal asthma or nonfatal asthma and in control subjects in all airway size groups. Blood vessels were distended to a mean value of 80% of their estimated maximal area. The increased number of larger vessels in patients with fatal asthma raises the possibility that vascular congestion associated with an acute severe asthma attack may distend blood vessels. The finding of similar numbers of blood vessels per square millimeter of submucosa in control subjects and in patients with asthma suggests that blood vessels increase in number in patients with asthma only in proportion to increased airway wall area. It is unlikely that submucosal vessels could act as capacitance vessels and significantly alter inner airway wall thickness.

Adult↗

PubMed1996

Is salmeterol ergogenic?

OBJECTIVE: To assess the effects of 50 micrograms of inhaled salmeterol on pulmonary function, selected physical capacities, and fine motor control in 16 nonasthmatic male cyclists and triathletes, mean age of 23.2 (SD = 3.5) years. DESIGN: Randomized double-blind placebo-controlled crossover trial. SETTING: Human Physical Performance Laboratory, the University of Western Australia. SUBJECTS: Sixteen healthy male high-performance nonasthmatic athletes with a mean age of 23.2 years participated in the study. INTERVENTION: Subjects attended three experimental testing sessions at which salmeterol (50 micrograms), a placebo, or "no treatment" was administered in random order in a double-blind fashion, on separate occasions, prior to exercise. MAIN OUTCOME MEASURES: During each testing, session lung function was measured before and 10 min after the treatment. Tests of reaction time and hand steadiness and then two anaerobic cycle tests followed. The first, a 10-s all-out sprint was followed, after a 3-min rest, by a 30-s all-out sprint performed on a front access bicycle ergometer. After 10 min recovery, leg flexion-extension peak torque was measured on a Biodex isokinetic dynamometer at speeds of 120 and 180 degrees s-1. MAIN RESULTS: Lung function variables, reaction time, movement time, alactic anaerobic power, lactacid anaerobic power, and leg-flexion and leg-extension muscular strength were similar among the three treatment groups. CONCLUSIONS: The preexercise administration of 50 micrograms of inhaled salmeterol has no performance-enhancing effects in nonasthmatic athletes. We believe that athletes with asthma should be permitted to use salmeterol before competition.

Administration, Inhalation↗