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S Lanes

Publications and source records attributed to S Lanes.

7 recordsLinked to original sources
PubMed1993

Casual inference.

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Epidemiologic Methods↗
PubMed1986

Differences in airway responsiveness to leukotriene D4 in allergic sheep with and without late bronchial responses.

Allergic sheep respond to inhaled Ascaris suum antigen with either acute and late bronchial obstructions (dual responders) or only acute bronchoconstriction (acute responders). In this study we tested the hypothesis that one factor which may distinguish between these two populations is the difference in sensitivity to a specific mediator of airway anaphylaxis, leukotriene (LT) D4 (a major component of slow reacting substance of anaphylaxis). We postulated that if the hypothesis was correct then dual responders should demonstrate increased airway responses to inhaled LTD4 and that this increased responsiveness should also be reflected by a more severe response to inhaled antigen. To test this we used animals from both groups with the same degree of non-specific airway responsiveness to carbachol and determined their airway responses to controlled inhalation challenges with synthetic LTD4 and Ascaris suum antigen. Airway responsiveness to carbachol was determined by measuring the change in specific lung resistance (SRL) to increasing concentrations of carbachol aerosol, and then identifying, by linear interpolation, the provocative carbachol concentration which produced a 150% increase (PC150) in SRL. Airway responses to LTD4, and antigen were determined by measuring the percentage change in SRL after a controlled inhalation challenge with either aerosol. Airway responsiveness to carbachol was not different between the two groups. There was, however, a difference (p less than 0.05) in the airway response to the same dose of LTD4 in the two groups. Dual responders showed a 297 +/- 72% increase in SRL as compared to a 90 +/- 13% increase in SRL in the acute responders. Dual responders also showed a greater immediate and more prolonged response to antigen than did acute responders. These results suggest that increased responsiveness to LTD4 may be one factor which may distinguish dual responders from acute responders.

Airway Resistance↗
PubMed1986

Indomethacin and FPL-57231 inhibit antigen-induced airway hyperresponsiveness in sheep.

We compared the development of antigen-induced airway hyperresponsiveness (AHR) 24 h after challenge with Ascaris suum antigen in allergic sheep with acute (n = 7) and with dual (n = 7) airway responses and then attempted to modify this AHR. Cholinergic airway responsiveness was determined by measuring the carbachol dose required to increase specific lung resistance (sRL) 150% (i.e., PC150). Subsequently the sheep were challenged with antigen and sRL was measured at predetermined times to document the presence or absence of a late response. PC150 was redetermined 24 h later followed by bronchoalveolar lavage (BAL) to assess inflammation. Only dual responders developed AHR (PC150 decreased, P less than 0.05). There were no significant differences in BAL between the two groups. Six dual responders were then, on separate occasions (greater than or equal to 3 wk), pretreated with placebo, indomethacin (2 mg/kg iv), or a leukotriene antagonist, FPL-57231 (30 mg inhaled). Neither agent significantly affected the acute response to antigen. Only FPL pretreatment blocked the late response, but both agents blocked the antigen-induced AHR 24 h later. BAL at 24 h showed no significant differences. These results indicate that only dual responders develop AHR 24 h after antigen challenge. This AHR appears independent of the late increase in sRL or the severity of pulmonary inflammation. AHR appears to be sensitive to agents that interfere with the early release or actions of cyclooxygenase and lipoxygenase metabolites in dual responders.

Airway Resistance↗
PubMedDate not supplied

Effect of an inhaled glucocorticosteroid (budesonide) on post-antigen induced increases in airway responsiveness.

We examined the effects of an inhaled glucocorticosteroid, budesonide, on antigen-induced early and late bronchial responses and the development 24 h after challenge of increased airway responsiveness to carbachol in allergic sheep. Six allergic sheep were used for this study and, on occasions separated by at least three weeks, they were treated: with placebo (treatment 1); 16 h and 20 min prior to antigen challenge with budesonide (treatment 2); 16 h and 20 min prior to and 8 h after antigen challenge with budesonide (treatment 3); or 16 h and 1 h prior to and 8 h after antigen challenge with budesonide (treatment 4). Airway responsiveness to carbachol was determined prior to and 24 h after antigen challenge by measuring specific lung resistance (sRL) after administering increasing doses of carbachol aerosol (0.5, 1 and 2.5% w/v) and determining the concentration of carbachol needed to increase sRL 150% over baseline (PC150). Placebo treatment did not affect the early or late increases in sRL after airway challenge with Ascaris suum antigen; 24 h after challenge, airway responsiveness to carbachol increased (p less than 0.05); at this time, PC150 was (mean +/- SEM) 0.88 +/- 0.15% as compared to 1.56 +/- 0.26% before challenge. Both treatments 2 and 3 blunted the early response to antigen and blocked the late response, but treatment 2 did not modify the antigen-induced increase in airway responsiveness, whereas treatment 3 did. Treatment 4 blocked both antigen-induced responses and was effective in blunting the increased airway responsiveness. These results suggest that antigen-induced increases in airway responsiveness: occur 24 h after a challenge in allergic sheep with early and late responses; can be blunted by budesonide; and are not dependent on the late response.

Administration, Inhalation↗