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At least 1,477 records · Page 82Linked to original sources
PubMed1998

Sensitivity of aerosol bolus behavior to methacholine-induced bronchoconstriction.

STUDY OBJECTIVES: Airway narrowing causes alterations in the shape of an exhaled aerosol bolus that can serve as indexes of airway changes during bronchoprovocation. We compared the sensitivities of aerosol bolus behavior and specific airway conductance (SGaw) during bronchoprovocation in normal subjects. DESIGN AND PARTICIPANTS: Fifteen normal, nonsmoking subjects were studied. Doubling methacholine (MCh) concentrations were delivered during tidal breathing. After each dose, SGaw was determined followed by inhalation of narrow pulses of 1-microm particles introduced into 1-L breaths. Inhaled and exhaled particle concentrations were measured with light scattering photometry. Using plots of concentration vs volume, the exhaled bolus was compared with the inhaled bolus for measurements of volumetric change in mode location (modal shift), particle deposition, and dispersion. To determine baseline intrasubject variability, sham studies using buffer solution were performed on five subjects. RESULTS: MCh caused a proximal modal shift, and increased dispersion and deposition of the exhaled bolus. At most doses, a greater percentage of subjects showed significant change (p<0.05) from baseline for modal shift and deposition than for SGaw. Aerosol bolus behavior displayed less intrasubject variability than did SGaw during sham studies. CONCLUSION: Aerosol bolus behavior is at least as sensitive as SGaw in detecting MCh-induced airway constriction in normal subjects and exhibits less intrasubject variability.

Administration, Inhalation↗
PubMed1998

Effects of cysteinyl-leukotriene receptor antagonist, thromboxane A2 receptor antagonist, and thromboxane A2 synthetase inhibitor on antigen-induced bronchoconstriction in patients with asthma.

BACKGROUND: Leukotriene (LT) and thromboxane A2 (TXA2) receptor antagonists have been used in the treatment of asthma. OBJECTIVES: We examined the effects of an LT receptor antagonist, TXA2 receptor antagonist, and TXA2 synthetase inhibitor on bronchoprovocation test (BPT) in patients with mild-to-moderate atopic asthma. METHODS: BPT was performed four times in each of six asthmatics. Development of the immediate asthmatic reaction (IAR) and late asthmatic reaction (LAR) was confirmed on the first BPT (BPT1). After a 7-day washout period, an LT receptor antagonist (pranlukast, 450 mg/d), TXA2 receptor antagonist (seratrodast, 80 mg/d), or TXA2 synthetase inhibitor (ozagrel, 800 mg/d) was administered orally over 7 days at random using a cross-over method (BPT2-4). Blood levels of LTB4, LTC4, LTD4, 11-dehydrothromboxane B2, eosinophil cationic protein, and histamine were measured at reaction phases of pre-BPT, IAR, and LAR. RESULTS: Administration of pranlukast suppressed IAR by 80.5% (p < 0.0001) and LAR by 54.6% (p = 0.0391). Ozagrel significantly suppressed IAR by 39.5% (p = 0.0413), but the fall in FEV1 was >20% (21.56+/-4.173%). Seratrodast did not suppress IAR or LAR. Blood levels of chemical mediators did not correlate with the suppressive effects of the tested drugs. CONCLUSIONS: The LT receptor antagonist was considered to be the most effective. LT might play a more important role in the pathogenesis of asthma than TXA2. Our data showed that measurement of blood levels of chemical mediators is not useful in identifying the pathogenic mechanisms of asthma.

Administration, Oral↗
PubMed2000

Ethnic differences: word descriptors used by African-American and white asthma patients during induced bronchoconstriction.

STUDY OBJECTIVES: To determine if African-American and white patients with asthma (1) differ in the words they use to describe their breathlessness, and (2) differ in their perception of breathlessness. DESIGN: Descriptive cross-sectional design. SETTING AND PARTICIPANTS: The study setting was located in Northern California, an ethnically and economically diverse area. A total of 32 subjects, 16 per group, completed the study. MEASUREMENTS: All had a provocation concentration of methacholine chloride causing a 30% fall in FEV(1) (PC(30)) of </= 8 mg/mL. Serial pulmonary function testing was performed. Breathlessness was measured using the Borg scale and the visual analog scale. Word descriptors were measured by an open-ended word descriptor questionnaire. RESULTS: Significant ethnic differences in the words used to describe the sensation of breathlessness were present at PC(30). African Americans used upper airway word descriptors: tight throat (p < 0. 0004), scared-agitated (p < 0.006), voice tight (p < 0.04), itchy throat (p < 0.03), and tough breath (p < 0.04). Whites used lower airway or chest-wall symptom descriptors: deep breath (p < 0.03), light-headed (p < 0.03), out of air (p < 0.01), aware of breathing (p < 0.03), and hurts to breathe (p < 0.06). In addition, African Americans required a significantly smaller, 44.3% (mean), dose of methacholine to achieve PC(30) (p < 0.02). CONCLUSION: This study provides valuable new information about ethnicity and the words used to describe breathlessness during airflow obstruction. Asthmatic African Americans used primarily upper airway word descriptors; whites used lower airway or chest-wall word descriptors. Effective symptom monitoring requires asking the correct question and awareness that ethnic differences in the words used to describe breathlessness may exist.

Administration, Inhalation↗
PubMed1998

The effects of ipratropium bromide on histamine-induced bronchoconstriction in subjects with cervical spinal cord injury.

Previously, we reported that a majority of subjects with chronic cervical spinal cord injury (SCI) demonstrated airway hyperreactivity in response to inhaled methacholine. To further investigate mechanisms of airway hyperreactivity, 15 male subjects with cervical SCI were challenged with aerosolized histamine, and on a separate day responders were rechallenged 30 min after the inhalation of 72 micrograms of ipratropium bromide. Twelve of 15 subjects demonstrated airway hyperresponsiveness to histamine (geometric mean PC20 of 1.27 mg/ml), which was not blocked by pretreatment with ipratropium bromide (geometric mean PC20 1.50 mg/ml). Baseline forced vital capacity and forced expiratory volume in 1 sec were not significantly different between responders and nonresponders (2.8 +/- 0.6 vs. 3.0 +/- 0.4 L and 2.3 +/- 0.6 vs. 2.4 +/- 0.2 L, respectively). Findings that subjects with cervical SCI are hyperresponsive to methacholine and histamine, chemical agents with direct action through distinct receptor systems, suggest that bronchial hyperreactivity in these subjects represents a nonspecific process similar to that observed in patients with asthma.

Adult↗
PubMed1996

PGF2 alpha causes bronchoconstriction and pulmonary vasoconstriction via thromboxane receptors in rat lung.

We determined the vascular and airway effects of PGF2 alpha and its mechanism of action on isolated-perfused lungs of rats were isolated and perfused at 50 ml/kg/min with Krebs-Henseleit bicarbonate buffer solution containing 3% bovine serum albumin. The lungs were ventilated with 21% O2 and 5% CO2 at a tidal volume of 2 ml. frequency of 60 per minute and positive end expiratory pressure of 3 cmH2O. Following injection of 50 micrograms PGF2 alpha into the afferent pulmonary catheter, there was a marked rise in pulmonary arterial pressure (Ppa) and in resistance to airflow across the lung (RL) and a fall in dynamic lung compliance (Cdyn). Double vascular occlusion technique revealed that 29% of the rise in Ppa was due to an increase in upstream and 71% to downstream resistance. N omega-nitro-L-arginine, 100 microns, a NO synthase inhibitor potentiated the Ppa response two-fold with significant change in airway mechanics. Rat atrial natriuretic factor (r-ANF), 40 micrograms quickly reversed the changes in Ppa, RL and Cdyn. Infusion of r-ANF prior to PGF2 alpha attenuated the Ppa response by 38%, RL by 44% and Cdyn by 12%. SQ 29548, a thromboxane receptor blocker and Cl, a protein kinase C (PKC) inhibitor, fully blocked both the vascular and airway responses to PGF2 alpha. PGF2 alpha is a constrictor of pulmonary vessels and airways in rat lungs via thromboxane SQ 29548 receptors, thansduced by intracellular PKC.

Animals↗
PubMed2002

[Bronchoconstriction in administration of ACE inhibitors].

The aim of the study was assessment of bronchial capacity in the treatment with ACE inhibitors. 92 patients with essential hypertension stage I-II (mean age 52 years), ischemic heart disease and bronchial asthma (a mild, moderate and severe course) in a relative remission were treated for arterial hypertension with ACE inhibitors enalapril and diroton. Enalapril improved cough indices by 38.3%, diroton--by 13.3%. This was accompanied by a rise in the level of natural antibodies to bradikinin.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

[Inhibitory effect of vasoactive intestinal peptide (VIP) and peptide histidine isoleucine (PHI) on bronchoconstriction in guinea pigs].

The present studies were conducted to investigate whether or not VIP and PHI have a bronchodilator effect in vivo. VIP or PHI was administered intravenously in guinea pigs, and dynamic respiratory resistance was measured. Intravenous administration of VIP and PHI reduced dynamic respiratory resistance; however, the effect was significantly less than that of isoprenaline. VIP and PHI inhibited the increase in dynamic respiratory resistance by intravenous administration of histamine in a dose-dependent manner, suggesting that VIP and PHI may be involved in the pathogenesis of airway hyperresponsiveness through inhibiting the effect of mediators on the airway.

Airway Resistance↗
PubMed1992

[Content and localization of leukotriene C4 in lung tissue during biphasic allergic bronchoconstriction in the guinea pig].

Leukotriene C4 (LTC4) is a very potent bronchoconstrictor, and is believed to be an important mediator during immediate (IAR) and late asthmatic response (LAR). No direct measurement of LTC4 in lung tissue during IAR and LAR has been reported, however, and its localized site in the lung remains unclear. In an effort to clarify these issues, the content of LTC4 in lung tissue was evaluated at the onset of antigen-induced IAR and LAR, and the distribution of LTC4 was examined by immunohistochemistry. IAR and LAR were induced by inhalation of aerosolized ovalbumin (OA) in conscious guinea pigs. The development of IAR and LAR following inhaled OA exposure was determined in sensitized guinea pigs by measurement of respiratory resistance using the oscillation method. LTC4 in lung tissue was measured by radioimmunoassay at six different stages (S1: non-treated group; S2: group before OA-challenge following sensitization; S3: IAR group; S4: group two hours after IAR; S5: LAR-positive group; S6: LAR-negative group). For immunohistochemistry, non-treated guinea pigs and the sensitized animals at the onset of LAR were used. Lung sections were stained with anti-LTC4 antibody by avidin biotin peroxidase complex method (ABC method). About 70% of the guinea pigs displayed IAR, followed by LAR that peaked at 6-20 hours after OA challenge. The LTC4 content in lung tissue was significantly increased (p less than 0.01) at the onset of IAR, but was significantly decreased (p less than 0.01) after two hours, and significantly increased (p less than 0.01) at the onset of LAR.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMedDate not supplied

[Effect of vitamin C on exercise-induced bronchoconstriction].

The effect of vitamin C on exercise-induced airway constriction was studied. Pretreatment with ascorbic acid prevented the significant alteration in airway geometry induced by exercise asthmatic patients. These results suggest that vitamin C deficiency might augment airway responses to exercise and other bronchospasmogenic factors, and treatment with vitamin C may decrease airway hyperresponsiveness.

Adolescent↗