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At least 1,153 records · Page 64Linked to original sources
PubMed1981

Bronchoconstriction induced by intratracheal administration of platelet-activating factor (PAF-acether) in baboons.

Intratracheal administration of PAF-acether (60 microgram.kg-1) was performed in six premedicated, curarized and mechanically ventilated baboons. Whereas intratracheal administration of an equal amount of solvent (200 microliter of 80 degrees alcohol in 2 ml of saline) caused no measurable changes in lung mechanics, administration of PAF-acether caused an almost immediate bronchoconstriction that was spontaneously reversible within about 30 min. The concomitant fall in platelet count in peripheral blood and reduction of perfusion of ventilated lung territories estimated from the alveolar-arterial difference in CO2 tension provide circumstantial evidence that PAF-acether also caused aggregation of platelets in the lung microcirculation. In keeping with the release of PAF-acether by human alveolar macrophages, our findings suggest that this mediator may play a role in human asthma.

Airway Resistance↗
PubMed1981

Leukotrienes C and D induce aspirin-sensitive bronchoconstriction in the guinea-pig.

Branchoconstriction in the guinea-pig due to leukotrienes C4 and D4 in vivo and in vitro was suppressed by aspirin. Since contracting effects of putative mediators of bronchial asthma should be refractory to inhibition of cyclooxygenase, our results indicate that release of leukotrienes in the guinea-pig does not alone account for anaphylactic bronchoconstriction.

Airway Resistance↗
PubMed1993

Inhalation of calcium channel blocking agents protects against methacholine-induced bronchoconstriction.

The calcium channel blockers, diltiazem and verapamil, and the beta agonist orciprenaline sulfate all demonstrated significant protection against methacholine-induced bronchoconstriction in 11 stable asthmatics (5 males and 6 females). Ten and 20 mg of inhaled diltiazem, 5 mg of verapamil or 30 mg of orciprenaline administered 15 min before stepwise increasing doses of methacholine hydrochloride produced significant reduction in respiratory resistance (Rrs), minimum dose of methacholine hydrochloride required for Rrs increase (Dmin) and bronchial reactivity measured with an Astograph. The mechanism of action of the calcium channel blockers is presumably at the level of the smooth muscle cells themselves. The combination of positive influence and lack of any adverse effect on blood pressure or heart rate with any of the agents tested indicates that their clinical application for alleviation of acute asthma can be recommended.

Journal Article↗
PubMed1983

Tolerance to sulfur dioxide-induced bronchoconstriction in subjects with asthma.

A study to determine whether the bronchoconstriction induced by low concentration of sulfur dioxide in subjects with asthma decreases with repeated exposure was undertaken. Eight subjects with asthma performed 3 min of voluntary eucapnic hyperpnea with 0.5 ppm of SO2 in humidified filtered air three times at 30-min intervals and we measured specific airway resistance (SRaw) before and after each period of hyperpnea. Specific airway resistance increased significantly more after the first exposure to SO2 [(from 7.6 +/- 1.7 to 15.5 +/- 2.0 L x cm H2O/liter/sec (mean +/- SEM)] than after the second (from 8.1 +/- 1.3 to 10.8 +/- 1.6) or third (from 7.6 +/- 1.6 to 10.1 +/- 1.9) exposures (P less than 0.025). When seven subjects repeated hyperpnea with SO2 24 hr and 7 days later, SRaw increased as much as it had after the first exposure (from 8.2 +/- 2.5 to 15.5 +/- 4.5 at 24 hr and from 6.6 +/- 1.4 to 15.4 +/- 2.1 at 7 days). In four subjects repeated exposure to SO2 caused short-term inhibition of the bronchomotor response to SO2 but did not inhibit the bronchomotor response to histamine aerosol. It was concluded that repeated exposures to a low concentration of SO2 over a short period (on 1 day) can induce tolerance to the bronchomotor effects of SO2 in subjects with asthma. Tolerance to the bronchomotor effects of SO2 is not caused by decreased responsiveness of airway smooth muscle or a generalized decrease in the responsiveness of vagal reflex pathways since the bronchomotor response to histamine is preserved.

Adult↗
PubMed1983

The effects of nifedipine and verapamil on antigen-induced bronchoconstriction in dogs.

The effects of calcium channel blockers, nifedipine and verapamil (i.v. and aerosol), were investigated in beagle dogs natively allergic to Ascaris suum antigen. Control exposures to an aerosol of Ascaris antigen provoked significant bronchopulmonary changes, i.e., increases in pulmonary resistance (RL) and decreases in dynamic lung compliance (CDYN). Pretreatment with either nifedipine or verapamil (200 micrograms/kg, i.v.) provided significant inhibition in the RL responses to Ascaris antigen (P less than 0.015) while neither agent significantly affected CDYN changes. When administered as an aerosol, verapamil (1.0%; 10 breaths) significantly inhibited both the RL and CDYN responses to Ascaris antigen (P less than 0.05), whereas a similar concentration of nifedipine was without effect. Resting basal levels of RL and CDYN were unaffected by either the i.v. route or by aerosols of either nifedipine or verapamil. These results suggest that calcium channel blockers may have beneficial effects against allergen-provoked bronchoconstriction; however, differences appear to exist in the choice of agent, route of administration and site of action.

Animals↗
PubMed1989

Inhibition of cholinergic and non-adrenergic, non-cholinergic bronchoconstriction in the guinea pig mediated by neuropeptide Y and alpha 2-adrenoceptors and opiate receptors.

The mechanisms underlying the regulatory influence of neuropeptide Y (NPY) and of alpha 2-adrenoceptor and opiate receptor activation on cholinergic and excitatory non-adrenergic, non-cholinergic (e-NANC) neurotransmission were studied in guinea pig hilus bronchi in vitro. NPY inhibited both the cholinergic and e-NANC bronchial contractions evoked by field stimulation. The NPY attenuation of the e-NANC contraction could not be antagonized by the alpha 2-antagonist, idazoxan, or naloxone. UK 14,304 a specific alpha 2-agonist, also reduced the two nervous components of bronchial contraction and this action was inhibited by idazoxan. NPY and UK 14,304 exerted a minor influence on the bronchial smooth muscle tone per se or on contractions evoked by acetylcholine or neurokinin A. This suggested that the inhibitory responses were caused by a prejunctional action reducing the release of transmitter substances from sensory and cholinergic nerve endings. Furthermore NPY (10(-7) M) seemed to be more potent to inhibit both contractile components than noradrenaline (10(-6) M) in the presence of propranolol (3 X 10(-6) M). Morphine was able to reduce the e-NANC response via a naloxone-sensitive mechanism. The capsaicin-evoked bronchoconstriction and the bronchodilator NANC effect evoked by field stimulation were, however, not influenced by UK 14,304. It is concluded that NPY, alpha 2-receptor and opiate receptor activation inhibit the release of sensory transmitters evoked by field stimulation but not by capsaicin.

Animals↗
PubMed1981

Airway anesthesia and respiratory response to methylcholine induced bronchoconstriction.

P0.1 and breathing pattern in response to acute methylcholine induced bronchoconstriction were studied with and without previous airway anesthesia in 6 normal subjects. In a randomized cross-over study, on two successive days, the subjects inhaled either 4% lidocaine hydrochloride or isotonic saline for 12 min, and then methylcholine for 3 min. FEV1, P0.1, and breathing patterns were measured at baseline and following each inhalation. Baseline values were changed neither by saline, nor by lidocaine, and methylcholine induced the same 18% decrease in FEV1 after each agent. Bronchospasm was not accompanied by a change in PACO2. After saline, methylcholine bronchospasm was associated with an increase of P0.1 from 1.0 +/- 0.2 (SEM) to 1.8 cm H2O +/- 0.3 (SEM) (P less than 0.05). During bronchospasm following airway anesthesia. P0.1 was increased from 1.1 +/- 0.2 (SEM) to 1.3 cm H2O +/- 0.3 (SEM), which was not significant. Comparing bronchospasm after saline to that after xylocaine we observed an increase in Ti afer xylocaine, which was correlated with the decrease in P0.1, suggesting that both were affected by airway anesthesia. We concluded that vagal airway receptors contribute to the increase in inspiratory drive which accompanies acute bronchospasm and also may contribute to the regulation of resting breathing pattern during bronchospasm in humans.

Adult↗
PubMed1982

Possible involvement of thromboxane in bronchoconstrictive and hypertensive effects of LTC4 and LTD4 in guinea pigs.

The actions of leukotriene (LT) C4 and D4 on the systemic arterial pressure and the insufflation pressure in guinea pigs and rabbits were examined. In guinea pigs, 0.3 - 3 nmole/kg of LTC4 and 0.1 - 1.0 nmole/kg of LTD4 administrated from left jugular vein caused dose-dependent increase of the airway resistance measured by the Konzett-Rössler method and a triphasic blood pressure response; an initial hypotension, a secondary hypertension and a third long-lasting hypotension. All of the hypertensive phase and 100 - 150% of the increase of the airway resistance by LTC4 and LTD4 were inhibited by a selective thromboxane synthetase inhibitor, OKY-1581 (10 mg/kg, i.v.) and only the hypotension was observed. Indomethacin (10 mg/kg, i.p.) also inhibited not only the airway resistance increase, but also the prolonged hypotension by LTC4 and shortened the duration of the hypotension by LTD4. It is suggested that thromboxane might be involved in bronchoconstriction and hypertensive effects by LTC4 and LTD4 and that hypotensive prostaglandin might be involved in the hypotensive phase after LTC4 and LTD4. In rabbits, the increase of the airway resistance by LTC4 and LTD4 (upto 100 nmole/kg, i.v.) was negligible and only the hypotension was observed.

Airway Resistance↗
PubMed1983

Enhanced bronchoconstriction responses to prostaglandin F2 alpha following inhalation of sulfur dioxide.

The effect of chronic sulfur dioxide (SO2) inhalation was investigated in pharmacologic-induced bronchoconstriction in beagle dogs. Increases in pulmonary resistance (RL) and decreases in dynamic lung compliance (CDYN) were observed with i.v. and aerosol administration of prostaglandin F2 alpha (PGF2 alpha). After control historical data were accumulated, the animals received exposures of 500 ppm of SO2 for two hours twice a week. After six months of chronic SO2 exposure, a significant enhancement in the RL response to i.v. and aerosolized PGF2 alpha was observed as compared to pre-SO2 data. Tracheobronchial inflammation, as observed by fiberoptic bronchoscopy, occurred as a result of the chronic inhalation of SO2; however, only a small increase in mucous production was observed visually. In addition, hypercapnic and acidotic changes in blood gas profiles were found. Therefore, beagle dogs chronically exposed to SO2, developed hyperactive airways as seen by increased sensitivity to PGF2 alpha. This model appears to reflect many of those changes observed in clinical bronchial hyperreactivity and may provide an additional insight into obstructive airways disease.

Animals↗
PubMed1985

Leukotriene A4-induced bronchoconstriction in the guinea pig in vivo.

Administration of leukotriene A4 (0.03-0.3 microgram kg-1 i.v.) to anesthetized spontaneously breathing guinea pigs produced pronounced changes in pulmonary resistance, dynamic compliance and blood pressure. The pulmonary responses were unaffected either by pretreatment with indomethacin or following desensitization to leukotriene B4 but were significantly attenuated by the leukotriene D4 receptor antagonist, FPL-55712. Following administration of leukotriene A4 increased levels of leukotriene C4-immunoreactive material were determined in the plasma and neutrophil accumulation was observed in the lung. It was concluded that leukotriene A4 induced bronchoconstriction in the guinea pig either by acting directly on the leukotriene D4 receptor site or more probably through efficient metabolism in the lung to peptido-lipid leukotrienes which in turn exerted direct bronchoconstrictor actions.

Airway Resistance↗
PubMed1986

A study with BN 52021 demonstrates the involvement of PAF-acether in IgE-dependent anaphylactic bronchoconstriction.

The involvement of platelet activating factor (PAF) in anaphylaxis was examined by recording the pulmonary responses of anesthetized passively sensitized guinea-pigs to the aerosolization of ovalbumin. Animals were tested with and without BN 52021 (a ginkgolide B, PAF receptor antagonist) pretreatment. Aerosolization of ovalbumin produced a bronchoconstriction (BC) which could be made refractory to additional challenges with the antigen. In animals desensitized to ovalbumin, aerosolization of PAF produced an unattenuated BC. Guinea pigs desensitized by repeated aerosolizations of PAF subsequently showed reduced responses to aerosolized antigen suggesting that PAF may be involved in the BC. Animals pretreated with BN 52021, were protected against the effects of systemically administered PAF and also showed reduced responses to aerosolized antigen. Aerosolization of the leukotriene antagonist, FPL 55712, was ineffective against anaphylactic BC under conditions where catecholamine and histamine release were blocked.

Aerosols↗
PubMed1988

Secondary release of thromboxane A2 in aerosol leukotriene C4-induced bronchoconstriction in guinea pigs.

Effect of a thromboxane synthetase inhibitor (OKY-046) on bronchoconstriction induced by aerosol leukotriene C4 and histamine was studied in anesthetized, artificially ventilated guinea pigs in order to examine whether secondary release of thromboxane A2 is produced by aerosol leukotriene C4 or not. 0.01-1.0 micrograms/ml of leukotriene C4 and 12.5-400 micrograms/ml of histamine inhaled from ultrasonic nebulizer developed for small animals caused dose-dependent increase of pressure at airway opening (Pao) which is considered to be an index representing bronchial response. Pretreatment of the animals with intravenous OKY-046 (100mg/kg) significantly reduced the airway responses produced by inhalation of 0.1, 0.33 and 1.0 micrograms/ml of leukotriene C4, while the pretreatment did not affect the histamine dose-response curve. Based on these findings and previous reports (6,7), it is suggested that aerosol leukotriene C4 activates arachidonate cyclooxygenase pathway including thromboxane A2 synthesis and the released cyclooxygenase products have bronchodilating effect as a whole.

Aerosols↗
PubMed1988

The effect of an orally active leukotriene (LT) D4 antagonist WY-48, 252 on LTD4 and antigen-induced bronchoconstrictions in allergic sheep.

In this study we examined the effects of a new orally active leukotriene (LT) D4 receptor antagonist, WY-48,252 (1,1,1-trifluoro-N-[3-(2-quinolinylmethoxy)phenyl]methanesulfonamide), on LTD4-induced bronchoconstriction and antigen-induced early and late responses in allergic sheep. For all studies WY-48,252 10 mg/kg, was administered via intragastric tube 1 h prior to airway challenge. In seven sheep, airway challenge with LTD4 [delivered dose mean +/- SE, 53 +/- 2 micrograms] resulted in an immediate increase in SRL to 600 +/- 18% over baseline. When these same sheep were treated with WY-48,252, airway challenge with LTD4 (delivered dose, 61 +/- 5 micrograms) resulted in only a 220 +/- 50% increase in SRL (p less than 0.05 vs placebo). The drug had no effect on baseline SRL. WY-48,252 was also effective in reducing early responses and blocking late responses to inhaled antigen in allergic sheep (n = 7). In the control trial, airway challenge with Ascaris suum antigen resulted in immediate and late (i.e. 6-8 h) increases in SRL of 499% and 138% over baseline (both responses, p less than 0.05). When these same sheep were pretreated with WY-48,252 the immediate antigen-induced increase in SRL was 171% and the late response was 49% over baseline (both responses p less than 0.05 vs control). These results indicate that WY-48,252 is a LTD4 antagonist in allergic sheep. The ability of this compound to modify antigen-induced early responses and to block antigen-induced late responses suggests that the generation of LTD4 during airway anaphylaxis contributes to both responses.

Aerosols↗
PubMed1977

A canine model for reaginic hypersensitivity and allergic bronchoconstriction.

Immunization of neonatal dogs with a conjugate of 2,4-dinitrobenzene and ovalbumin (DNP2-OA), using aluminum hydroxide as the adjuvant, elicited long-lasting (over 30 wk) anti-DNP and anti-OA IgE antibody responses of high titers as determined by homologous passive cutaneous anaphylaxis. Low antigen doses of 10 or 50 mug were more effective than the higher doses of 250 or 1,250 mug in inducing high IgE antibody levels. However, this method of immunization failed to elicity any detectable IgE antibody response in adult dogs. Bronchoprovocation with antigen of sensitized animals having IgE antibody titers in excess of 64 resulted in a marked increase in airflow resistance, which could be corrected by the administration of nebulized isoproterenol. On the other hand, sensitized animals with IgE antibody titers in the order of 64 did not manifest significant bronchoconstriction on inhalation challenge but developed anaphylaxis following intravenous injection of the antigen.

Aging↗
PubMed1981

Effects of ascorbic acid and indomethacin on the airways of healthy male subjects with and without induced bronchoconstriction.

We have investigated the effects of ascorbic acid (1.0 gm orally) and indomethacin (50 mg orally) on airway tone in the basal state in six health nonsmoking male adults. Airway tone was assessed from measurements of specific airway conductance and flow rates interpolated from partial expiratory flow-volume curves by means of whole-body plethysmography and spirometry, respectively. Neither ascorbic acid nor indomethacin alone produced a significant change in basal tone. However, both the duration and intensity of the bronchoconstriction induced by methacholine aerosol (10 mg/ml for 30 sec) were significantly reduced by prior administration of ascorbic acid. This ameliorating action of ascorbic acid was blocked by ingestion of indomethacin. The results suggest that ascorbic acid exerts its effects by altering the production of a bronchodilator prostaglandin.

Airway Resistance↗
PubMed1982

Further investigation of the association between gastroesophageal reflux and bronchoconstriction.

A double-blind modification of the intraesophageal acid perfusion challenge (Bernstein procedure) was performed in asthmatic subjects with and without gastroesophageal reflux, nonasthmatic subjects with reflux, and normal subjects. Conventional spirometric functions and total respiratory resistance (Rrs) were measured prior to and after the infusion. There were no changes in pulmonary functions except in the asthmatic subjects who had had a positive acid challenge. The greatest changes occurred in Rrs, which increased significantly with reflux symptoms (p less than 0.01) and decreased toward baseline (p less than 0.05) when these symptoms were relieved with antacids. The response was even greater in asthmatic subjects who associated reflux symptoms with attacks of asthma. These results support previous findings that acid reflux symptoms could cause a bronchoconstrictive response in certain asthmatic patients.

Airway Resistance↗
PubMed1983

Inhaled verapamil in histamine-induced bronchoconstriction.

Fifteen asthmatic subjects participated in a double-blind trial comparing the protective effects of inhaled verapamil, salbutamol, and saline against inhaled histamine. Inhaling verapamil between four repeated histamine inhalation tests produced no significant protection against histamine-induced bronchoconstriction, while there was significant protection with salbutamol (p less than 0.001). Inhaling verapamil before a single inhalation test produced limited but significant protection (p less than 0.05) compared with a saline control in eight asthmatic subjects. This small protective effect in the two-treatment study of eight asthmatics suggests that either the protective effect of verapamil is variable among subjects or a preceding histamine inhalation test blocks the verapamil effect.

Adult↗
PubMed1984

Inhibition of antigen-induced bronchoconstriction by methylprednisolone succinate.

We investigated whether the glucocorticoid methylprednisolone succinate mg/kg) could prevent antigen-induced bronchoconstriction in conscious sheep. Ten allergic ewes were subjected to inhalation challenge with Ascaris suum antigen, with and without methylprednisolone pretreatment, administered intravenously either 20 min or 3 hr before antigen challenge. Antigen challenge alone resulted in increased airflow resistance, pulmonary hyperinflation, and decreases in dynamic lung compliance and arterial oxygen tension. Methylprednisolone administered 20 min before antigen challenge had no effect on these antigen-induced changes. In contrast, administration of methylprednisolone 3 hr before antigen challenge effectively prevented all the responses to antigen challenge. We suggest that pretreatment with glucocorticoids can attenuate airway anaphylaxis if sufficient time is allowed between the pretreatment and the antigen challenge.

Animals↗