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PubMed1999

Effect of CPAP on breathlessness perception in healthy subjects during methacholine induced bronchoconstriction.

Application of continuous positive airway pressure (CPAP) in asthmatic patients decreases breathlessness (B). The effect of CPAP on induced bronchoconstriction was studied in healthy subjects. The changes in B were related to changes in lung function indices. In nine healthy volunteers, males aged 20-27 years, acute bronchoconstriction was induced by inhalation of 1 to 128 mg/ml methacholine (M). CPAP (0.5 kPa) was then applied for 1 min. It was followed by inhalation of albuterol. Forced expiratory volume in 1 s (FEV1) and vital capacity (VC) were measured by spirometry and end expiratory lung level (EELL), to derive inspiratory capacity (IC), by inductive plethysmography. B was assessed by Borg scale. After the maximal concentration of M, FEV1 decreased by 14% (p < 0.01) as compared to the control values and Borg score (BS) increased to 2.4 (p < 0.01). In 7 out of 9 subjects we found a significant (p < 0.05) correlation between the changes in FEV1 and BS. BS decreased during CPAP (p < 0.01) and it further decreased significantly after albuterol. There was no correlation between the changes in IC and FEV1 during bronchoconstriction, or between IC and BS during CPAP. In conclusion, in healthy subjects with induced bronchoconstriction CPAP decreased significantly BS, which was further improved by inhalation of albuterol. B was related to changes in FEV1 but not in IC.

Adult↗

PubMed2001

Differences between peptide and nonpeptide B(2) bradykinin receptor antagonists in blocking bronchoconstriction and hypotension induced by bradykinin in anesthetized Guinea pigs.

We have compared the in vivo activity of the bradykinin B(2) receptor peptide antagonists MEN 11270 and Icatibant versus the nonpeptide antagonist FR 173657, after intravenous (i.v.) and intratracheal (i.t.) administration, on the bradykinin (BK)-induced bronchoconstriction and hypotension in anesthetized guinea pigs. We have also assessed the affinity of these antagonists for B(2) receptors in guinea pig lung membranes by radioligand binding and the metabolic stability of peptide antagonists in guinea pig plasma and tissue homogenates. The i.v. administration of MEN 11270, Icatibant, or FR 173657 induced a dose-dependent (10-100 nmol/kg) inhibition of both hypotension and bronchoconstriction induced by bradykinin (10 nmol/kg i.v.). The inhibitory effect of MEN 11270 and Icatibant was comparable both in terms of potency and time course, whereas FR 173657 was less potent and shorter acting. After i.t. administration MEN 11270 and Icatibant (10-100 nmol/kg) dose dependently inhibited both bronchoconstriction and hypotension, whereas FR 173657 (10-100 nmol/kg) reduced bronchoconstriction without affecting hypotension. The antibronchoconstrictor effect of MEN 11270 was more prolonged than that of Icatibant and FR 173657, whereas no differences were found between the peptide antagonists in inhibiting hypotension. These findings indicated that, in vivo, the peptide antagonists are more potent and longer lasting than FR 173657 acting on bradykinin B(2) receptors in guinea pig airways and in the vascular system. The greater efficacy of the antagonists in blocking airway compared with vascular B(2) receptors after topical administration suggests that they can block airway B(2) receptors with little systemic effects.

Animals↗

PubMed2003

Airway eosinophil accumulation on sensory neuropeptide release in a guinea pig model of distilled-water-induced bronchoconstriction.

BACKGROUND: Increased numbers of eosinophils in the airways is characteristic of asthma. However, it remains unclear whether airway eosinophils enhance or reduce the release of neuropeptides in the airways in vivo. This study was conducted to elucidate the influence of airway eosinophil accumulation on the ultrasonically nebulized distilled water (UNDW)-induced bronchoconstriction in our newly developed animal model, which is mediated by sensory neuropeptides. METHODS: Guinea pigs were transnasally treated with 100 mg/kg of platelet activating factor (PAF), or vehicle, twice a week for 3 weeks. We then conducted three experiments. In the first, UNDW was inhaled 20 min after aerosolized antigen challenge, and bronchoalveolar lavage (BAL) was performed in PAF-treated and passively sensitized animals. In the second, PAF-treated animals were exposed for 20 s to ascending doses of methacholine at intervals of 5 min In the third, passively sensitized animals were administered selective NK1 antagonist, SR 140333, selective NK2 antagonist, SR 48968, or vehicle, intravenously 5 min before UNDW-induced bronchoconstriction. RESULTS: The proportion of eosinophils in BAL fluid was significantly increased in guinea pigs treated with PAF, compared with the vehicle. The PAF treatment did not affect antigen-induced immediate asthmatic response, UNDW-induced bronchoconstriction, or bronchial responsiveness to inhaled methacholine. SR 140333, but not SR 48968, inhibited the UNDW-induced bronchoconstriction. CONCLUSION: We conclude that eosinophils accumulated in the airways, caused by repeated intranasal administration of PAF, does not affect the release of substance P induced by UNDW inhalation, or the action of released substance P in vivo.

Aerosols↗

PubMedDate not supplied

The effect of inhaled furosemide and acetazolamide on bronchoconstriction induced by deep inspiration in asthma.

In some asthmatics deep inspiration causes a sustained bronchoconstration, which is dependent on Ca2+ uptake. Inhaled diuretics protect against bronchoconstriction induced by a variety of indirect stimuli, by inhibiting the ionic fluxes involving Ca2+ uptake across the cell membrane of airway epithelium. The aim of this study was therefore to investigate the protective effect of inhaled furosemide on the bronchoconstriction induced by deep inspiration in asthma and to compare it with the effect of acetazolamide, an inhibitor of carbonic anhydrase devoid of effect on ion cotransport but possessing inhibitory effects on chloride ion influx and Na+/K+ exchange. The study was carried out on three different study days according to a randomized, double-blind, placebo-controlled, crossover design. Nine non smoking asthmatic subjects first performed a series of 9 controlled deep inspirations to TLC followed by forced expirations to RV within 20 min, which caused a decrease of FEV1 > 20% from baseline. Two hours later, the subjects inhaled either furosemide (40 mg), or acetazolamide (500 mg), or saline (placebo) in random order, and then two more deep-inspiration challenges were performed after 30 and 140 mins. The progressive percent decrement of FEV1 caused by deep-inspiration challenge was taken as an index of bronchoconstriction. Bronchoconstriction was significantly blunted at 30 mins, but not 140 mins, after inhaling furosemide (p < 0.01) or acetazolamide (p < 0.05) compared to control. We interpret these results as due to a modulation of ionic fluxes across the smooth muscle cell membrane afforded by inhaled furosemide and acetazolamide.

Acetazolamide↗

PubMed1992

[Effect of enkephalinase inhibitor on endothelin-1 induced bronchoconstriction in guinea pigs].

Endothelin-1 (ET-1) is one of the most potent bronchoconstrictors in the guinea pig. The mechanism of its metabolism is still unclear. Phosphoramidon is known to be an enkephalinase inhibitor. We studied the effect of phosphoramidon on bronchoconstriction induced by ET-1. In the first in vitro study, a tracheal preparation was mounted in oxygenated Krebs-Ringer solution. The response was monitored by isometric transducer. Dose-response curves to ET-1 with or without phosphoramidon were obtained. Phosphoramidon potentiated ET-1 induced bronchoconstriction significantly. Next, the specific airway conductance (sGaw) was measured in conscious guinea pigs exposed to an aerosol of phosphoramidon or saline, followed by ET-1 aerosol inhalation. The ET-1 dose was increased by successively doubling the concentration. sGaw, after inhalation of phosphoramidon, was significantly reduced when exposed to ET-1. Phosphoramidon also potentiated ET-1 induced bronchoconstriction in vivo. Next, lung parenchymal tissues were prepared and placed in oxygenated Krebs-Ringer solution with or without phosphoramidon. ET-1 was added and incubated, and samples were injected into a high performance liquid chromatography column. Phosphoramidon inhibited an analysis of ET-1. These data suggest that enkephalinase plays a role in the break down of ET-1 in the airway of the guinea pig. Under the condition of decreased enkephalinase, ET-1 would potentiate bronchoconstriction.

Animals↗

PubMedDate not supplied

The influence of misoprostol (synthetic analogue of prostaglandin E1) on aspirin-induced bronchoconstriction in aspirin-sensitive asthma.

It is believed that aspirin (ASA) and other nonsteroidal anti-inflammatory drugs elicit dyspnea in ASA-sensitive asthmatics by blocking cyclooxygenase. It is unclear whether this bronchospasm is due to the shunting of arachidonic acid into the lipoxygenase pathway or to the removal of a cyclooxygenase product which prevents bronchospasm. Diminished tissue concentration of PGE may cause bronchoconstriction. PGE also modulates mast cells, decreasing the release of anaphylaxis mediators. The authors investigated the influence of a synthetic analogue of PGE1-misoprostol (Cytotec, Searle)-on post-aspirin bronchoconstriction in seven ASA-sensitive asthmatics. On the first day, the effect of a placebo was studied. On the second day, the bronchodilatory effect of misoprostol (Cytotec, Searle) alone was examined. After a few days, a predetermined threshold dose of ASA was administered. Seven days later, at least 400 micrograms of misoprostol +200 micrograms 2 h later, together with a predetermined ASA dose, were administered. In all but one patient, the protective influence of misoprostol on ASA-induced bronchoconstriction was observed. The maximum drop in FEV1 (forced expiratory volume in one second) in % after ASA in each of the patients was 40, 25, 24, 33, 47 and 54, and after ASA with misoprostol 10, 9, 4, (+8), 10, (+2) and 45, respectively. Misoprostol given together with ASA attenuated aspirin-induced bronchoconstriction, reaching statistical significance at 3 and 3.5 h. It also diminished extrapulmonary symptoms.

Adult↗

PubMed1996

[The effect of droperidol and sevoflurane on serotonin-induced bronchoconstriction in dog].

Serotonin is a potent bronchoconstrictor, but the site of bronchoconstriction has not been determined. The present study was performed in dogs to clarify the site of bronchoconstriction induced by serotonin as well as to clarify the bronchodilating effect of droperidol and sevoflurance on the serotonin-induced bronchoconstriction by means of deflation flow-volume curve (DFVC) method, passive expiratory flow volume curve (PEFVC) method and respiratory system impedance measurement by forced oscillation method. Infusion of serotonin (60 micrograms.kg-1.min-1) induced a significant decrease in maximal expiratory flow at 10% of maximal expiratory volume (DEF10) by DFVC method and a significant increase in respiratory system impedance (Z). After droperidol (0.1 mg.kg-1) injection, DEF10 and Z returned to the control level and they remained unchanged even after the termination of serotonin infusion. Respiratory system compliance and resistance by PEFVC were unchanged by both serotonin and droperidol infusion or sevoflurane. Inhalation of 5% sevoflurane during serotonin infusion caused no significant change in DEF10. These findings indicate that serotonin-induced bronchoconstriction involves the small airway as well as the large airway. It is suggested that droperidol reversed serotonin-induced small airway constriction probably due to the antagonism of serotonin receptor in the airway. Bronchodilating effect of sevoflurane is probably limited in the small airway constricted by serotonin.

Anesthetics, Inhalation↗

PubMed1996

[Hypertonic saline induced bronchoconstriction in sensitized rabbits].

Hypertonic saline is a potent stimulus to airway narrowing in most asthmatic patients. However, the mechanism of airway narrowing induced by a change in osmolarity is not clearly understood. In ovalbumin-sensitized rabbits, we found that bronchoconstriction occurred after inhalation of hypertonic saline, and then studied the mechanisms responsible for this bronchoconstriction. Eighteen anesthetized, paralyzed, mechanically ventilated (40 breath/min, TV 7 ml/kg) ovalbumin-sensitized rabbits were exposed to aerosols of hypertonic saline (ultrasonic nebulizer, 0.5 ml/min, 1 min). Total lung resistance (RL) and dynamic compliance (Cdyr) of the lung were measured before and after the exposure. The concentration of NaCl was increased from 0.9% to 7.2% in 0.9% steps. RL increased and Cdyr decreased as the dose of NaCl rose and they reached plateaus at doses of 6.3% and 7.2%, respectively. These responses were markedly inhibited by treatment with atropine (5 mg/kg i.v., p < 0.05 vs. control group), but treatment with chlorpheniramine (1 mg/kg iv.) suppressed the responses only at low concentrations of NaCl. In contrast, treatment with indomethacin, did not significantly change the responses. We conclude that inhalation of hypertonic saline can cause bronchoconstriction in sensitized rabbits, and that vagal stimulation plays a major role in this bronchoconstriction.

Animals↗

PubMed1996

Role of sensory neuropeptides in post-allergic propranolol-induced bronchoconstriction in guinea pigs in vivo.

BACKGROUND: Administration of propranolol can provoke bronchoconstriction in asthmatic patients. We hypothesized that such bronchoconstriction may result from the inflammatory mediators released by an allergic reaction. We recently developed a guinea pig model for propranolol-induced bronchoconstriction (PIB). Neuropeptides which are released from C-fibre nerve endings have been postulated to induce bronchial hyperresponsiveness through neurogenic inflammation. OBJECTIVE: The purpose of this study was to examine whether sensory neuropeptides are involved in the development of PIB after allergic reaction. METHODS: Propranolol at a concentration of 10 mg/ml was inhaled 20 min after antigen challenge in passively sensitized, anaesthetized and artificially ventilated guinea pigs. The animals were treated intravenously with a NK1 and NK2 dual antagonist, FK224, in a dose of 1 or 10 mg/kg or vehicle or a selective NK1 antagonist, FK888, in a dose of 1 or 10 mg/kg or vehicle 10 min before or 15 min after antigen challenge. RESULTS: Propranolol inhaled 20 min after antigen challenge caused bronchoconstriction. FK224 or FK888 administered 15 min after antigen challenge as well as 10 min before antigen challenge did not reduce the PIB. CONCLUSION: We conclude that neuropeptides such as neurokinin A and substance P do not directly contribute to the development of PIB after allergic reaction.

Adrenergic beta-Antagonists↗

PubMed1997

Activity of inhaled lysine acetylsalicylate (L-ASA) on bradykinin-induced bronchoconstriction in asthmatics: evidence of contribution of prostaglandins.

When administered by inhalation, bradykinin provokes dose-related bronchoconstriction in asthmatic subjects by a mechanism believed to involve activation of sensory nerve endings. However, little is known of the change in airway responsiveness to bradykinin after cyclo-oxygenase blockade. The aim of the present study was to investigate the effect of the potent cyclo-oxygenase inhibitor, lysine acetylsalicylate (L-ASA), administered by inhalation, on bradykinin-induced bronchoconstriction in a group of 12 asthmatic subjects. The subjects attended the laboratory on four separate occasions to receive nebulized L-ASA (solution of 90 mg x mL(-1)) or matched placebo (glycine, solution of 30 mg x mL(-1)) 15 min prior to bronchoprovocation tests with bradykinin and methacholine in a randomized, double-blind order with at least a 5 day interval. Changes in airway calibre were followed as forced expiratory volume in one second (FEV1), and responsiveness to agonists was expressed as the provocative concentration causing a 20% fall in FEV1 from baseline (PC20). Administration both of L-ASA and glycine solution caused a small but significant acute fall in FEV1 from baseline, with gradual recovery within 20 min. When compared to placebo, inhaled L-ASA reduced the airway responsiveness to bradykinin in 11 of the 12 subjects studied, the geometric mean (range) values for PC20 bradykinin increasing significantly (p<0.001) by 1.7 doubling dose from 0.55 (0.11-5.05) to 1.72 (0.26-6.05) mg x mL(-1) after placebo and L-ASA, respectively. No significant change in airway responsiveness to methacholine was recorded after L-ASA. It is concluded that administration of lysine acetylsalicylate by inhalation protects the asthmatic airways against bradykinin-induced bronchoconstriction, thus suggesting that endogenous prostaglandins may play a contributory role in the bronchoconstriction to kinins in human asthma.

Administration, Inhalation↗

PubMed1998

Correlative alteration of thromboxane A2 with antigen-induced bronchoconstriction and the role of platelets as a source of TXA2 synthesis in guinea pigs: effect of DP-1904, an inhibitor of thromboxane synthetase.

A marked and sustained bronchoconstriction after antigen challenge was produced in actively sensitised guinea pigs, and correlated with increments of thromboxane (TX) A2 level in both the plasma and bronchoalveolar lavage fluid. DP-1904 given orally relieved the bronchoconstriction and increase in TXA2 in a dose-dependent manner. In platelet-depleted animals, antigen-induced bronchoconstriction and TXA2 release in the plasma were significantly reduced compared to those of non-platelet-depleted animals, indicating that platelets are a major cell source of TXA2 production, the remainder originating from the other cells excluding platelets. In the platelet-deprived animal, DP-1904 showed further significant inhibition of the constriction and plasma TXA2 level, and therefore likely inhibits TXA2 synthesis of various cells, including platelets, in the bloodstream. The results suggested that TXA2 is an important mediator responsible for producing antigen-induced bronchoconstriction, and endogenously originated from various cells including platelets in guinea pigs.

Animals↗

PubMed1979

The role of upper airways and of sensoric receptors on reflex bronchoconstriction.

The influence of bilateral transection of the nervi laryngici cranialis, laryngici caudalis and glossopharyngici on ACH and allergen-induced bronchoconstriction was tested in 15 dogs. In three dogs the free preparation of bilateral nervi laryngici cranialis was performed for control measurements. Partial transection of pulmonary left nervus vagus was performed in three dogs and compared to radical transection of the same nerve in three animals. Transection of the nervi laryngici cranialis as well as of the nervi glossopharyngici was followed by the inhibition of the allergen-induced bronchoconstriction. The bronchoconstriction following ACH challenge was not influenced by transection. Bronchoconstriction induced by allergen returned to the same values within three weeks after surgical intervention. Partial unilateral dissection of the vagus nerve on lung hilus shows a small decrease in bronchial constriction induced by allergen and by ACH. Complete unilateral dissection of the vagus nerve on the lung hilus reduced the bronchial constrictoric response to both substances significantly.

Acetylcholine↗

PubMed1979

Mechanisms of bronchoconstriction and of thrombocytopenia induced by collagen in the guinea pig.

Collagen injected to guinea pigs i.v. increased the pulmonary resistance to inflation (bronchoconstriction) and induced thrombocytopenia. Immune platelet depletion protected against the effects of collagen, and has been shown not to prevent bronchoconstriction induced by the prostaglandin/thromboxane A2 precursor arachidonic acid. Use of inhibitors demonstrated that histamine, serotonin, acetylcholine and bradykinin were not involved with the effects of collagen in the guinea pig. Aspirin and indomethacin inhibited collagen-induced bronchoconstriction completely and thrombocytopenia partly, supporting the hypothesis that the former is prostaglandin cyclo-oxygenase dependent, whereas the latter has a thromboxane A2-independent mechanism as well. Carrageenan, heparin and reserpine inhibited the in vivo effects of collagen to various extents, but their precise mechanism of action could not be discovered. Collagen-induced bronchoconstriction is strictly platelet and thromboxane A2-dependent.

Airway Resistance↗

PubMed1982

Inhibition by sulphinpyrazone of the platelet-dependent bronchoconstriction due to platelet-activating factor (PAF-acether) in the guinea pig.

Platelet-activating factor (PAF-acether) injected into guinea-pigs induced platelet-dependent bronchoconstriction and thrombocytopenia. Treatment of the animals with sulphinpyrazone suppressed bronchoconstriction without affecting thrombocytopenia. When tested ex vivo and in vitro, sulphinpyrazone suppressed the PAF-acether-induced platelet release reaction, as measured by the release of ATP, more efficiently than platelet aggregation. In contrast, bronchoconstriction and thrombocytopenia in vivo, as well as platelet aggregation and the release reaction ex vivo and in vitro, induced by arachidonic acid (AA), were suppressed by sulphinpyrazone. This effect is accounted for by the known anti-arachidonate cyclooxygenase activity of sulphinpyrazone. Finally, aggregation by ADP was only marginally inhibited by sulphinpyrazone, and the inhibition was easily surmounted when the amounts of ADP added were increased. Sulphinpyrazone exerts a specific and cyclooxygenase-independent protective effect towards platelet activation by PAF-acether, which results in inhibition of platelet-dependent bronchoconstriction even though aggregation, and consequently in vivo thrombocytopenia, may persist.

Adenosine Diphosphate↗

PubMed1987

Ipratropium bromide potentiates bronchoconstriction induced by vagal nerve stimulation in the guinea-pig.

In anaesthetised guinea-pigs, bronchoconstriction induced by vagal nerve stimulation was potentiated by low doses of the antimuscarinic bronchodilator drug, ipratropium (0.01-1.0 microgram/kg); the maximum effect was obtained with 1.0 microgram/kg which doubled the bronchoconstriction. When the dose was increased above 1.0 microgram/kg potentiation no longer occurred; instead the vagally induced bronchoconstriction was antagonised. This was accompanied by reduction in the bronchoconstriction and bradycardia induced by i.v. acetylcholine, due to blockade of post-junctional muscarinic receptors in the airways and heart. With 10 micrograms/kg ipratropium responses elicited both by vagal stimulation and by exogenous acetylcholine were abolished. The results show that ipratropium is an antagonist for pre-junctional muscarinic inhibitory receptors on pulmonary parasympathetic nerves and also confirm its potent antagonist actions on post-junctional muscarinic receptors in the airway smooth muscle. The effect of ipratropium in the lung depends, therefore, on the balance between the pre- and post-junctional effects.

Animals↗

PubMed1981

Effect of bronchoconstriction on the firing behavior of pulmonary stretch receptors.

To study the effect of bronchoconstriction on the activity of pulmonary stretch receptors (PSRs), acetylcholine aerosols (0.05% solution) were delivered continuously into the lungs while the afferent activity of a single PSR was recorded from a filament of the vagus nerve. The relationship between the PSR frequency (fPSR) and the transpulmonary pressure (Ptp) was examined during both constant volume ventilation and hyperinflation. During bronchoconstriction, the peak fPSR for the same tidal volume increased significantly (P less than 0.05) compared to the control response obtained with saline aerosols. However, the fPSR at functional residual capacity decreased in the receptors above the carina but increased in those below. Bronchoconstriction induced a hysteresis in the dynamic Ptp-fPSR relationship during hyperinflation in 11 out of the 21 receptors studied: a clockwise hysteresis was found in those receptors above the carina whereas a counterclockwise one in those below. Results of these studies suggest that the response of PSRs to bronchoconstriction depends on their locations in the tracheobronchial tree.

Acetylcholine↗

PubMed1983

Effect of inhibition of thromboxane production on the leukotriene D4-mediated bronchoconstriction in the guinea pig.

Leukotriene D4 (LTD4) administered intravenously to anesthetized, spontaneously breathing guinea pigs elicited decreases in dynamic lung compliance (Cdyn) and airway conductance (GAW) with a maximal response achieved at 0.5 min. Simultaneously, plasma levels of the thromboxane metabolite, TxB2, and the prostacyclin metabolite, 6-keto-PGF1 alpha, increased 10-fold over pre-LTD4 levels. Pretreatment of the guinea pigs with meclofenamic acid delayed the onset of the LTD4-induced bronchoconstriction, antagonized the magnitude of the decreases in Cdyn and GAW, and blocked the increase in plasma TxB2 and 6-keto-PGF1 alpha levels. The thromboxane synthetase inhibitor, UK 37,248, suppressed the LTD4-induced bronchoconstriction, while it completely blocked TxB2 production without significantly affecting 6-keto-PGF1 alpha. The SRS-A end organ antagonist, FPL 55712, blocked both the LTD4-induced bronchoconstriction and the production of the arachidonic acid metabolites. These results suggest that thromboxane A2 plays an important role in mediating part of the bronchoconstriction elicited by intravenously administered LTD4 in the guinea pig.

6-Ketoprostaglandin F1 alpha↗

PubMed1984

Propranolol potentiates leukotriene D4-induced bronchoconstriction and enhances antagonism by FPL 55712.

Aerosol LTD4-induced bronchoconstriction in anesthetized, spontaneously breathing guinea pigs was potentiated by either pretreatment with propranolol or bilateral adrenalectomy, whereas bilateral vagotomy did not affect the LTD4 response. The dose-response curve describing LTD4-induced changes in dynamic lung compliance (CDYN) and pulmonary resistance (RL) [as reflective indices of bronchoconstriction] was shifted to the left by approximately 20-fold by propranolol. Against an equal degree of LTD4-induced bronchoconstriction, the leukotriene antagonist, FPL 55712, had an apparent 20-fold greater potency in propranolol-pretreated animals vis a vis saline-treated controls. The duration of action of aerosol FPL 55712 was similar in both propranolol-treated and saline-treated animals. These results demonstrate that aerosol LTD4-induced bronchoconstriction is modulated by an adrenergic compensatory bronchodilator mechanism that is apparently dependent upon the adrenals and independent of vagal influences. Inhibition of the effect of this reflex with propranolol also enhances the apparent potency of an aerosol leukotriene antagonist, FPL 55712, presumably reflecting a constant LTD4 to antagonist ratio in the saline-treated and propranolol-pretreated guinea pigs.

Adrenalectomy↗