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PubMed1991

Tachykinin recovery during postmortem bronchoconstriction in guinea pig lungs.

We examined the role of substance P (SP) and neurokinin A (NKA) in the postmortem bronchoconstriction in guinea pig lungs using isolated lungs superfused via the trachea. Airway opening pressure (Pao) during superfusion was monitored and the superfusate collected for analysis of SP- and NKA-like immunoreactivities (SP-LI and NKA-LI, respectively). Peak Pao (39.0 +/- 3.9 cmH2O) was reached 10 min after starting superfusion; Pao decreased slowly thereafter, reaching only 9.9 +/- 2.2% of the peak value 2 h after starting superfusion (P less than 0.005); 12.6 +/- 2.6 and 34.0 +/- 9.7 fmol of SP-LI and NKA-LI, respectively, were found in the fraction corresponding to 10-20 min of superfusion. Recovered immunoreactivities decreased to 5.2 +/- 0.3 and 9.3 +/- 1.8 fmol of SP-LI and NKA-LI, respectively, in the fraction corresponding to 110-120 min of superfusion (P less than 0.05). Inhibition of neutral endopeptidase with thiorphan resulted in significantly greater increases in Pao (P less than 0.005) and augmentation of the recovery of SP-LI and NKA-LI (P less than 0.05 and P less than 0.001, respectively). Capsaicin treatment of animals 7-10 days before the removal of their lungs abolished the increase in Pao during superfusion and resulted in a significant decrease in the amount of SP-LI and NKA-LI recovered. Our data confirm that tachykinin release occurs during postmortem bronchoconstriction in guinea pig lungs and, furthermore, that tachykinin degradation by NEP modulates the intensity of this response.

Animals↗
PubMedDate not supplied

Management of exercise-induced bronchoconstriction.

Exercise-induced bronchoconstriction (EIB) is a common clinical manifestation of asthma, occurring in 70% to 80% of asthmatics. Evidence suggests that exercise and the ensuing bronchoconstriction do not contribute to a worsening of asthmatic inflammation. Asthmatics should not be discouraged from exercising, and, with adequate management, most patients should be able to exercise regularly with only minor symptoms. The first step in the management of patients with EIB should be to obtain optimum control of the underlying asthma, often requiring regular treatment with inhaled steroids. Regular treatment with inhaled corticosteroids usually reduces the extent of EIB by 50% or more. Frequently, despite optimal management of the underlying asthma, patients develop EIB symptoms requiring additional treatment. Short and long acting inhaled beta2-agonists are highly effective at reducing the magnitude of EIB, although there are concerns that the extent of protection diminishes during periods of regular use of these agents. Inhaled cromolyn and nedocromyl are effective at reducing the extent of EIB in some patients, although this protection does not extend beyond 2 to 3 h after treatment. The recently developed leukotriene receptor antagonists are effective at reducing the extent of EIB by 40% to 70%, and have the advantage that this protection lasts throughout the day and does not appear to diminish with regular use. Other agents, including anticholinergics and antihistamines, have been shown to offer partial protection against EIB, suggesting the possibility of using a combination treatment to manage some patients' symptoms. Finally, there is encouraging evidence suggesting that modifications of the pattern of exercise can markedly reduce the extent of EIB.

Adrenergic beta-Antagonists↗
PubMed1988

Azelastine, a new antiallergic/antiasthmatic agent, inhibits PAF-acether-induced platelet aggregation, paw edema and bronchoconstriction.

Azelastine is a phthalazinone derivative with a wide spectrum of pharmacologically relevant activities. Since PAF-acether has been considered to be a potent mediator of asthma, azelastine was assayed for its ability to counteract PAF-acether-induced platelet aggregation, paw edema development and bronchoconstriction. Azelastine exerted a concentration-dependent inhibition of PAF-acether-induced platelet aggregation in human platelet rich plasma with an IC50 of 87 mumol/l and was as effective as ketotifen. PAF-acether-induced paw edema was reduced by intraperitoneal administration of azelastine resulting in an ID50 of 14.4 mg/kg after 2 h. By contrast, ketotifen was not able to inhibit edema development up to a dose of 32 mg/kg i.p. Azelastine and ketotifen, administered intravenously, dose-dependently inhibited PAF-acether-induced bronchoconstriction, starting from the dose of 0.01 mg/kg and resulting in ID50s of 0.03 and 0.02 mg/kg, respectively. These results show that azelastine is endowed with a peculiar anti-PAF-acether action, which may be advantageous in its therapeutic use, in the treatment of asthma.

Animals↗
PubMed1977

Exercise-induced bronchoconstriction in patients with bronchial asthma. Its prevention with an antihistaminic agent.

14 asthmatic patients developing regularly exercise-induced bronchoconstriction were subjected to a submaximal exercise on a bicycle ergometer. On the first day the exercise was not preceded by any medication; on the second, 50 mg thiazinamium was given, and on the third day 2 mg atropine was given before the exercise. The changes in the calibre of the bronchi were assessed with a Wright peak flow meter. With thiazinamium a complete protection against the bronchoconstriction was observed in 12 patients, in one the protection was partial and in an other no beneficial effect of the drug was found. It seems that protection given by thiazinamium was due to its antihistaminic property and not to the anticholinergic one, as among 10 patients protected by thiazinamium, only 2 were also protected by the atropine.

Adult↗
PubMed1979

The location of sensoric bronchoconstricting receptors in the upper airways.

The bronchoconstrictoric influence of allergen and acetylcholine aerosol was tested in 16 boxer dogs. The animals were exposed to these substances through a mask. The aerosol was also administered directly to three restricted areas of the trachea. Both substances induced a strong bronchoconstriction when administered through the mouth. Only the allergen showed a similar strong bronchoconstriction when administered to a restricted area in the upper third of the trachea.

Acetylcholine↗
PubMed1979

The side of action of bronchodilating drugs (beta 2-stimulators) on antigen-induced bronchoconstriction.

The prophylactic effect of a sympathicomimetic drug (Fenoterol) was tested separately for the upper and the lower respiratory tract on 14 boxer dogs exposed to antigen challenge. In the lower airways, a restricted short-lasting diminution of bronchoconstriction was observed when both antigen and Fenoterol were administered to these airways. Administration of Fenoterol to the upper respiratory tract showed a long-lasting strong local effect in prevention of antigen-induced bronchoconstriction. There is a strong long-lasting effect of sympathicomimetic bronchodilators on the sensoric part of the reflex way into the airways. There is, with similar dosages, a weak short-lasting direct effect of these drugs on bronchial muscles.

Aerosols↗
PubMed1982

Contribution of residual volume to the increased alveolar plateau with bronchoconstriction.

We studied 10 normal volunteers with single-breath nitrogen tests before and after methacholine-induced bronchoconstriction. On the first day we challenged each subject with increasing methacholine concentrations to obtain a 20% drop in the partial forced expired volume in 1 s/partial forced vital capacity ratio. This resulted in an increased residual volume (RV) from 1,536 +/- 138 to 2,371 +/- 216 ml (mean +/- SEM, p less than 0.01). On the following day we did single-breath nitrogen tests from RV, RV + delta V (delta V is the individual's RV increase after bronchoprovocation) and after a similar methacholine rechallenge. Baseline slope of phase III was 0.88 +/- 0.11% N2/1 (mean +/- SEM), 1.36 +/- 0.22% N2/1 with the RV + delta V test (p less than 0.01), and 2.84 +/- 0.68% N2/1 with bronchoconstriction (p less than 0.05). The results show that the changes in RV per se accounted for 24% of the increase in the slope of phase III seen with bronchoprovocation.

Adult↗
PubMed1984

Partial sensory denervation of the upper respiratory tract on allergen- and histamine-induced bronchoconstriction.

The influence of partial denervation of the upper part of the respiratory tract on histamine- and antigen-induced bronchoconstriction was investigated in a series of 12 boxer dogs. To achieve this purpose, the superior laryngeal, hypoglossal and glossopharyngeal nerves were sectioned. The prophylactic effect of unilateral transection of these nerves on antigen-induced bronchoconstriction originating in the upper respiratory tract could be demonstrated.

Aerosols↗
PubMed1988

Effect of sodium cromoglycate and nifedipine on adenosine-induced bronchoconstriction.

Inhaled adenosine causes bronchoconstriction in asthmatic patients. In 7 symptom-free asthmatics a study was performed to investigate the effect of sodium cromoglycate and nifedipine on adenosine-induced bronchoconstriction. All patients were challenged with increasing doses (from 0.03 to 2 mg) of nebulized adenosine to assess airway reactivity. The same procedure was repeated on different days at the same time each morning after administration of placebo and drugs in a randomized double-blind study. Airway response was measured as the forced expiratory volume in 1 s (FEV1). The PD20 value and the fall of FEV1 at the provocative dose were calculated. The PD20 data were modified in log values and the statistical analysis was performed by two-way analysis of variance. Mean decrease of FEV1 after adenosine challenge was 26.02 and 28.87% with placebo sodium cromoglycate and placebo nifedipine, respectively. Sodium cromoglycate and nifedipine gave a mean decrease of FEV1 of 6.44% (p less than 0.05) and 22.22%, respectively. PD20 values (geometric mean) after adenosine inhalation were 0.72 and 0.74 mg for placebo sodium cromoglycate and placebo nifedipine and 0.86 mg for nifedipine. Sodium cromoglycate gave a significant protection against adenosine in all subjects and in no case did the maximum dose used (2 mg) result in a fall in FEV1 value greater than 20%. Adenosine antagonism could be considered as a possible factor contributing to the pharmacologic efficacy of sodium cromoglycate in asthmatic patients. No protective effect was noticed with nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1989

Inhibition of fog-induced bronchoconstriction by nedocromil sodium and sodium cromoglycate in intrinsic asthma: a double-blind, placebo-controlled study.

The efficacy of pretreatment with two doses of nedocromil sodium (4 and 8 mg) and sodium cromoglycate 12 mg were compared with placebo in inhibiting the bronchoconstriction induced by inhalation of ultrasonically nebulized distilled water ('fog') in 10 subjects with intrinsic asthma. Each fog challenge consisted of three inhalations of 30, 60 and 120 s duration, respectively, given at 4-min intervals, and the bronchoconstrictor response was assessed as the postchallenge percentage fall in FEV1 from baseline. Statistically significant drug effects (p less than 0.05) were observed after 120 s of fog challenge: both nedocromil sodium 4 and 8 mg and sodium cromoglycate were significantly more effective than placebo in inhibiting fog-induced bronchoconstriction; in addition, nedocromil sodium 4 mg proved statistically significantly more effective than sodium cromoglycate.

Administration, Inhalation↗
PubMed1976

IgE-mediated anaphylactic bronchoconstriction in the guinea pig and the effect of disodium cromoglycate.

Using guinea pigs, the development of anaphylactic hypersensitivity with time after Trichinella spiralis infection has been studied, the response being assessed in terms of bronchoconstriction at 5, 12, 19 and 26 days after infection. In addition, the susceptibility of these reactions to treatment with disodium cromoglycate (DSCG) has been determined. At 12 days after infection, DSCG significantly reduced the severity of anaphylactic bronchoconstriction, suggesting that IgE competes with IgG1 antibody for sensitisation sites in the lung.

Anaphylaxis↗
PubMed1983

Time course of morphometric changes after acute allergic bronchoconstriction in the guinea pig.

Experimental allergic bronchoconstriction was induced in guinea pigs by passive sensitization with a standard dose of homologous antiserum followed by challenge with aerosolized antigen. Lungs were removed from animals at intervals of up to 6 days thereafter, and several parameters of the reaction were assessed morphometrically by comparison with lungs from unsensitized guinea pigs. We determined all changes in volume of the lung tissue resulting from fixation through to the preparation of histologic sections, but no significant differences were observed between the time course subgroups. The size of both large and small airways was assessed by a point-counting technique, as well as by measurement of the percentage of the diameter of the airways contributed by the mean thickness of the muscular layer. Maximal bronchoconstriction was observed morphometrically to correspond with the peak of a response as determined clinically by the use of a strain gauge around the chest. This was followed by a return to normal of the airway size. The number of mast cells and eosinophils around large and small airways, around branches of the pulmonary artery and in random fields of the lung parenchyma was tabulated. The maximal decrease in mast cells was seen in animals which died immediately following challenge, but the numbers were not restored to the control level even in animals which had survived for 6 days. The greatest increase in eosinophil response occurred in lungs obtained 10 min following challenge. This model will be of value in determining the effects at the tissue level of pharmacological inhibitors of this reaction.

Acute Disease↗
PubMed1985

Inhibition of the presumably leukotriene-dependent component of antigen-induced bronchoconstriction in the guinea pig by piriprost (U-60,257).

Piriprost (U-60,257), a selective inhibitor of the 5-lipoxygenase, inhibited bronchoconstriction in a modification of the Konzett-Rossler procedure in which bronchoconstriction in sensitized guinea pigs may reflect leukotriene production. The duration of action of this compound and also the possible development of tachyphylaxis to its action upon repeated dosing were studied using a newly developed procedure for dosing conscious animals via the aerosol route. Duration of action with the lowest concentration which afforded maximum protection (180 s exposure to a 0.01% solution) was approximately 1.5 h. No decrease in drug potency was observed after 7 daily drug treatments.

Administration, Oral↗
PubMed1987

The role of histamine in allergen and adenosine-induced bronchoconstriction.

We have investigated the role of histamine in allergen and adenosine-5'-monophosphate (AMP)-induced bronchoconstriction in asthmatic subjects by performing inhalation challenge tests with histamine, AMP and allergen after treatment with placebo or the potent H1 histamine receptor antagonist, terfenadine. Single concentrations of each agonist which had previously been shown to produce a 30% fall in FEV1 were used. After placebo, AMP and histamine both produced rapid bronchoconstriction reaching a maximum within 5 min and returning to within 10% of baseline after 25 min. Terfenadine inhibited this reaction to histamine completely and to AMP by 86%. The response to allergen was slower in onset and was sustained over 45 min and was inhibited 50% by terfenadine. We interpret these results as reflecting the contribution of histamine to the various airway challenges, both histamine and newly generated mediators comprise the response to allergen, whereas AMP selectively enhances mast cell degranulation without affecting the production of arachidonic acid derived mediators.

Adenosine Monophosphate↗
PubMed1988

Effect of a novel leukotriene D4 antagonist with 5-lipoxygenase and cyclooxygenase inhibitory activity, Wy-45,911, on leukotriene-D4-and antigen-induced bronchoconstriction in the guinea pig.

Wy-45,911 (4-[hydroxy-[3-(2-quinolinylmethoxy)phenyl] amino]-4-oxabutanoic acid, methyl ester) was found to inhibit competitively leukotriene D4 (LTD4)-induced contractions of the isolated guinea pig trachea but not those of leukotriene C4 (LTC4), even in the presence of a gamma-glutamyltranspeptidase inhibitor, reduced glutathione (GSH). Tracheal contractions induced by histamine or pilocarpine were also not significantly altered by Wy-45,911. The drug inhibited the tracheal contractions induced by antigen, even in the presence of GSH. This latter effect resulted from inhibition of 5-lipoxygenase (5-LO), as the synthesis of 5-LO products by rat polymorphonuclear leukocytes and by mouse macrophages was markedly reduced by Wy-45,911. The drug inhibited both LTD4-induced and antigen-induced bronchoconstriction when injected intraduodenally or intragastrically into intact guinea pigs though it was more potent against LTD4-induced bronchoconstriction. We conclude that Wy-45,911 is a novel, orally active LTD4 antagonist in the guinea pig, with some 5-LO inhibitory activity.

Animals↗
PubMed1994

Refractoriness of eucapnic hyperventilation-induced bronchoconstriction in rabbits.

The mechanism of refractoriness in bronchoconstriction after repeated hyperventilation was investigated in 18 sensitized rabbits. Rabbits were separated into three groups: an untreated control group (n = 7), a cimetidine-treated group (n = 6), and an indomethacin-treated group (n = 5). After anesthetization, hyperventilation was performed for 15 min (120 breaths/min, 7 ml/kg tidal volume) with dry air containing 5% CO2. Total lung resistance (RL) and dynamic compliance (Cdyn) were measured before (baseline) and after hyperventilation challenge. After RL and Cdyn had returned to baseline values, the hyperventilation challenge was repeated. In the control group maximal increase in percent RL (max %RL) was 49 +/- 9% after the first challenge, but 16 +/- 4% after the second challenge, indicating refractoriness. A similar tendency was observed in percent Cdyn. In the cimetidine- and indomethacin-treated groups, max %RL were 42 +/- 3% and 60 +/- 15% after the first challenge, and 35 +/- 8% and 60 +/- 7% after the second challenge, respectively, indicating no refractoriness. These results suggest that the H2-receptor and bronchodilating prostanoids play an important role in producing the refractoriness to bronchoconstriction observed in sensitized rabbits after repeated hyperventilation.

Airway Resistance↗
PubMed2000

Exhaled nitric oxide and exercise-induced bronchoconstriction in asthmatic children.

It is known that exhaled nitric oxide (ENO) is increased in asthmatic individuals, probably as an expression of airway inflammation, but no studies have been reported of ENO and exercise-induced bronchoconstriction (EIB). We assessed the effect of a treadmill exercise challenge on ENO concentration in 24 asthmatic children aged 11.2 +/- 0.4 yr (mean +/- SEM). According to the presence or absence of EIB, the children were divided into an EIB group (n = 10) and a non-EIB group (n = 14). ENO was measured with a single-breath reservoir technique. FEV(1), ENO, and heart rate were measured at baseline and 1, 6, 12, and 18 min after the end of exercise. We also measured ENO in 18 healthy control children aged 10.8 +/- 0.6 yr, of whom nine underwent an exercise challenge identical to that of the asthmatic children. After the exercise test, the mean decrease in FEV(1) was 34% in the EIB group and 5% in the non-EIB group. The EIB group had higher baseline ENO values (12.3 +/- 1.6 ppb) than the healthy children (6.1 +/- 0.2 ppb) (p < 0.01). The time course of ENO was similar in the EIB, non-EIB, and control groups, with no significant changes after exercise (p = NS). In the overall group of asthmatic children there was a significant correlation (r = 0.61, p < 0.01) between baseline (preexercise) ENO and magnitude of the maximal decrease in FEV(1) after exercise. In conclusion, our study shows that ENO levels do not change during acute airway obstruction induced by exercise challenge in asthmatic children. In addition, baseline ENO values correlate with the magnitude of postexercise bronchoconstriction, suggesting that NO may be a predictor of airway hyperresponsiveness to exercise.

Adolescent↗
PubMed1987

Symptomatic bronchoconstriction after short-term inhalation of sulfur dioxide.

We studied the relationship between duration and concentration of exposure in SO2-induced bronchoconstriction in 8 asthmatic subjects. On separate days, we administered SO2 in humidified air through a mouthpiece at 2 concentrations (0.5 and 1.0 ppm) for 3 time periods (1, 3, and 5 min) during eucapnic hyperpnea (60 L/min). Humidified air was administered for 5 min as a control. Bronchoconstriction was assessed by measurement of specific airway resistance (SRaw). The magnitude of the bronchoconstrictor response to both concentrations of SO2 increased progressively over the 3 time periods studied. The mean (+/- SE) increase in SRaw (in L x cm H2O/L/s) and percent increase above baseline (in parentheses) after each exposure to SO2 were as follows: 2.5 +/- 0.3 (34%) after 0.5 ppm for 1 min; 7.5 +/- 4.7 (93%) after 1.0 ppm for 1 min; 13 +/- 3.2 (173%) after 0.5 ppm for 3 min; 31.4 +/- 7.4 (395%) after 1.0 ppm for 3 min; 19.6 +/- 4.0 (234%) after 0.5 ppm for 5 min; 44.1 +/- 9.8 (580%) after 1.0 ppm for 5 min; 3.5 +/- 1.5 (46%) after humidified air for 5 min. For the group, the increases in SRaw caused by inhalation of both concentrations of SO2 for 1 min were small. However, 2 of 8 subjects did develop large increases in SRaw and chest tightness after inhalation of 1.0 ppm for 1 min. Seven of 8 subjects developed wheezing, chest tightness, or dyspnea and used an inhaled bronchodilator after inhalation of 0.5 ppm for 3 and 5 min and 1.0 ppm for 3 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗