Disease relevance of Bronchoconstriction

• Inhaled heparin prevents exercise-induced asthma without influencing histamine-induced bronchoconstriction [1].
• Injection of synthetic PAF-acether induces similar effects, including bronchoconstriction, respiratory arrest, systemic hypotension, neutropenia, and thrombocytopenia [2].
• Lipopolysaccharide from Escherichia coli reduces antigen-induced bronchoconstriction in actively sensitized guinea pigs [3].
• Prostaglandin F2alpha is associated with bronchoconstriction and its increased production in children with C.F. might be causally related to their chronic pulmonary disease [4].
• Allergen-induced asthma is characterized by chronic pulmonary inflammation, reversible bronchoconstriction, and airway hyperreactivity to provocative stimuli [5].

Psychiatry related information on Bronchoconstriction

• Selective histamine-H1 receptor antagonists inhibit adenosine 5'-monophosphate (AMP)-induced bronchoconstriction by greater than 80% when expressed as a percentage inhibition of the FEV1 time-response curve following inhalation of the provocation concentration of AMP required to produce a 20% decrease in FEV1 from baseline (PC20) [6].

High impact information on Bronchoconstriction

• The morning dose of salmeterol attenuated the degree of bronchoconstriction at all times (decrease in FEV1 on day 1, 5+/-2 percent; on day 14, 10+/-3 percent; and on day 29, 9+/-3 percent; P=0.10) [7].
• RESULTS: At 12 weeks, montelukast therapy offered significantly greater protection against exercise-induced bronchoconstriction than placebo therapy (expressed as the percentage of inhibition of the end points), as evidenced by the improvement in the area under the FEV1 curve (degree of inhibition, 47.4 percent; P=0.002) [8].
• On the first treatment day, salmeterol afforded significant protection against methacholine-induced bronchoconstriction, as shown by a 10-fold increase in the PC20 as compared with the value at entry (P less than 0.001) [9].
• Inhibition of exercise-induced bronchoconstriction by MK-571, a potent leukotriene D4-receptor antagonist [10].
• Inhibition of exercise-induced bronchoconstriction by MK-571, a potent leukotriene D4-receptor antagonist [11].

Chemical compound and disease context of Bronchoconstriction

• Unlike adenosine, which non-selectively activates all four Ado R subtypes and produces unwanted effects, tecadenoson appears to terminate AV node-dependent supraventricular tachycardias without hypotension and bronchoconstriction [12].
• Therefore, we tested in awake volunteers with bronchial hyperreactivity the effect of lidocaine on histamine-induced bronchoconstriction administered either intravenously or as an aerosol [13].
• In hay fever subjects deep inspiration had no effect on Gaw/Vtg if it was performed in the control state; however, when methacholine-induced bronchoconstriction was present, deep inspiration transiently increased Gaw/Vtg [14].
• Ten allergic subjects with exercise-induced bronchospasm were studied to determine whether albuterol could prevent sulfur dioxide (SO2)-induced bronchoconstriction [15].
• Inhaled PAF provokes bronchoconstriction, causes peripheral blood neutropenia with rebound neutrophilia, and generates urinary production of the bronchoconstrictor eicosanoids, thromboxane (TX)A2, and the cysteinyl leukotrienes [16].

Biological context of Bronchoconstriction

• INTERPRETATION: The results suggest that bronchoconstriction after bradykinin inhalation is greatly inhibited by the formation of NO in airways of asthmatic patients and that NO could have a bronchoprotective role in asthma [17].
• Compared with Aqp5(+/+) mice, Aqp5(-/-) mice show a significantly increased concentration-dependent bronchoconstriction to intravenously administered Ach, as shown by an increase in total lung resistance and a decrease in dynamic lung compliance (P < 0.05) [18].
• Endothelin is a 21-amino acid peptide with a striking diversity of important biological responses, including, vasoconstriction, bronchoconstriction, and mitogenesis [19].
• 5. Alterations in core body temperature, bronchial constriction, plasma histamine, and PN-specific IgE levels were all significantly reduced [20].
• In addition, increased vagal reflex bronchoconstriction and the delayed effects of the fall in plasma cortisol level may also contribute to nocturnal wheezing [21].

Anatomical context of Bronchoconstriction

• After methacholine, there were no significant changes in neutrophil chemotactic activity or percentages of complement rosettes, despite bronchoconstriction [22].
• Activated eosinophils release major basic protein, which blocks inhibitory M2 muscarinic receptors (M2Rs) on nerves, increasing acetylcholine release and potentiating vagally mediated bronchoconstriction [23].
• Inhibitory M2 muscarinic receptors on parasympathetic nerve endings in the lungs decrease release of acetylcholine, inhibiting vagally induced bronchoconstriction [24].
• The hyperreactivity to bronchoconstriction observed in the Aqp5(-/-) mice was not due to differences in tracheal smooth muscle contractility in isolated preparations or to altered levels of surfactant protein B. These data suggest a novel pathway by which AQP5 influences bronchoconstriction [18].
• Leukotriene C4 is converted to the more potent leukotriene D4 by the action of gamma-glutamyltransferase on guinea pig ileum during bioassay. gamma-Glutamyltransferase may represent a control feature in the biosynthesis of leukotriene D4, and thus be involved in leukotriene-induced bronchoconstriction in the lung [25].

Associations of Bronchoconstriction with chemical compounds

• To control for the effects of bronchoconstriction, the same studies were done after a challenge with methacholine [22].
• The purpose of this study was to investigate the importance of LTD4 as a mediator of exercise-induced bronchoconstriction [11].
• These results suggest that prostaglandin D2 may be involved in the pathogenesis of bronchoconstriction in allergic asthma [26].
• Treatment with MK-571 attenuated exercise-induced bronchoconstriction in all the subjects [11].
• Subcutaneous infusion of rats with albuterol for 7 days compromised the ability of albuterol, given acutely, to protect against acetylcholine-induced bronchoconstriction [27].

Gene context of Bronchoconstriction

• Aspirin may remove PGE2-dependent suppression in all subjects, but only in AIA patients does increased bronchial expression of LTC4 synthase allow marked overproduction of cys-LTs leading to bronchoconstriction [28].
• Likewise, Penh, a measure of bronchoconstriction, was significantly enhanced in Aqp5(-/-) mice challenged with aerosolized methacholine (P < 0.05) [18].
• Heparin, in combination with SLPI demonstrated in vivo efficacy reducing early and late phase bronchoconstriction [29].
• BACKGROUND: Subjects with aspirin-intolerant asthma (AIA) respond with bronchoconstriction and extrapulmonary adverse reactions to conventional nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit the cyclooxygenase (COX) step in the biosynthesis of prostaglandins [30].
• Pretreatment of lungs with BQ 610, BQ 123, or bosentan aggravated the bronchoconstriction induced by 1 nmol ET-1 so that it was comparable to that induced by 1 nmol IRL 1620 [31].

Analytical, diagnostic and therapeutic context of Bronchoconstriction

• Treatment for 2 weeks impaired the ability of terbutaline to protect against histamine-induced bronchoconstriction, and was followed by a rebound increase in bronchial responsiveness after cessation of treatment [32].
• Evidence from animal models has implicated nerve growth factor (NGF) as a mediator of pulmonary inflammation, bronchoconstriction, and airway hyperreactivity, all of which are hallmarks of asthma [33].
• Hoe140 had no effect on OA-induced BHR to acetylcholine (ACh) and bronchoalveolar lavage fluid (BALF) cellular profiles, but inhibited bronchoconstriction to BK (p < 0.04) [34].
• In a randomized, double-blind, placebo-controlled crossover study, we examined the effect of the specific LTRA montelukast at 5 mg/d for 2 d on the bronchoconstriction induced by hyperventilation of cold, dry air in 13 asthmatic children 3 to 5 yr old [35].
• Neither in these three patients nor in another patient known already to respond with bronchoconstriction to 30 to 50 mg of hydrocortisone did intravenous injections of 20 mg of methylprednisolone, 4 mg of dexamethasone, or 4 mg of betamethasone produce any signs of bronchial obstruction [36].

References