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PubMed1982

Inhibition of bronchoconstriction in the guinea pig by a calcium channel blocker, nifedipine.

We investigated the inhibitory effects of nifedipine, a calcium channel blocker, on airway smooth muscle constriction in the guinea pig. In vitro, nifedipine (0.003 to 3.0 microM) caused significant dose-dependent reversal of intrinsically existing tone in both tracheal spirals and parenchymal strips. Nifedipine also inhibited the constriction of tracheal spirals and parenchymal strips induced by two different agonists, histamine and carbachol. At a concentration of 3.0 microM, nifedipine increased by 48-fold the concentration of carbachol required to produce a 50% of maximal contraction of parenchymal strips, and by 5-fold the concentration of histamine. Increasing extracellular calcium ion concentration in the tissue baths significantly diminished the inhibitory action of nifedipine. In vivo, nifedipine (30 micrograms/kg body weight given intravenously) did not alter pulmonary resistance or dynamic compliance. It did, however, attenuate histamine-induced bronchoconstriction in 3 of 5 animals studied. In response to the maximal dose of histamine infused, mean pulmonary resistance rose 40 +/- 16% (SEM) after nifedipine versus 182 +/- 65% in the control animals (p less than 0.025) and mean dynamic compliance decreased 35 +/- 8% after nifedipine versus 58 +/- 6% in the control animals (p less than 0.01). Thus, this calcium channel blocker inhibits mediator-induced constriction of both central and peripheral airway contractile tissues, a finding of potential clinical applicability.

Animals↗
PubMed1982

Naloxone does not affect bronchoconstriction induced by isocapnic hyperpnea of subfreezing air.

Although respiratory heat loss with cooling of the tracheobronchial mucosa is responsible for the airway obstruction that develops after inhalation of subfreezing air in asthmatics, the mechanism by which airway cooling results in bronchoconstriction is not known. In order to test whether release of endogenous opiate peptides might play a role in mediating this response, asthmatic subjects were studied before and after isocapnic hyperventilation of subfreezing air after the administration of placebo or naloxone, given in a double-blind fashion. Five asthmatic subjects were tested with low-dose (0.8 mg) and 5 with high-dose (10 mg) naloxone given intravenously. Pretreatment with naloxone at either dose did not attenuate the decrease in FVC, FEV1, or FEF25--75 after cold air in comparison with placebo pretreatment. A slightly greater decrease in FEV1 and FEF25--75 after low-dose naloxone than placebo pretreatment can be partially explained by a difference in the temperature achieved during cold air inhalation. We conclude that endogenous opiate peptides are not involved in mediating the bronchoconstrictor response to cold air inhalation in asthmatics.

Adult↗
PubMed1983

Effects of nifedipine on antigen-induced bronchoconstriction.

We have investigated the effects of the calcium antagonist nifedipine on antigen-induced bronchoconstriction in vivo and in vitro. Eight grass-pollen-sensitive asthmatics were given either nifedipine (20 mg sublingually) or placebo 30 min before antigen challenge. The fall in forced expiratory volume in one second after pretreatment with placebo was 42.8 +/- 10.1%. After nifedipine this fall was significantly reduced to 26.5 +/- 11.7% (p less than 0.005). Two in vitro models of allergic asthma have been studied: actively sensitized guinea pig tracheal strips (GPT) and passively sensitized human bronchial muscle (HBM). Contraction of GPT by acetylcholine, histamine, and antigen challenge was unaffected by nifedipine 10(-4)M. Contraction of HBM by acetylcholine, histamine and grass pollen antigen challenge was significantly reduced by nifedipine 10(-4)M and 10(-6)M. The magnitude of the reduction in contraction to antigen challenge was comparable to the inhibition of acetylcholine and histamine responses. It would appear most likely that nifedipine exerts its effect mainly on bronchial muscle contractility rather than by stabilizing mast cells.

Adult↗
PubMed1983

Bronchoconstriction stimulated by airway cooling. Better protection with combined inhalation of terbutaline sulphate and cromolyn sodium than with either alone.

We compared the effect of inhaled terbutaline sulphate (1,000 micrograms), cromolyn sodium (20 mg), terbutaline plus cromolyn, and placebo on the response to respiratory heat loss (RHL) in 10 asthmatics in whom terbutaline alone did not completely inhibit the response to RHL. The medications were taken double-blind in random order 20 min before voluntary isocapnic hyperventilation of subfreezing air (-14 degrees C, 0% humidity) in twofold-increasing amounts. The response was expressed as the provocative dose of RHL to cause a 10 and 20% fall in forced expiratory volume in one second (FEV1). When compared with placebo, terbutaline produced bronchodilation and inhibition of the response to RHL. The degree of bronchodilation was small (mean delta FEV1, 3.9%) and did not correlate with the degree of protection. Cromolyn produced no bronchodilation and similar inhibition. The effect of terbutaline and cromolyn together was additive. We conclude that when bronchoconstriction stimulated by airway cooling is not prevented by a beta agonist or cromolyn given individually, that it will be more effectively inhibited by the 2 drugs given in combination.

Adult↗
PubMed1985

Respiratory heat loss is not the sole stimulus for bronchoconstriction induced by isocapnic hyperpnea with dry air.

It is uncertain if respiratory heat loss or respiratory water loss is the stimulus for bronchoconstriction induced by isocapnic hyperpnea or exercise with dry air in subjects with asthma. We partially separated these 2 stimuli by having 18 subjects with asthma breathe dry air (0 mg/L water content) at increasing ventilations by isocapnic hyperpnea while we measured the increase in specific airway resistance (SRaw). The study was divided into 2 phases. In Phase 1, we used an apparatus with a single respiratory valve and evaluated the subjects' responses at 3 different inspired temperatures (-8.4, 20.5, and 39.4 degrees C). Seven of the subjects had esophageal catheters with 2 thermocouples in place to measure retrocardiac and retrotracheal temperatures. In this phase, we found that there were no significant differences in the ventilation required to cause a 100% increase in SRaw among the 3 different inspired temperatures (48.4 L/min, cold; 47.5 L/min, room temperature; 44.2 L/min, hot), even though the retrotracheal temperature fell more when the subjects breathed cold air at 40 L/min (2.1 degrees C) than when they breathed hot air (1.2 degrees C), suggesting greater airway cooling with the cold air. In Phase 2, in order to accurately measure inspired and exhaled temperatures and exhaled water content, we used 2 separate systems for delivering the inspired air and collecting the exhaled air at 2 different inspired temperatures (-21.4 and 38.9 degrees C). Again, we found that there was no significant difference in the ventilation required to cause a 100% increase in SRaw between the 2 different inspired temperatures (28.3 L/min, cold; 33.6 L/min, hot). When the subjects inhaled cold air, exhaled temperature was warmer than previously reported.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Factors that contribute to inhibition of methacholine-induced bronchoconstriction.

To evaluate the factors that contribute to inhibition of airways reactivity, we compared the effect of inhaled isoproterenol, 125 micrograms, on the response to methacholine-induced bronchoconstriction in 10 normal and 10 asthmatic subjects. We measured in each subject baseline lung function, response to inhaled bronchodilator, dose of bronchodilator causing 50% maximal response, and degree of airways reactivity to inhalation of methacholine before and after isoproterenol. In asthmatics, but not normal subjects, inhalation of isoproterenol led to significant inhibition of methacholine-induced bronchospasm. In asthmatics, the greater the airways reactivity to methacholine the greater the inhibition by isoproterenol (p less than 0.05). In both groups, there was significant correlation between baseline lung function and level of airways reactivity. In neither normal subjects nor asthmatics did the maximal bronchodilator response to isoproterenol inhalation correlate with inhibition of airways reactivity. Studies evaluating inhibition of airways reactivity should take into account the population tested, baseline lung function, and baseline level of airways reactivity.

Adult↗
PubMed1986

Bronchoconstriction induced by distilled water. Sensitivity in asthmatics and relationship to exercise-induced bronchospasm.

We studied the ability of bronchial challenge with an ultrasonically produced, distilled water aerosol to detect airways hyperreactivity in asthmatics and also evaluated its relationship to exercise-induced bronchoconstriction. Fifteen asthmatics and 10 normal subjects inhaled, at room temperature, distilled water aerosol in increasing concentrations. On a separate day, each subject performed a standard methacholine challenge. On the third day, all asthmatics exercised on a treadmill for 6 min at 90% maximal heart rate while breathing room-temperature, dry air. Pulmonary mechanics (FEV1 and SGaw) were measured before and after each challenge. Seven of the asthmatics and all of the normal subjects did not react to challenge with distilled water. Distilled-water challenge caused a 20% decrease in FEV1 in only 53% (8 of the 15) asthmatics, whereas all of the asthmatics reacted to methacholine challenge with a 20% fall in FEV1. Thus, distilled water was not a sensitive challenge procedure for the detection of airways hyperreactivity in asthma and it cannot be used as a routine screening test. However, in the asthmatics, the response to distilled water challenge correlated significantly with the response to exercise (r = 0.81, p less than 0.001). Seven asthmatics were reactive to both exercise and water, 7 were reactive to neither exercise nor water, and 1 reacted to water but not to exercise. Cromolyn completely or partially blocked both distilled-water- and exercise-induced bronchospasm in the reactive asthmatics.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerosols↗
PubMed2002

Mannitol as a challenge test to identify exercise-induced bronchoconstriction in elite athletes.

Bronchial provocation tests provide objective criteria for asthma and exercise-induced bronchoconstriction (EIB) and were recommended to justify the use of inhaled beta2-agonists by athletes at the Winter Olympics 2002. Eucapnic voluntary hyperpnea (EVH) was one test recommended to identify EIB. Provocation with EVH requires a special dry gas mixture limiting its availability. Provocation tests with osmotic aerosols require less expensive equipment that is easily portable. We assessed the sensitivity of a challenge with mannitol to identify responsiveness to EVH in 50 elite summer sport athletes who were unselected if they had respiratory symptoms. Asthma was previously diagnosed by a doctor in 27 subjects, and 21 subjects were currently under treatment for EIB or asthma. The mean predicted FEV1 was 103.6 +/- 10.8%, FVC was 99 +/- 13.3%, and mean forced expiratory flow during the middle half of the FVC was 104 +/- 22.7%. A total of 25 subjects were positive to EVH challenge (mean percentage of fall in FEV1 was 25.4 +/- 15% SD), and 26 subjects had a positive mannitol challenge (geometric mean [95% confidence interval] provoking dose causing a 10% fall in forced expiratory volume in one second [PD10] was 202 mg [134, 300], with 24 of the subjects positive to both challenges). Mannitol had a sensitivity of 96% and specificity of 92% to identify a positive response to EVH and, as such, could be used as an alternative to EVH to identify EIB.

Adolescent↗
PubMed2003

Fish oil supplementation reduces severity of exercise-induced bronchoconstriction in elite athletes.

In elite athletes, exercise-induced bronchoconstriction (EIB) may respond to dietary modification, thereby reducing the need for pharmacologic treatment. Ten elite athletes with EIB and 10 elite athletes without EIB (control subjects) participated in a randomized, double-blind crossover study. Subjects entered the study on their normal diet, and then received either fish oil capsules containing 3.2 g eicosapentaenoic acid and 2.2 g docohexaenoic acid (n-3 polyunsaturated fatty acid [PUFA] diet; n = 5) or placebo capsules containing olive oil (placebo diet; n = 5) taken daily for 3 weeks. Diet had no effect on preexercise pulmonary function in either group or on postexercise pulmonary function in control subjects. However, in subjects with EIB, the n-3 PUFA diet improved postexercise pulmonary function compared with the normal and placebo diets. FEV1 decreased by 3 +/- 2% on n-3 PUFA diet, 14.5 +/- 5% on placebo diet, and 17.3 +/- 6% on normal diet at 15 minutes postexercise. Leukotriene (LT)E4, 9alpha, 11beta-prostaglandin F2, LTB4, tumor necrosis factor-alpha, and interleukin-1beta, all significantly decreased on the n-3 PUFA diet compared with normal and placebo diets and after the exercise challenge. These data suggest that dietary fish oil supplementation has a markedly protective effect in suppressing EIB in elite athletes, and this may be attributed to their antiinflammatory properties.

Adult↗
PubMed1969

Maximum expiratory flow rates in induced bronchoconstriction in man.

We evaluated changes of maximum expiratory flow-volume (MEFV) curves and of partial expiratory flow-volume (PEFV) curves caused by bronchoconstrictor drugs and dust, and compared these to the reverse changes induced by a bronchodilator drug in previously bronchoconstricted subjects. Measurements of maximum flow at constant lung inflation (i.e. liters thoracic gas volume) showed larger changes, both after constriction and after dilation, than measurements of peak expiratory flow rate, 1 sec forced expiratory volume and the slope of the effort-independent portion of MEFV curves. Changes of flow rates on PEFV curves (made after inspiration to mid-vital capacity) were usually larger than those of flow rates on MEFV curves (made after inspiration to total lung capacity). The decreased maximum flow rates after constrictor agents are not caused by changes in lung static recoil force and are attributed to narrowing of small airways, i.e., airways which are uncompressed during forced expirations. Changes of maximum expiratory flow rates at constant lung inflation (e.g. 60% of the control total lung capacity) provide an objective and sensitive measurement of changes in airway caliber which remains valid if total lung capacity is altered during treatment.

Acetylcholine↗
PubMed1998

Tolerance to the protective effects of salmeterol on methacholine-induced bronchoconstriction: influence of inhaled corticosteroids.

Long-acting beta2-adrenoceptor agonists such as salmeterol reduce airway responsiveness for at least 12 h, but this effect seems to decrease with regular use. We evaluated the time-course of the protective effects of salmeterol on methacholine-induced bronchoconstriction, its modulation by inhaled corticosteroids (ICS) and its influence on asthma control. Thirty two subjects (13 males and 19 females) with mild to moderate stable asthma were divided into two groups according to their medication needs: bronchodilators (BD) alone (n=16) or with ICS (n=16). After a 2 week run-in period, a double-blind crossover study was conducted. Subjects from both groups received salmeterol 50 microg b.i.d. or a placebo for 4 weeks each in random order, separated by a 2 week washout period. The provocative concentration of methacholine causing a 20% fall in forced expiratory volume in one second (PC20) was measured before and after each treatment period, 1 h prior to inhalation of salmeterol or placebo and 1 and 12 h after. Baseline forced expiratory volume in one second (FEV1) increased significantly after salmeterol, both after the first dose and at 4 weeks (BD group: 19 and 17%; ICS: 22 and 13%). On the first day of administration, salmeterol provided significant protection in both groups up to 12 h with a PC20 before and 1 and 12 h postdose of 2.2, 21.7 and 12.4, mg x mL(-1), respectively, in the BD group and 2.1, 11.6 and 55 mg x mL(-1), respectively, in the ICS group. After 4 weeks, this effect was significantly attenuated in both groups with a PC20 before, 1 and 12 h postdose of 3.3, 10.9 and 7.1 mg x mL(-1), respectively, in the BD group and 2.1, 5.0 and 2.3 mg x mL(-1), respectively, in the ICS group. This loss of protective effect was of similar magnitude in both groups. Respiratory symptoms, rescue beta2-agonist use and baseline FEV1 did not change significantly throughout the study in both groups. In conclusion, the bronchoprotective effect of salmeterol decreased with regular use both 1 and 12 h postdose; inhaled corticosteroids did not prevent this reduction. However, the development of tolerance was not associated with loss of asthma control.

Administration, Inhalation↗
PubMed1981

Mode of action of bronchodilating drugs on histamine-induced bronchoconstriction in asthmatic children.

The bronchodilatory response of three beta 2-agonists (fenoterol, salbutamol, and terbutaline), administered by a metered aerosol inhaler, was assessed in 19 asthmatic children after histamine-induced bronchoconstriction. At 1-min intervals, the changes in total pulmonary flow resistance (R1) and dynamic lung compliance (C dyn) were measured. After rank-ordering according to the base line value of C dyn (62 to 200% predicted), the patients were divided into two groups according to lung compliance: (1) patients with greater compliance (C dyn, 129 to 200% predicted) and (2) patients with lesser compliance (C dyn, 69 to 116% predicted). The effect of the three bronchodilators on the mean decrease of R1 and on the increase of C dyn was studied and analyzed for each drug separately. In all patients, salbutamol was the most efficient bronchodilator of small airways (P less than 0.02). The most striking feature of this beta 2-mimetic was observed in patients whose lungs were initially overinflated (functional residual capacity over 120% predicted) but not obstructed before the histamine challenge (P less than 0.005). In these subjects C dyn and R1 are normalized after inhalation of salbutamol. After fenoterol and terbutaline inhalation, obstruction of the large airways was not fully alleviated. In addition, these two drugs seemed not to affect the ventilatory asynchronism (C dyn alterations) in patients whose lungs had been overinflated before drug inhalation (C dyn again around 150% predicted).

Adolescent↗
PubMed2004

Baseline lung function, exercise-induced bronchoconstriction, and asthma-like symptoms in elite women ice hockey players.

PURPOSE: Exercise-induced bronchoconstriction (EIB) is high among ice rink athletes and may be related to exercise ventilation of rink air pollutants. Impaired postchallenge expiratory flows are common for this population; however, baseline lung function and symptoms have not been fully evaluated. METHODS: We examined resting lung function and asthma-like symptoms in relation to airway hyperresponsiveness in National Team female ice hockey players (N = 43). Subjects were grouped according to observed symptoms and medical history as symptomatic ('S') or asymptomatic ('A'). Baseline and postexercise lung function was determined. RESULTS: Seventeen (39.5%) presented symptoms and 9 (21%) had EIB. Baseline FEV1, FEV1/FVC, and FEF25-75 were different between 'S' and 'A' (102 +/- 14% vs 116 +/- 12%, 77.7 +/- 7.5 vs 88.2 +/- 4.5, and 74 +/- 22% vs 118 +/- 24%, respectively; P < 0.05); FVC and PEF were not different. Ten 'S' athletes had <80% FEV1/FVC; 9 had <70% predicted FEF25-75. Six of 9 EIB+ subjects had symptoms; cough occurred in all six and was related to EIB (chi 2 = 4.23, OR = 6.5, CI = 1.1-44.1; P = 0.039). CONCLUSION: Baseline lung function is related to symptoms and precludes EIB in some rink athletes, suggesting that EIB and its development is a heterogeneous and may involve fibrotic as well as inflammatory processes. Small airway dysfunction in ice arena athletes is likely related to internal combustion pollutants emitted from ice resurfacing machines.

Adult↗
PubMed2001

Effects of heparin on hypertonic potassium chloride-induced bronchoconstriction.

BACKGROUND: Changes in bronchial osmolarity is a well-known factor for bronchoconstricion. Recenty, nonisotonic aerosols have begun to be used for the assessment of bronchial hyperreactivity. Hypertonic KCl can cause bronchoconstriction even in non-symptomatic asthmatic patients. OBJECTIVE: To evaluate the protective role of heparin on hypertonic KCl-induced bronchospasm in asthma. METHODS: Thirty-eight asthmatic patients were included in this double-blind, placebo-controlled study. On day 1 of the study, after performing the respiratory function test (RFT), patients had inhaled KCl 10% and RFTs were done after 20 minutes. On day 2 of the study, after the basal RFT, 18 patents inhaled NaCl 0.9% 0.2 mLkg solution. After the completion of this procedure, patients waited for 20 minutes and inhaled KCl 10% 10 mL, and RFTs were repeated 20 minutes later. The second group consisted of 20patients who inhaled heparn 1,000 units/kg after the RFTs were performed. Twenty minutes later, they inhaled KCl 10% and waited for 20 minutes. Finally, RFTs were done and compared with those from the other group. RESULTS: In the control group, forced expiratory volume in one second (FEV1) decreased 17.4% on day 1 and 16.4% on day 2. In the heparin-treated group, FEV1 decreased 18.6% on day 1, but almost no change occurred after this group was treated with heparin before inhalation of hypertonic KCl on day 2. CONCLUSIONS: Heparin was found to be highly protective against hypertonic KCl induced bronchospasm in bronchial asthma.

Adolescent↗
PubMed1976

Regional bronchoconstriction in asthma. 133Xenon washout scans following parenteral methacholine.

To determine the influence of bronchoconstriction on the distribution of ventilation during an asthma attack, pulmonary clearance of 133xenon was evaluated in four normal and eight asthmatic subjects within three to five minutes after intramuscular injection of methacholine. In asthmatics, administration of 4-10 mg methacholine resulted in a decrease of forced vital capacity of 28.5 +/- 5.1 (SE) percent and a decrease in expiratory flow at 60 percent vital capacity of 44.2 +/- 6.9 percent (P less than 0.001). The cumulative ventilation required to reach 50 percent of the pre-washout radioactivity increased from 3.6 +/- 0.8 to 9.9 +/- 1.6 L after administration of the drug (P less than 0.05). The normal subjects showed no ventilatory effects after receiving 10 mg methacholine. Comparison of clearance of 133xenon from ten areas of lung (each representing approximately 6 percent of the surface area of one lung) showed that all areas were affected to approximately the same extent during drug-induced asthma. These findings suggest that parenteral methacholine is an effective way to demonstrate airway hyperreactivity and that the airway response to methacholine in asthmatics is relatively generalized throughout the lung.

Adult↗
PubMed1985

Comparative effects of oral and inhaled verapamil on antigen-induced bronchoconstriction.

We investigated the comparative effects of oral and inhaled verapamil on specific airway conductance (SGaw) and allergic bronchial reactivity. Ten asymptomatic subjects with ragweed hypersensitivity and a history of bronchial asthma were studied on four different days, without and with pre-treatments by oral (160 mg) or inhaled (20 mg) verapamil. Bronchial reactivity was measured as the cumulative provocative dose of ragweed antigen which caused a 35 percent decrease in SGaw, ie PD35. The amount of inhaled verapamil actually deposited in the tracheobronchial tree was estimated to be 0.56 mg. Mean SGaw was not affected by either mode of administration; mean SGaw (SE) was 0.13(.02) and 0.12(.02) L/sec-1 before and .14(.02) and 0.12(.02) L/sec-1 after oral and inhaled verapamil, respectively. Mean (SE) PD35 was reproducible on two control days, ie 0.9(.4) and 0.8(.4) breath units, respectively. Inhaled verapamil increased mean PD35 to 18.8 (10.8) breath units (p less than 0.02), while oral verapamil had no significant effect on mean PD35. This study demonstrates that route of administration of calcium antagonist verapamil is an important factor in protection against antigen-induced bronchoconstriction. Inhalation of verapamil appears to be more effective than oral administration.

Administration, Oral↗
PubMed1987

The inhibitory effect of azelastine and ketotifen on histamine-induced bronchoconstriction in asthmatic patients.

We studied the antihistaminic property of a new compound, azelastine, on histamine-induced bronchoconstriction and compared it with ketotifen and placebo. In 12 patients with bronchial asthma we performed histamine bronchial challenges before and four hours after ingestion of placebo, 2.0 mg ketotifen, and 4.4 mg azelastine given in a double-blind, randomized, cross-over fashion. Ketotifen and azelastine provided significant protection compared with placebo. No statistically significant difference between ketotifen and azelastine could be detected. As the antihistaminic effect of azelastine does not predict the therapeutic usefulness in the maintenance therapy of bronchial asthma, further studies are indicated.

Adult↗
PubMed1989

New assessment of airway responsiveness. Effect of pretreatment with procaterol on allergen-induced bronchoconstriction.

We examined airway responsiveness to allergen inhalation using a novel technique by which dynamic compliance (Cdyn) and pulmonary resistance (Rl) are simultaneously calculated by Fourier-series analysis of flow and transpulmonary pressure during tidal breathing. C0 and C0.5 (Cdyn at the frequency of zero and 0.5 Hz, respectively) were computed using the regression line of Cdyn versus frequency measured at the fundamental and first three harmonics in each breathing cycle. First, the validity of this system was tested by comparing Rl, C0 and C0.5 during five consecutive breaths with those obtained by the conventional method. A good correlation was seen in Rl, C0 and C0.5 between the two methods. Second, we studied airway response to allergen inhalation before and after oral administration of a long-acting beta 2-stimulant (procaterol, 50 micrograms or 100 micrograms) or placebo in a double-blind crossover trial in six atopic asthmatic subjects. In control allergen inhalation tests by administration of placebo, Rl increased progressively, and C0.5, expressed as percentage of control compliance at zero frequency (C0.5/COcont), decreased progressively. After 100 micrograms procaterol, Rl response to allergen was almost completely inhibited. However, a decrease in C0.5/C0cont was still observed. These findings suggest that pretreatment of asthmatic patients with procaterol can release allergen-induced bronchoconstriction of the central airways, but cannot release that of the peripheral airways.

Adult↗