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Biomedical subjects

K F Chung

Publications and source records attributed to K F Chung.

At least 235 records · Page 13Linked to original sources
PubMed1994

Inhaled platelet-activating factor worsens gas exchange in mild asthma.

To investigate the potential effects of inhaled platelet-activating-factor (PAF) (12 micrograms) to perturb pulmonary gas exchange in bronchial asthma, six patients (mean +/- SE, 23 +/- 2 yr) with intermittent asthma (FEV1, 90% predicted) were studied before and 5, 15, and 45 min after challenge. Circulating white blood cells, respiratory system resistance (Rrs), systemic and pulmonary hemodynamics, and respiratory and inert pulmonary gas exchange were measured. Five minutes after PAF leukocytes fell, Rrs increased (by 27%). PaO2 decreased (by 15 mm Hg), and AaPO2 increased (twofold) (p < 0.05 each). Ventilation-perfusion (Va/Q) distributions worsened in a pattern similar to that commonly observed in patients with moderate to severe asthma. Dispersions of pulmonary blood flow (log SD Q) and of alveolar ventilation (log SD V), and an overall index of Va/Q heterogeneity (DISP R-E*) increased significantly (123% for DISP R-E*; p < 0.05, each). Gas exchange indices and Rrs were still minimally abnormal at 15 min but returned towards baseline at 45 min. Ventilatory and hemodynamic variables remained unaltered throughout the study. These results suggest that endogenous PAF may be implicated in the arterial blood gas abnormalities shown during exacerbations of bronchial asthma.

Administration, Inhalation↗
PubMed1994

Role of nitric oxide and superoxide anions in interleukin-1 beta-induced airway hyperresponsiveness to bradykinin.

We investigated the role of endogenous nitric oxide (NO) and superoxide anions in recombinant human interleukin-1 beta (rhIL-1 beta)-induced bronchial hyperresponsiveness (BHR) and neutrophilia in Brown-Norway rats. Aminoguanidine (100 mg/kg/d) administered subcutaneously for 3 d, an inhibitor of inducible NO synthase, L-arginine (100 mg/kg/d administered subcutaneously for 3 d, a specific precursor for the synthesis of NO, and apocynin (5 mg/kg/orally), an inhibitor of superoxide anion (O2-)-generating NADPH oxidase in macrophages and neutrophils, were administered prior to administration of rhIL-1 beta (500 U) intratracheally. Aminoguanidine in addition to another inhibitor of NO synthase, NW-nitro-L-arginine methyl ester (L-NAME) 100 mg kg/d administered subcutaneously for 3 d augmented bronchial responsiveness to inhaled bradykinin (BK) but not to acetylcholine (ACh), an effect reversed by L-arginine. rhIL-1 beta-treated rats also demonstrated BHR to BK but not to ACh, associated with neutrophilia in bronchoalveolar lavage fluid (BALF). rhIL-1 beta-induced BHR and neutrophilia were neither further increased by aminoguanidine nor inhibited by L-arginine. Apocynin, however, significantly inhibited rhIL-1 beta-induced BHR but not the BALF neutrophilia. Suppression of NO generation and generation of O2- from macrophages and infiltrating neutrophils may be important in rhIL-1 beta-induced airway hyperresponsiveness to bradykinin.

Acetophenones↗
PubMed1994

Platelet-activating factor causes ventilation-perfusion mismatch in humans.

We hypothesized that platelet-activating factor (PAF), a potent inflammatory mediator, could induce gas exchange abnormalities in normal humans. To this end, the effect of aerosolized PAF (2 mg/ml solution; 24 micrograms) on ventilation-perfusion (VA/Q) relationships, hemodynamics, and resistance of the respiratory system was studied in 14 healthy, nonatopic, and nonsmoking individuals (23 +/- 1 [SEM]yr) before and at 2, 4, 6, 8, 15, and 45 min after inhalation, and compared to that of inhaled lyso-PAF in 10 other healthy individuals (24 +/- 2 yr). PAF induced, compared to lyso-PAF, immediate leukopenia (P < 0.001) followed by a rebound leukocytosis (P < 0.002), increased minute ventilation (P < 0.05) and resistance of the respiratory system (P < 0.01), and decreased systemic arterial pressure (P < 0.05). Similarly, compared to lyso-PAF, PaO2 showed a trend to fall (by 12.2 +/- 4.3 mmHg, mean +/- SEM maximum change from baseline), and arterial-alveolar O2 gradient increased (by 16.7 +/- 4.3 mmHg) (P < 0.02) after PAF, because of VA/Q mismatch: the dispersion of pulmonary blood flow and that of ventilation increased by 0.45 +/- 0.1 (P < 0.01) and 0.29 +/- 0.1 (P < 0.04), respectively. We conclude that in normal subjects, inhaled PAF results in considerable immediate VA/Q inequality and gas exchange impairment. These results reinforce the notion that PAF may play a major role as a mediator of inflammation in the human lung.

Adolescent↗
PubMed1994

Coughing frequency in patients with persistent cough: assessment using a 24 hour ambulatory recorder.

Cough is an important symptom of many respiratory disorders. We determined the frequency and diurnal variation of cough in normal subjects and in patients with asthma or with persistent cough of unknown cause. We used a portable, solid-state, multiple-channel recorder to record cough sounds over a 24 h period. The audio-signal was recorded from a unidirectional microphone strapped over the chest wall, and electromyographic (EMG) signals from the lower respiratory muscles were simultaneously registered with surface electrodes. The recorded digital data were examined on an IBM-compatible computer, and the typical signals induced by cough (as assessed by voluntary or experimentally-induced cough) were counted. In 12 normal subjects, only 0-16 coughs were recorded over 24 h. In 21 stable asthmatics with a history of chronic cough ("asthma") the median number was 282 (ranges: 45-1,577), and in 14 patients with the predominant symptom of daily dry coughs ("chronic coughers") the median number was 794 (64-3,639). In both groups of patients, there was a diurnal variation of coughs, such that the least numbers occurred between 2 and 5 a.m. (< 3% of total). In the asthma group, there was no significant correlation between forced expiratory volume in one second (FEV1) (% predicted) or diurnal variation of peak expiratory flow and cough frequency. In the chronic coughers, there was a significant correlation between daytime cough numbers and daytime cough symptoms scores but not for the night-time values. Our data show that cough frequency is not determined by the severity of asthma in relatively stable asthmatics on inhaled steroids, and is reduced during sleep in both asthmatics and chronic cough patients. This portable cough recorder may be useful in the assessment of drug therapy for chronic cough.

Adult↗
PubMed1994

Alveolar macrophage-induced suppression of peripheral blood mononuclear cell responsiveness is reversed by in vitro allergen exposure in bronchial asthma.

Little information is available on the specific role of alveolar macrophages (AMs) in modulating local cellular reactions to inhaled allergens in atopic asthma. We investigated the influence of alveolar macrophages obtained by bronchoalveolar lavage (BAL) on the proliferative responses of lavage and peripheral lymphocytes from 12 patients with atopic asthma, 6 nonasthmatic symptomatic atopic subjects, and 6 nonatopic normal volunteers, in the context of in vitro exposure to relevant and nonrelevant allergens. Fresh nonadherent bronchoalveolar lavage cells from atopic asthmatic patients, depleted of alveolar macrophages, proliferated spontaneously more than nonadherent bronchoalveolar lavage cells from normal subjects. Addition of autologous asthmatic alveolar macrophages reduced this endogenous "activation". Asthmatic and normal alveolar macrophages also inhibited phytohaemagglutinin-stimulated proliferation of both autologous and allogeneic nonadherent peripheral blood mononuclear cells (PBMC). In contrast, autologous asthmatic alveolar macrophages induced strong proliferation of peripheral blood mononuclear cells when stimulated with allergen to which the patient was skin test and radio allergosorbent test (RAST) reactive; however, no response was seen with allergens to which the patient was insensitive. No such allergen-specific proliferation was seen with alveolar macrophages from nonasthmatic atopic subjects. These data support the presence of functionally-active alveolar macrophages within the airways of atopic asthmatic patients, that under normal stable conditions suppress the induction of peripheral blood mononuclear cell responses, and which only on contact with specific allergen appear to switch to inducer alveolar macrophages, with consequent peripheral blood mononuclear cell hyperactivation.

Adult↗
PubMed1994

Inhaled frusemide does not affect lung mucociliary clearance in healthy and asthmatic subjects.

Inhaled frusemide has been shown to protect against the bronchoconstrictor effect of several inhaled agents in asthmatic subjects by mechanism(s) that are unclear. Since loop diuretics can modulate Cl- transport in the airway epithelium, frusemide may alter the quality and/or the quantity of the periciliary layer, which in turn may affect lung mucociliary transport. We investigated the effect of a single inhalation of nebulized frusemide (40 mg) on lung mucociliary clearance in four healthy subjects and in seven stable, mild asthmatics using an objective radioaerosol technique. Frusemide or placebo was inhaled in a double-blind, randomized, cross-over manner half an hour after the inhalation of 5 microns polystyrene particles labelled with 99mTc, used for assessing mucociliary clearance. The pulmonary function and initial radioaerosol distribution were similar between frusemide and placebo runs within each of the two study groups. The areas under the tracheobronchial retention curves over the 6 h observation period were similar between frusemide and placebo runs for both groups. Our findings show inhaled frusemide, at a dose known to inhibit bronchoconstrictor responses, does not affect lung mucociliary clearance.

Administration, Inhalation↗
PubMed1994

Inhibition of interleukin-8 expression by dexamethasone in human cultured airway epithelial cells.

Interleukin-8 (IL-8) is a neutrophil chemotactic factor expressed in many cell types, including human airway epithelial cells (HAEC). Inhaled corticosteroids are now used increasingly early in the treatment of airway inflammation such as in asthma, and directly interact with HAEC at relatively high concentrations. We have investigated the effect of dexamethasone on IL-8 expression in primary cultured HAEC obtained from transplantation donors. Northern blot analysis was used to measure IL-8 mRNA levels in HAEC, and radioimmunoassay was used to measure IL-8 protein in culture supernatant fluids. We demonstrated that IL-8 was expressed by primary cultured HAEC and that this was enhanced by IL-1 beta and tumour necrosis factor-alpha stimulation, but not by IL-6 or lipopolysaccharide. Dexamethasone suppressed IL-8 mRNA expression and protein synthesis dose-dependently in both resting and stimulated HAEC. The half-life of IL-8 mRNA determined in the presence of actinomycin D was less than 1 hr, and dexamethasone preincubation had no effect on mRNA stability. These results support the view that HAEC may play an important role in the pathogenesis of airway inflammatory diseases, and that glucocorticosteroids may exert their anti-inflammatory effects by blocking IL-8 gene expression and generation in these cells.

Adolescent↗
PubMed1993

Effect of CP-96,345, a non-peptide NK1 receptor antagonist, against substance P-, bradykinin- and allergen-induced airway microvascular leakage and bronchoconstriction in the guinea pig.

We have investigated the effect of a new non-peptide NK1 receptor antagonist, CP-96,345, against substance P (SP)-, bradykinin (BK)- and allergen-induced airway microvascular leakage, bronchoconstriction and hypotension in anesthetized guinea pigs. Lung resistance (RL) and mean systemic blood pressure (BP) were measured for 6 min after challenge, followed by measurement of extravasation of Evans blue dye into airway tissues, used as an index of airway microvascular leakage. I.v. (2 nmol/kg) and inhaled (1 mM, 45 breaths) SP, i.v. (15 nmol/kg) and inhaled (1 mM, 45 breaths) BK and aerosolized allergen (5 mg/ml of ovalbumin, 30 breaths) induced a significant increase in RL and leakage of dye at all airway levels, and decreased BP significantly except for inhaled BK. CP-96,345 (2 mg/kg i.v.) abolished the dye extravasation induced by both SP. CP-96,345 partly inhibited the responses induced by both BK but not by allergen. CP-96,345 markedly inhibited the increase in RL and fall in BP induced by SP but not by BK or allergen. NK1 receptor-mediated mechanisms may contribute to SP- and BK-induced airway microvascular leakage and SP-induced bronchoconstriction and hypotension. These mechanisms are not important in the acute airway responses induced by inhaled allergen.

Administration, Inhalation↗
PubMed1993

Effect of beta 2-adrenoceptor agonists against platelet-activating factor-induced airway microvascular leakage and bronchoconstriction in the guinea pig.

We have investigated the effect of inhaled formoterol (0.75 mg/ml, 60 breaths) and salbutamol (25 mg/ml, 60 breaths) against airway microvascular leakage and bronchoconstriction induced by inhaled platelet-activating factor (PAF) and histamine in anaesthetized guinea pigs. Lung resistance (RL) was measured for 6 min after challenge, followed by measurement of extravasation of Evans blue dye into airway tissues, used as an index of airway microvascular leakage. PAF (0.1, 0.4 and 1 mM; 30 breaths) caused a significant increase in RL and extravasation of dye, but the responses were smaller than those induced by histamine (5 mM, 30 breaths). Both formoterol and salbutamol caused a small but significant inhibition of extravasation in the distal intrapulmonary airways induced by PAF (0.1 and 0.4 mM for formoterol and 0.1 mM for salbutamol), and only formoterol reduced the increase in RL induced by 1 mM PAF. These drugs also inhibited both airway effects of histamine to a higher degree. In conclusion, formoterol and salbutamol can partly inhibit airway microvascular leakage and bronchoconstriction induced by inhaled PAF and histamine. The inhibitory potency of beta 2-adrenoceptor agonists may be dependent on the inflammatory mediator inducing the airway effects.

Administration, Inhalation↗
PubMed1993

Role played by NK2 receptor and cyclooxygenase activation in bradykinin B2 receptor mediated-airway effects in guinea pigs.

We have investigated the effects of SR-48968, an NK2 receptor antagonist, and indomethacin, a cyclooxygenase inhibitor, against bronchoconstriction and airway microvascular leakage induced by bradykinin (BK) in anesthetized guinea pigs. In addition, we have determined whether these effects were mediated via bradykinin B2 receptor activation, using a B2 receptor antagonist HOE 140. Lung resistance (RL) and extravasation of Evans blue dye into airway tissues were used as indexes of airway caliber and microvascular leakage, respectively. BK (15 nmol/kg i.v.) induced a significant increase in RL and leakage of dye at all airway levels, responses which were completely abolished by HOE 140 (0.13 mg/kg i.v.). SR-48968 (1.5 mg/kg i.v.) had no effect against BK-induced airway effects. Indomethacin (5 mg/kg i.v.) completely blocked the increase in RL and significantly inhibited the leakage of dye in peripheral intrapulmonary airway. In conclusion, bronchoconstriction induced by i.v. BK is mediated by release of cyclooxygenase products but not by stimulation of NK2 receptors, while the airway microvascular leakage only partly involves cyclooxygenase activation. Cyclooxygenase activation may occur following bradykinin B2 receptor stimulation.

Airway Resistance↗
PubMed1993

Effect of a topical corticosteroid on airway hyperresponsiveness and eosinophilic inflammation induced by trimellitic anhydride exposure in sensitized guinea pigs.

BACKGROUND: Topical corticosteroids are effective in the treatment of asthma by improving bronchial hyperresponsiveness and reducing airway inflammation. METHODS: We assessed the effect of a nebulized corticosteroid, budesonide, on airway hyperresponsiveness and inflammatory response provoked by inhalation of trimellitic anhydride (TMA) dust, a known cause of occupational asthma in human beings, in guinea pigs sensitized to the free hapten. Male Dunkin-Hartley guinea pigs (n = 24) were injected intradermally with 0.1 ml of 0.3% TMA in corn oil, followed by exposure 21 to 28 days later to five consecutive doses of budesonide aerosol (0.5 mg/ml) or saline solution, administered for 10 minutes every 12 hours. They were then exposed (noses only) to TMA dust (8 mg/m3) or air for 1 hour (four groups, n = 6 in each). Airway responsiveness to acetylcholine, defined as the concentration needed to cause a 200% increase in lung resistance (PC200), was measured 8 hours later. RESULTS: In saline-treated guinea pigs exposed to TMA, mean PC200 was 0.094 mmol/L (geometric SEM, 1.4 mmol/L) compared with 0.31 mmol/L (geometric SEM, 1.3 mmol/L, p < 0.05) in those guinea pigs pretreated with budesonide. In sham-exposed sensitized guinea pigs, PC200 was 0.35 mmol/L (geometric SEM, 1.2 mmol/L), which was not significantly different from the budesonide-treated group (0.36 mmol/L; geometric SEM, 1.3 mmol/L). There was a significant increase in the number of eosinophils in the subepithelium of guinea pigs further exposed to TMA dust (71.5 +/- 6.8 cells/unit area [mean +/- SEM]) compared with those exposed to air (22.7 +/- 6.7, p < 0.01). Budesonide did not inhibit the number of subepithelial eosinophils of guinea pigs exposed to TMA dust (54.0 +/- 3.7 cells/unit area) or in those exposed to air (24.3 +/- 6.7 cells/unit area) and did not affect the increase in eosinophils found in bronchoalveolar fluid. CONCLUSIONS: Budesonide significantly inhibited the increase in airway responsiveness but not the eosinophilic inflammation induced by exposure to TMA dust in sensitized guinea pigs.

Administration, Topical↗
PubMed1993

Effect of inhaled corticosteroids on peripheral blood eosinophil counts and density profiles in asthma.

BACKGROUND: Inhaled corticosteroids are effective in the treatment of asthma and reduce bronchial hyperresponsiveness. We examined the effect of inhaled budesonide (1600 micrograms/day for 14 days) on the number and density profile of peripheral blood eosinophils in 10 patients with mild stable asthma in a double-blind, placebo-controlled, crossover trial. METHODS: At the end of each study period, blood was collected immediately before measurement of bronchial responsiveness calculated as the concentration of methacholine causing a 20% fall in forced expiratory volume in 1 second (PC20). Plasma leukocyte suspension obtained after sedimentation of blood with 46% dextran was layered on a Percoll continuous-density gradient. After centrifugation, 20 sequential aliquots of increasing density gradients were removed for differential counts. Eosinophils recovered from density of gradients less than 1.080 gm/ml were defined as hypodense. RESULTS: Budesonide treatment resulted in a fall in mean eosinophil count from 0.37 +/- 0.05 x 10(9) L-1 after placebo to 0.16 +/- 0.03 x 10(9) L-1 (p < 0.01). A significant reduction occurred in the hypodense eosinophil population from 51.6% +/- 4.3% after placebo to 38.1% +/- 3.1% after budesonide (p < 0.05). Mean log PC20 increased from -0.26 +/- 0.12 after placebo to -0.004 +/- 0.14 after budesonide (p < 0.01). CONCLUSION: We conclude that inhaled steroid therapy reduces the number of circulating hypodense eosinophils, which is an effect that may underlie the improvement in bronchial hyperresponsiveness.

Administration, Inhalation↗
PubMed1993

Ultrastructural characterization of platelet-activating factor-stimulated human eosinophils from patients with asthma.

1. Purified human eosinophils from asthmatic patients were stimulated with platelet-activating factor in vitro and examined for morphological changes by transmission electron and light microscopy. Changes were also evaluated by morphometric analysis and were related to the platelet-activating factor-stimulated release of granular eosinophil cationic protein. 2. Stimulation of eosinophils with platelet-activating factor induced a dose-dependent shape change, including the elongation of cells, loss of microvilli and the formation of lamellipodia. This effect was maximal at 25 min and was reversible. 3. Stimulation with platelet-activating factor also induced granule movement to the cell periphery and fusion of adjacent granules. Granules became swollen and vesiculated, whereas both the matrix and core showed evidence of solubilization. 4. There was a time-dependent secretion of eosinophilic cationic protein from human eosinophils upon stimulation with platelet-activating factor which occurred without significant lactate dehydrogenase release. 5. Morphometric analysis of the transmission electron micrographs indicated a significant reduction in cytoplasmic area after 10 min of incubation with platelet-activating factor from 39.0 +/- 1.7 microns 2 for untreated eosinophils to 33.2 +/- 2.3 microns 2 (P < 0.02) for platelet-activating factor-treated cells, underscoring the observation that the cells change from spherical to ellipsoidal. No significant increase in the perimeter of the cells was found. 6. The number of granule-profiles in platelet-activating factor-stimulated eosinophils was slightly reduced when compared with control, and an increase in granule area was observed 10 min after platelet-activating factor challenge (0.215 +/- 0.011 microns 2 versus 0.246 +/- 0.016 microns 2).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effect of an oral potassium channel activator, BRL 38227, on airway function and responsiveness in asthmatic patients: comparison with oral salbutamol.

BACKGROUND: Potassium (K+) channel activators, such as cromakalim, open ATP sensitive K+ channels and relax airway smooth muscle in vitro and inhibit induced bronchoconstriction in vivo in animals. The prolonged half life of cromakalim gives it potential as an oral bronchodilator. The effect of orally administered BRL 38227 (the active enantiomer of cromakalim), at doses of 0.125, 0.25, and 0.5 mg, on airway function and airway responsiveness to histamine and methacholine has been investigated in asthmatic patients. METHODS: Seventeen patients with asthma were studied in three separate randomised double blind, placebo controlled studies. In the first study eight patients with moderately severe asthma were given 0.125, 0.25, and 0.5 mg of BRL 38227 or placebo, and responses to histamine were assessed before and five hours after treatment. In the second study responses to methacholine were measured before and five hours after 0.125 and 0.5 mg of BRL 38227 or placebo were given to nine patients with mild asthma. In the third study the effect of 0.5 mg of BRL 38227 or placebo was assessed in eight patients with mild asthma. Responses to histamine were measured before treatment and two and five hours after treatment. To provide a positive control study eight subjects who had taken part in studies 1 and 3 were also given oral salbutamol (8 mg) in a placebo controlled, double blind study. Responses to histamine were assessed before and two hours after treatment. RESULTS: BRL 38227 did not cause significant bronchodilatation or changes in airway responsiveness in any of the studies. Headache was reported in 19 of 25 of patients receiving (in some cases twice) 0.5 mg of BRL 38227. By contrast, oral salbutamol gave significant protection against histamine challenge (geometric mean 2.23 doubling dilutions). CONCLUSIONS: After a single oral dose of BRL 38227 no beneficial effect on airway function was detected, despite a high incidence of side effects, which indicates that the orally administered K+ channel activator BRL 38227 may not be useful in the management of asthma.

Adult↗
PubMed1993

Effect of inhaled lyso-platelet-activating factor on airway microvascular leakage in the guinea pig.

Lyso-platelet-activating factor (PAF), the precursor and metabolite of PAF, is considered inactive, although it may be converted to PAF by airway cells. We have investigated the effects of inhaled lyso-PAF on bronchoconstriction and airway microvascular leakage in anesthetized guinea pigs. Lung resistance (RL) was measured for 6 min after inhalation of lyso-PAF (0.3, 1, and 3 mM; 30 breaths) followed by measurement of extravasation of intravenous Evans blue dye into airway tissues, which was used as an index of airway microvascular leakage. Inhaled lyso-PAF caused an increase in RL and leakage of dye at all airway levels in a dose-dependent fashion, but intravenous lyso-PAF (0.25 mg/kg) had no airway effect. The maximum dose of inhaled lyso-PAF increased RL significantly by approximately 200%. The amount of extravasation of dye induced was 96 +/- 4 (SE) ng/mg of tissue in trachea, 77 +/- 8 ng/mg in main bronchi, and 65 +/- 7 and 25 +/- 1 ng/mg in proximal and distal intrapulmonary airways respectively; these values were all significantly higher (P < 0.01) than control values. These responses were completely abolished by a specific PAF-receptor antagonist WEB-2086 (2 mg/kg iv). Our results show that inhaled lyso-PAF is potent in increasing airway microvascular leakage. The effects of lyso-PAF may result from its metabolic transformation to PAF by lyso-PAF:acetyl-CoA acetyltransferase in the airway.

Administration, Inhalation↗
PubMed1993

Allergen-induced airway hyperresponsiveness in Brown-Norway rat: role of parasympathetic mechanisms.

Enhanced parasympathetic mechanisms may contribute to airway hyperresponsiveness. The present study examined whether the in vivo increase in airway responsiveness seen 18-24 h after either a single or chronic aerosolized allergen challenge protocol in actively sensitized Brown-Norway rats was due to altered parasympathetic mechanisms. The roles of central and reflex vagal mechanisms were studied by performing bilateral cervical vagotomy before measurement of airway responsiveness. Bilateral vagotomy failed to reduce the increase in airway responsiveness after either a single or chronic allergen challenge. The roles of increased neural release of acetylcholine (ACh) and increased end organ responsiveness were studied in vitro. The isometric responses of tracheal and bronchial strips to both electrical field stimulation and exogenously applied ACh from rats exposed both to single and chronic allergen challenges were compared with those from saline-exposed rats. The responses to electrical field stimulation and to exogenous ACh were not significantly enhanced 18-24 h after either protocol. We conclude that the airway hyperresponsiveness observed in this allergic rat model is not mediated through an enhancement of parasympathetic mechanisms.

Acetylcholine↗