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Biomedical subjects

J G Kirby

Publications and source records attributed to J G Kirby.

8 recordsLinked to original sources
PubMed1989

Effect of indomethacin on allergen-induced asthmatic responses.

Previous studies have suggested that inhibition of the cyclooxygenase pathway of arachidonic acid metabolism may suppress the late asthmatic responses to inhaled allergen. Both human and animal studies have suggested that prostanoids may also be involved in increases in airway responsiveness after ozone and allergen. We studied seven atopic subjects, who had a dual asthmatic response to inhaled allergen, during a control period and then after pretreatment with indomethacin (50 mg) or placebo twice daily for 2 days, administered in a randomized, double-blind manner. Indomethacin had no significant effect on the base-line airway responsiveness to histamine (P = 0.22) or the allergen-induced early or late asthmatic response (P = 0.49). However, indomethacin inhibited the increase in airway responsiveness (express as histamine PC20) after allergen inhalation. The log difference in preallergen to postallergen histamine PC20 was 0.49 +/- 0.08 (SE) during the control period, 0.46 +/- 0.08 (SE) after placebo (P = 0.81), and 0.22 +/- 0.10 (SE) after indomethacin (P = 0.02). Although indomethacin is useful for examining the role of cyclooxygenase products in asthmatic responses, it should not be considered in the treatment of asthma. We conclude that cyclooxygenase products are not significant mediators of allergen-induced early or late asthmatic responses but are involved in the pathogenesis of airway hyperresponsiveness after allergen inhalation.

Adult↗
PubMed1987

Bronchoalveolar cell profiles of asthmatic and nonasthmatic subjects.

Asthma is associated with increased airway responsiveness to pharmacologic agents such as methacholine. Increases in airway responsiveness after exposure to allergen or ozone are associated with increased inflammatory cells in bronchoalveolar lavage both in human and in animal studies. We studied the total and differential cell counts in 10 stable atopic asthmatics who had airway hyperresponsiveness but no clinical features of airway inflammation and 10 nonasthmatic subjects, using a conventional 100-ml lavage and a 20-ml washing. Metachromatic cell numbers and eosinophils were increased in both the lavage (p less than 0.01 for metachromatic cells; p = 0.05 for eosinophils) and washing (p less than 0.025 for metachromatic cells and p = 0.03 for eosinophils) compared with those in nonasthmatics. In asthmatics, metachromatic cell numbers in the lavage and washing, and total cell count and, to a lesser extent, eosinophils in lavage were significantly correlated with measurements of airway responsiveness. Major basic protein in lavage and blood did not differ between asthmatics and nonasthmatics. The washing, although it revealed a different cell profile from the lavage in both normal subjects and asthmatics, did not show differences between asthmatics and nonasthmatics undetected by the lavage specimen. We conclude that there is evidence of cellular inflammation in the airway of stable asthmatics and that small volume washings do not add to the information concerning the cell profile of asthmatics and nonasthmatics provided by conventional lavage.

Asthma↗
PubMed1987

Bronchoalveolar lavage does not alter airway responsiveness in asthmatic subjects.

Bronchoalveolar lavage (BAL) during fiberoptic bronchoscopy is being used increasingly for the investigation of asthma. Airway responsiveness to methacholine is a sensitive indicator of the presence and severity of asthma. Therefore, we studied the effect of BAL on methacholine airway responsiveness in stable asthmatics. Geometric mean methacholine PC20 was 1.34 mg/ml before and 1.80 mg/ml after BAL (p = 0.26) in asthmatics. Immediate symptoms of airway narrowing after BAL occurred only in the 3 asthmatics with moderate to severe hyperresponsiveness. These symptoms were rapidly relieved by inhaled bronchodilator. There was no relationship between the occurrence of symptoms and the amount of topical lidocaine used for local anaesthesia or the volume of lavage fluid returned. The absence of an effect of BAL on airway responsiveness supports the safety of this procedure in the controlled asthmatic patient with near normal FEV1, irrespective of the level of baseline airway responsiveness.

Albuterol↗
PubMed1986

Total lung capacity does not change during methacholine-stimulated airway narrowing.

The accurate measurement of changes in flow rates from partial flow-volume curves depends on their measurement at the same lung volume. This lung volume can be standardized from total lung capacity (TLC) if this does not change at the same time. We examined the effect of methacholine-stimulated maximal airway narrowing [change in mean forced expiratory volume in 1 s (delta FEV1) = 26.4%] on TLC, measured by whole-body plethysmography, in 10 normal subjects and of moderate airway narrowing (mean delta FEV1 = 34.9%) in 10 asthmatics. The TLC changed from 5.88 to 6.03 liters in normal subjects (P greater than 0.05) and from 6.92 to 6.95 liters (P greater than 0.5) in asthmatics. The results of this study suggest that TLC does not change significantly after methacholine-stimulated maximal airway narrowing in normal subjects and after moderate narrowing in asthmatics.

Adult↗
PubMed1986

Asthma and the role of inflammation.

Asthma has been defined as variable airflow obstruction. The symptoms of asthma are not specific for the condition and, therefore, the presence of variable airflow obstruction needs to be objectively confirmed. When airflow obstruction is present and when it can be completely reversed with treatment, confirmation of the diagnosis is easy. When spirometry is normal or when there is chronic airflow limitation, however, other methods of investigation are required. These methods include inhalation tests with histamine or methacholine, diurnal variation of peak flow rates and tests with exercise or hyperventilation. When spirometry is normal, methacholine or histamine tests appear to be the most sensitive method but, if results are normal, they do not exclude past or future asthma. However, when there is chronic airflow limitation neither variable airflow obstruction nor methacholine or histamine hyperresponsiveness are specific for asthma; tests with hyperventilation (and probably others that act through mediator release) may be more specific. The presence of asthma probably requires the release of chemical mediators, from mast cells and other cells, which can produce inflammation. This has been particularly studied after inhalation of allergens or chemical sensitizers which can trigger both early and late asthmatic responses. The late responses are associated with prolonged increases in airway responsiveness and are considered to be a result of the cellular phase of inflammation. It is possible that persistent or recurrent inflammation, due to these and other stimuli, is the cause of the persisting airway hyperresponsiveness and variable airflow obstruction in asthma, as well as the other features of cough and sputum, but this requires further investigation.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗