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Richard J. Martin - One of the best experts on this subject based on the ideXlab platform.
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Altered pituitary-adrenal interaction in Nocturnal Asthma.
The Journal of allergy and clinical immunology, 2003Co-Authors: E Rand Sutherland, Monica Kraft, Misoo C. Ellison, Richard J. MartinAbstract:Abstract Background: Increased airway inflammation at night contributes to the Nocturnal worsening of Asthma, but the mechanisms regulating circadian variations in airway inflammation are unknown. Objective: We hypothesized that altered hypothalamic-pituitary-adrenal axis function serves as an endogenous controller of inflammation in Nocturnal Asthma. Methods: Patients with Nocturnal Asthma (n = 7), patients with nonNocturnal Asthma (n = 13), and healthy control subjects (n = 11) adhered to a regular sleep-wake cycle for 1 week. Corticotropin and cortisol levels were assayed every 2 hours for 24 hours. Low-dose corticotropin stimulation was performed. Circadian hormonal flux was analyzed by means of cosinor modeling and calculation of the area under the 24-hour curve. Results: Corticotropin peak levels and areas under the 24-hour curve were significantly increased in patients with Nocturnal Asthma versus values in patients with nonNocturnal Asthma and control subjects. Patients with nonNocturnal Asthma demonstrated significantly increased areas under the 24-hour cortisol curve when compared with control subjects, but peak cortisol levels did not differ between groups. Cortisol levels after low-dose corticotropin stimulation did not differ between groups. Corticotropin and cortisol levels were not correlated with the degree of physiologic impairment. Conclusion: Nocturnal Asthma is marked by increased corticotropin levels that are not accompanied by commensurate increases in cortisol levels. This observation might indicate blunted adrenal responsiveness in the Nocturnal Asthma phenotype. Conversely, adrenal response to corticotropin might be enhanced in nonNocturnal Asthma, attenuating Nocturnal worsening of airway inflammation. (J Allergy Clin Immunol 2003;112:52-7.)
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Distal lung dysfunction at night in Nocturnal Asthma.
American journal of respiratory and critical care medicine, 2001Co-Authors: Monica Kraft, Richard J. Martin, Juno Pak, David A. Kaminsky, Charles G. IrvinAbstract:We have previously shown that patients with Nocturnal worsening of Asthma (Nocturnal Asthma) exhibit increased parenchymal inflammation at night. To evaluate the functional significance of this parenchymal inflammation, 10 subjects with Nocturnal Asthma (NA), four subjects with non-Nocturnal Asthma (NNA), and four normal control subjects underwent bronchoscopy with measurement of peripheral airways resistance (Rp) at 4:00 p.m. and at 4:00 a.m. Employing a wedged bronchoscope technique, Rp was measured. Flow was stopped, and the pressure reached after 10 s of decay was termed the plateau pressure. The time constant of this decay ( τ ) was measured, and the peripheral compliance (Cp) was calculated as τ /Rp. The NA group exhibited the highest Rp values at 4:00 p.m. and at 4:00 a.m. as compared with the NNA and control groups, but all groups were significantly different from each other at 4:00 p.m.: NA, 0.113 ± 0.02 cm H2O/ml/min; NNA, 0.033 ± 0.005 cm H2O/ml/min; Control subjects, 0.010 ± 0.001 cm H2O/ ml/m...
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Airway-parenchyma uncoupling in Nocturnal Asthma.
American journal of respiratory and critical care medicine, 2000Co-Authors: Charles G. Irvin, Juno Pak, Richard J. MartinAbstract:Airway flow resistance is well known to be dependent upon lung volume. The rise in lung volume that occurs in Asthma is therefore thought to be an important mechanism that defends airway patency. The purpose of the current study was to investigate the interdependence or mechanical coupling between airways and lung parenchyma during the inflammatory processes that occur in the patient with Nocturnal Asthma. Five patients with documented Nocturnal Asthma were studied in both a vertical and a horizontal body plethysmograph. Lung volume was altered with continuous negative pressure as applied to the chest wall with a poncho cuirass in different postures and during sleep. We found during the awake phase that an increase in lung volume decreased lower pulmonary resistance (Rlp); however, within 30 min of sleep onset, functional residual capacity (FRC) fell and Rlp rose more than would be expected for the fall in FRC. Restoring FRC to presleep values either at an early (half-hour) or a late (3-h) time point did not cause Rlp to significantly fall. A second phase of the study showed that the loss of Rlp dependence on lung volume was not due to the assumption of the supine posture. Indirect measurements of lung compliance were consistent with a stiffening of the lung. We conclude that with sleep there is an immediate uncoupling of the parenchyma to the airway, resulting in a loss of interdependence that persists throughout sleep and may contribute to the morbidity and mortality associated with Nocturnal Asthma.
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Lymphocyte and Eosinophil Influx into Alveolar Tissue in Nocturnal Asthma
American journal of respiratory and critical care medicine, 1999Co-Authors: Monica Kraft, Richard J. Martin, Susan J. Wilson, Ratko Djukanovic, Stephen T. HolgateAbstract:We have shown in Nocturnal Asthma that alveolar tissue eosinophils are increased at night as compared with the proximal airway, and that they correlate with the overnight decrement in lung function. As the CD4+ cell is thought to be the principal orchestrating cell in eosinophil recruitment, we evaluated its presence in the proximal and distal airways in Nocturnal Asthma. Eleven patients with Nocturnal Asthma (NA) and 10 patients with non-Nocturnal Asthma (NNA) underwent two bronchoscopies with proximal airway endobronchial and distal alveolar tissue transbronchial biopsy in a random order at 4:00 P.M. and at 4:00 A.M. separated by 1 wk. Immunohistochemical staining and morphometric analysis were used to determine the number of CD3+, CD4+, and CD8+ cells and EG2+ eosinophils per mm2 in the epithelium, lamina propria, and alveolar tissue. At 4:00 A.M., the NA group had a significantly greater number of CD4+ cells in the alveolar tissue than the NNA group (9.8 cells/ mm2 [5.6-30.8, interquartile (IQ)] versus 1.5 cells/mm2 [0-6. 3, IQ], p = 0.04). Within the NA group, there were significantly greater numbers of CD3+, CD4+, CD8+, and EG2+ cells in the proximal airway lamina propria than in the distal airway at both 4:00 P.M. and 4:00 A.M. There were no differences within the epithelium between the groups at either time point. Only alveolar tissue, not airway tissue, CD4+ cells correlated inversely with the percentage predicted FEV1 at 4:00 A.M. (r = -0.68, p = 0.0018) and positively with the number of alveolar tissue EG2+ cells (r = 0.66, p = 0.01). These findings suggest that the CD4+ lymphocyte is increased in the alveolar tissue at night in Nocturnal Asthma as compared with non-Nocturnal Asthma.
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Circadian variation in exhaled nitric oxide in Nocturnal Asthma.
The Journal of asthma : official journal of the Association for the Care of Asthma, 1999Co-Authors: George Georges, Richard J. Martin, Becki Bucher Bartelson, Philip E. SilkoffAbstract:Asthma is characterized by airway inflammation and shows a circadian variation with Nocturnal exacerbations. Because exhaled nitric oxide (ENO) measurement appears to be a noninvasive marker of airway inflammation, we examined the hypothesis that ENO would increase at night. In five Nocturnal and five non-Nocturnal Asthmatics, ENO was measured at 4 P.M., 10 P.M., and 4 A.M. before and after bronchodilator. Both pre- and post-bronchodilator ENO (mean pre- and post-bronchodilator ± SEM, ppb) unexpectedly fell significantly in Nocturnal Asthma from 4 P.M. (77.2 ± 8.2) compared to 10 P.M. (68.4 ± 8.7, p < 0.003) and 4 A.M. (66.0 ± 8.5, p < 0.001) with no significant difference between 10 P.M. and 4 A.M., In contrast, there were no significant differences in mean ENO at 4 P.M., 10 P.M., and 4 A.M. in non-Nocturnal Asthma. (51.3 ± 10.8, 57.7 ± 13.4, 53.8 ± 12.5 ppb, respectively). Following bronchodilator, ENO rose significantly by 10.5 ± 1.8 ppb in the Nocturnal Asthma group alone. The circadian rhythm of ENO ...
Neil J. Douglas - One of the best experts on this subject based on the ideXlab platform.
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Inhaled salmeterol or oral theophylline in Nocturnal Asthma
American journal of respiratory and critical care medicine, 1997Co-Authors: Colin Selby, Michael Fitzpatrick, Heather M. Engleman, Patricia M. Sime, T. W. Mackay, Neil J. DouglasAbstract:Nocturnal cough and wheeze are common in Asthma and often treated with beta2 agonists or theophyllines. As Nocturnal Asthma and these therapies may affect sleep and cognition, we compared 50 microg salmeterol inhaled every 12 h with individually dose-titrated sustained-release oral theophylline on sleep quality and cognitive performance in 15 patients with stable Nocturnal Asthma (overnight peak expiratory flow rate [PEFR] fall > or = 15%, > or = 1 Asthmatic awakening/week) using a double-blind, double-dummy, crossover design with 14-d therapy limbs. Cognitive testing and polysomnography were performed on Nights 13 and 14. Trough plasma theophylline concentration after Night 14 on theophylline was median 11.1 (interquartile range 8.3, 15.2) microg/ml. Overnight PEFR falls were similar [salmeterol 2.3 (0, 10.6), theophylline 3.5 (-0.3, 9.6)%, p = 0.4] but on salmeterol there were more nights without awakenings [median difference 1 (0, 2), p < 0.01], fewer Nocturnal arousals [difference -3 (-7, 2) h(-1), p ...
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Role of inflammation in Nocturnal Asthma.
Thorax, 1994Co-Authors: T. W. Mackay, Martin K. Church, William Wallace, Sarah E. M. Howie, P H Brown, Andrew P. Greening, Neil J. DouglasAbstract:BACKGROUND--Nocturnal airway narrowing is a common problem for patients with Asthma but the role of inflammation in its pathogenesis is unclear. Overnight changes in airway inflammatory cell populations were studied in patients with Nocturnal Asthma and in control normal subjects. METHODS--Bronchoscopies were performed at 0400 hours and 1600 hours in eight healthy subjects and in 10 patients with Nocturnal Asthma (> 15% overnight fall in peak flow plus at least one awakening/week with Asthma). The two bronchoscopies were separated by at least five days, and both the order of bronchoscopies and site of bronchoalveolar lavage (middle lobe or lingula with contralateral lower lobe bronchial biopsy) were randomised. RESULTS--In the normal subjects there was no difference in cell numbers and differential cell counts in bronchoalveolar lavage fluid between 0400 and 1600 hours, but in the Nocturnal Asthmatic subjects both eosinophil counts (median 0.11 x 10(5) cells/ml at 0400 hours, 0.05 x 10(5) cells/ml at 1600 hours) and lymphocyte numbers (0.06 x 10(5) cells/ml at 0400 hours, 0.03 x 10(5) cells/ml at 1600 hours) increased at 0400 hours, along with an increase in eosinophil cationic protein levels in bronchoalveolar lavage fluid (3.0 micrograms/ml at 0400 hours, 2.0 micrograms/l at 1600 hours). There were no changes in cell populations in the bronchial biopsies or in alveolar macrophage production of hydrogen peroxide, GM-CSF, or TNF alpha in either normal or Asthmatic subjects at 0400 and 1600 hours. There was no correlation between changes in overnight airway function and changes in cell populations in the bronchoalveolar lavage fluid. CONCLUSIONS--This study confirms that there are increases in inflammatory cell populations in the airway fluid at night in Asthmatic but not in normal subjects. The results have also shown a Nocturnal increase in eosinophil cationic protein levels in bronchoalveolar lavage fluid, but these findings do not prove that these inflammatory changes cause Nocturnal airway narrowing.
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Circulating histamine and eosinophil cationic protein levels in Nocturnal Asthma.
Clinical science (London England : 1979), 1992Co-Authors: Michael Fitzpatrick, Stephen T. Holgate, Thomas W. Mackay, C. Walters, Po-chun Tai, Martin K. Church, Neil J. DouglasAbstract:1. To investigate the role of mast cells and eosinophils in the pathogenesis of Nocturnal Asthma, the plasma methylhistamine concentration, serum eosinophil cationic protein level and peak expiratory flow rate were measured 2-hourly for 24 h in 10 patients with Nocturnal Asthma and in 10 healthy control subjects. Nocturnal Asthma was defined as at least one Nocturnal awakening per week due to cough, wheeze or breathlessness with an average overnight fall in peak expiratory flow rate of at least 15% during a 2-week run-in period. 2. The lowest peak expiratory flow rate occurred at 02.00-04.00 hours in the group with Nocturnal Asthma, whose overnight fall in peak expiratory flow rate was 29 +/- 5% in comparison with 5 +/- 1% (means +/- SEM) in the normal subjects. 3. Plasma methylhistamine levels at night (0.200-04.00 hours) were lower than during the day (10.00-20.00 hours) in both Asthmatic patients and normal subjects (Asthmatic patients: day, median 0.22 ng/ml, 95% confidence intervals 0.18-0.34 ng/ml; night, 0.17 ng/ml, 0.13-0.24 ng/ml; P < 0.01; normal subjects: day, 0.31 ng/ml, 0.24-0.41 ng/ml; night, 0.24 ng/ml, 0.21-0.33 ng/ml; P < 0.01). 4. The serum eosinophil cationic protein level was higher by day (30 ng/ml, 8-47 ng/ml) than by night (21 ng/ml, 5-34 ng/ml; P < 0.04) in the group with Nocturnal Asthma, but did not change significantly with the time of day in the normal subjects (day: 8 ng/ml, 4-14 ng/ml; night: 8 ng/ml, 5-21 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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Morbidity in Nocturnal Asthma: sleep quality and daytime cognitive performance.
Thorax, 1991Co-Authors: Michael Fitzpatrick, C M Shapiro, Heather M. Engleman, K. F. Whyte, Ian J. Deary, Neil J. DouglasAbstract:Most patients with Asthma waken with Nocturnal Asthma from time to time. To assess morbidity in patients with Nocturnal Asthma Nocturnal sleep quality, daytime sleepiness, and daytime cognitive performance were measured prospectively in 12 patients with Nocturnal Asthma (median age 43 years) and 12 age and intellect matched normal subjects. The median (range) percentage overnight fall in peak expiratory flow rate (PEF) was 22 (15 to 50) in the patients with Nocturnal Asthma and 4 (-4 to 7) in the normal subjects. The patients with Asthma had poorer average scores for subjective sleep quality than the normal subjects (median paired difference 1.1 (95% confidence limits 0.1, 2.3)). Objective overnight sleep quality was also worse in the Asthmatic patients, who spent more time awake at night (median difference 51 (95% CL 8.1, 74) minutes), had a longer sleep onset latency (12 (10, 30) minutes), and tended to have less stage 4 (deep) sleep (-33 (-58, 4) minutes). Daytime cognitive performance was worse in the patients with Nocturnal Asthma, who took a longer time to complete the trail making tests (median difference 62 (22, 75) seconds) and achieved a lower score on the paced serial addition tests (-10 (-24, -3)). Mean daytime sleep latency did not differ significantly between the two groups (2 (-3, 7) minutes). It is concluded that hospital outpatients with stable Nocturnal Asthma have impaired sleep quality and daytime cognitive performance even when having their usual maintenance Asthma treatment.
William W. Busse - One of the best experts on this subject based on the ideXlab platform.
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Cytokines in bronchoalveolar lavage fluid of patients with Nocturnal Asthma.
American journal of respiratory and critical care medicine, 1995Co-Authors: Nizar N. Jarjour, William W. BusseAbstract:Airflow obstruction can have a circadian pattern with Nocturnal worsening. Airway inflammation is a cardinal feature of Asthma, and it has been shown to increase at night in association with the decline in pulmonary function. Although the mechanisms regulating enhanced airway inflammation in Asthma at night have yet to be ascertained, we hypothesized that circadian variation in cytokine expression or production is an important factor in the development of Nocturnal airflow limitation. To investigate this possibility, spirometry and bronchoscopy were performed; the bronchoalveolar lavage (BAL) fluid obtained at 4:00 A.M. and at 4:00 P.M. were measured for IL-1 beta in Asthmatics with (n = 5) and without (n = 9) Nocturnal Asthma. In addition, the activity of IL-3, IL-5, and GM-CSF was measured using a biologic assay (eosinophil survival-enhancing activity). BAL fluid concentrations of IL-1 beta were significantly greater at 4:00 A.M. than at 4:00 P.M. (1.14 +/- 0.6 versus 0.7 +/- 0.6 pg/ml; p = 0.05) in Asthmatics with Nocturnal airflow obstruction. Moreover, IL-1 beta levels at 4:00 A.M. tended to be higher in subjects with Nocturnal Asthma than in those without nighttime airflow reduction (1.14 +/- 0.6 versus 0.3 +/- 0.4 pg/ml; p = 0.1). On the other hand, eosinophil survival-enhancing activity in BAL fluid, which is usually associated with IL-3, IL-5, or GM-CSF, was not detected in relationship to Nocturnal Asthma. Because IL-1 beta can activate air-space cells, particularly alveolar macrophages, we propose that an increased release of this cytokine is a significant contributor to Nocturnal airway inflammation and obstruction in Asthma.
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Relationship of plasma epinephrine and circulating eosinophils to Nocturnal Asthma.
American Journal of Respiratory and Critical Care Medicine, 1994Co-Authors: Mary Ellen Bates, William J Calhoun, Nizar N. Jarjour, T Schultz, J Sedgwick, Lara M. Schrader, Murray K. Clayton, Kristen M. Geiger, Cheri A. Swenson, William W. BusseAbstract:The mechanisms of nighttime airway obstruction are not fully established, but include circadian fluctuations in epinephrine and cortisol. To evaluate the relationship of circadian patterns in epinephrine and cortisol to nighttime airflow obstruction, 10 young adult Asthma patients (ages 19 to 25 yr) were admitted to a hospital clinical research unit for a 3-day study during which plasma concentrations of epinephrine, cortisol, and histamine were determined along with white blood cell and eosinophil counts every 6 h (1600, 2200, 0400, and 1000 h). Six of the 10 patients experienced at least one episode of Nocturnal Asthma (defined by more than a 15% decrease in antemeridian (A.M.) to postmeridian (P.M.) FEV1 values). Plasma epinephrine levels (pg/ml) showed a circadian pattern, and the concentration at 2200 h was significantly (p = 0.039) different for the Nocturnal and non-Nocturnal Asthma groups. Circulating eosinophil numbers were greater in subjects who had more frequent episodes of Nocturnal Asthma, a...
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relationship of plasma epinephrine and circulating eosinophils to Nocturnal Asthma
The American review of respiratory disease, 1994Co-Authors: Mary Ellen Bates, William J Calhoun, Nizar N. Jarjour, T Schultz, J Sedgwick, Lara M. Schrader, Murray K. Clayton, Kristen M. Geiger, Cheri A. Swenson, William W. BusseAbstract:The mechanisms of nighttime airway obstruction are not fully established, but include circadian fluctuations in epinephrine and cortisol. To evaluate the relationship of circadian patterns in epinephrine and cortisol to nighttime airflow obstruction, 10 young adult Asthma patients (ages 19 to 25 yr) were admitted to a hospital clinical research unit for a 3-day study during which plasma concentrations of epinephrine, cortisol, and histamine were determined along with white blood cell and eosinophil counts every 6 h (1600, 2200, 0400, and 1000 h). Six of the 10 patients experienced at least one episode of Nocturnal Asthma (defined by more than a 15% decrease in antemeridian (A.M.) to postmeridian (P.M.) FEV 1 values)
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Enhanced Production of Oxygen Radicals in Nocturnal Asthma
The American review of respiratory disease, 1992Co-Authors: Nizar N. Jarjour, William W. Busse, William J CalhounAbstract:Although the mechanisms of Nocturnal worsening of pulmonary function in Asthmatics have not been entirely established, airway inflammation is felt to be a major factor in disease severity. Consequently, to determine whether changes in branchoalveolar lavage (BAL) fluid cellular components and their functions are related to Nocturnal airway obstruction, we performed BAL at 4:00 a.m. and at 4:00 p.m. in Asthma subjects with (n = 5) and without (n = 10) Nocturnal Asthma. No significant changes were observed from 4:00 p.m. to 4:00 a.m. in the concentration of total cells or the percentage or concentration of eosinophils or neutrophils in BAL fluid from subjects with or without Nocturnal Asthma. However, superoxide anion generation by air-space cells from subjects with Nocturnal Asthma was significantly greater at 4:00 a.m. than at 4:00 p.m. (6.9 ± 1.7 versus 1.8 ± 0.5 nmol/500K cells/h, p < 0.05). Moreover, superoxide production at 4:00 a.m. was greater in subjects with than in those without Nocturnal Asthma ...
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Characteristics of Peripheral Blood Eosinophils in Patients with Nocturnal Asthma
The American review of respiratory disease, 1992Co-Authors: William J Calhoun, Mary Ellen Bates, Lara M. Schrader, Julie B. Sedgwick, William W. BusseAbstract:A number of mechanisms have been proposed to explain Nocturnal exacerbations of Asthma including circadian patterns in circulating cortisol and catecholamines. These factors may influence airway smooth muscle tone and circulating eosinophil characteristics and function. Because recent evidence has indicated that eosinophils contribute to airway inflammation and the severity of Asthma, we evaluated the relationship among peripheral blood eosinophils, their density distribution, and the appearance of Nocturnal Asthma. Fifteen patients with Asthma were evaluated. Spirometry (FEV1 and FVC) was determined at 0400 and 1600, and the number and density distribution of peripheral blood eosinophils were determined. Five patients had Nocturnal Asthma, defined as a 15% or greater fall In FEV1 at 0400 versus 1600. The patients with Nocturnal Asthma had greater numbers of eosinophils (cells × 106/ml) at 0400 (0.845 ± 0.13 versus 0.351 ± 0.03) and 1600 (0.651 ± 0.18 versus 0.319 ± 0.07) and a greater circadian variation...
Stanley J. Szefler - One of the best experts on this subject based on the ideXlab platform.
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Airways Inflammation in Nocturnal Asthma
The American review of respiratory disease, 1991Co-Authors: Richard J. Martin, Lisa Cicutto, Hunter R. Smith, Robert D. Ballard, Stanley J. SzeflerAbstract:Nocturnal Asthma is a frequent problem, but the mechanism is unclear. We investigated the possibility that airways inflammation occurred during the night. Bronchoalveolar lavage fluid was analyzed in Asthmatic patients with (n = 7) and without Nocturnal Asthma (n = 7) at 1600 and 0400 h. The Nocturnal Asthma group had an increase in the total leukocyte count (24.0 +/- 7.0 to 41.1 +/- 9.9 x 10(4) cells/ml, p less than 0.05), neutrophils (1.1 +/- 0.6 to 3.7 +/- 1.5 x 10(4) cells/ml, p less than 0.05), and eosinophils (0.5 +/- 0.1 to 1.7 +/- 0.7 x 10(4) cells/ml, p less than 0.05) from 1600 to 0400 h. Cellular components for the non-Nocturnal Asthma group did not change. Between groups, the 1600-h cells were similar. At 0400 h the Nocturnal Asthma group had significantly higher total leukocyte, neutrophil, eosinophil, lymphocyte, and epithelial cell counts. For all subjects, the overnight fall in peak expiratory flow rates was correlated to the change in neutrophils (r = 0.54, p less than 0.05) and eosinophils (r = 0.77, p less than 0.05). We conclude that the Nocturnal worsening of Asthma has an associated cellular inflammatory response that is not seen in patients without overnight decrements in lung function. This inflammatory response together with epithelial damage may be important factors in the etiology of Nocturnal Asthma.
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Plasma histamine, epinephrine, cortisol, and leukocyte β‐adrenergic receptors in Nocturnal Asthma
Clinical pharmacology and therapeutics, 1991Co-Authors: Stanley J. Szefler, Lisa Cicutto, Richard Ando, Wendy Surs, Malcolm R. Hill, Richard J. MartinAbstract:Plasma histamine, cortisol, epinephrine, cyclic adenosine monophosphate (cAMP), and leukocyte β-adrenergic receptors were measured in Asthmatic patients with (n = 7) and without (n = 10) Nocturnal Asthma at 4 PM and 4 AM and compared with those of normal subjects (n = 10). A twofold higher plasma histamine concentration was observed at 4 AM compared with 4 PM in all groups, with no change in plasma cortisol, epinephrine, and cAMP concentrations. At 4 AM compared with 4 PM, only patients with Nocturnal Asthma had a significant 33% decrease (p < 0.05) in mononuclear and polymorphonuclear leukocyte β-adrenergic receptor density, with no difference in binding affinity in all three groups. Polymorphonuclear leukocytes from patients with Nocturnal Asthma had significantly impaired response to iso-proterenol at 4 AM (17% ± 7.3% SEM increase in cAMP; p < 0.05) compared with those of patients without Nocturnal Asthma (69.4% ± 13.7%) and normal (80.2% ± 21.3%) subjects. A significant change in β-adrenergic receptor density and function occurs at night in patients with Nocturnal Asthma. Clinical Pharmacology and Therapeutics (1991) 49, 59–68; doi:10.1038/clpt.1991.11
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plasma histamine epinephrine cortisol and leukocyte β adrenergic receptors in Nocturnal Asthma
Clinical Pharmacology & Therapeutics, 1991Co-Authors: Stanley J. Szefler, Lisa Cicutto, Richard Ando, Wendy Surs, Malcolm R. Hill, Richard J. MartinAbstract:Plasma histamine, cortisol, epinephrine, cyclic adenosine monophosphate (cAMP), and leukocyte β-adrenergic receptors were measured in Asthmatic patients with (n = 7) and without (n = 10) Nocturnal Asthma at 4 PM and 4 AM and compared with those of normal subjects (n = 10). A twofold higher plasma histamine concentration was observed at 4 AM compared with 4 PM in all groups, with no change in plasma cortisol, epinephrine, and cAMP concentrations. At 4 AM compared with 4 PM, only patients with Nocturnal Asthma had a significant 33% decrease (p < 0.05) in mononuclear and polymorphonuclear leukocyte β-adrenergic receptor density, with no difference in binding affinity in all three groups. Polymorphonuclear leukocytes from patients with Nocturnal Asthma had significantly impaired response to iso-proterenol at 4 AM (17% ± 7.3% SEM increase in cAMP; p < 0.05) compared with those of patients without Nocturnal Asthma (69.4% ± 13.7%) and normal (80.2% ± 21.3%) subjects. A significant change in β-adrenergic receptor density and function occurs at night in patients with Nocturnal Asthma. Clinical Pharmacology and Therapeutics (1991) 49, 59–68; doi:10.1038/clpt.1991.11
William J Calhoun - One of the best experts on this subject based on the ideXlab platform.
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Nocturnal Asthma.
Chest, 2003Co-Authors: William J CalhounAbstract:Lung function in a healthy individual varies in a circadian rhythm, with peak lung function occurring near 4:00 PM (1600 hours) and minimal lung function occurring near 4:00 AM (0400 hours). An episode of Nocturnal Asthma is characterized by an exaggeration in this normal variation in lung function from daytime to nighttime, with diurnal changes in pulmonary function generally of > 15%. The occurrence of Nocturnal Asthma is associated with increased morbidity and inadequate Asthma control, and has an important negative impact on quality of life (QOL). Newer data have shed light on physiologic and immunologic mechanisms that underlie the Nocturnal development of airway obstruction. It remains controversial whether Nocturnal Asthma is a distinct entity or is a manifestation of more severe Asthma. The current data do not resolve these two alternatives, as well-controlled studies have reached opposite conclusions. However, the clinical associations of gastroesophageal reflux disease and obesity appear to be strong. The treatment of Asthma with effective controller agents can reduce nighttime symptoms, improve psychometric outcomes, and improve QOL.
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Relationship of plasma epinephrine and circulating eosinophils to Nocturnal Asthma.
American Journal of Respiratory and Critical Care Medicine, 1994Co-Authors: Mary Ellen Bates, William J Calhoun, Nizar N. Jarjour, T Schultz, J Sedgwick, Lara M. Schrader, Murray K. Clayton, Kristen M. Geiger, Cheri A. Swenson, William W. BusseAbstract:The mechanisms of nighttime airway obstruction are not fully established, but include circadian fluctuations in epinephrine and cortisol. To evaluate the relationship of circadian patterns in epinephrine and cortisol to nighttime airflow obstruction, 10 young adult Asthma patients (ages 19 to 25 yr) were admitted to a hospital clinical research unit for a 3-day study during which plasma concentrations of epinephrine, cortisol, and histamine were determined along with white blood cell and eosinophil counts every 6 h (1600, 2200, 0400, and 1000 h). Six of the 10 patients experienced at least one episode of Nocturnal Asthma (defined by more than a 15% decrease in antemeridian (A.M.) to postmeridian (P.M.) FEV1 values). Plasma epinephrine levels (pg/ml) showed a circadian pattern, and the concentration at 2200 h was significantly (p = 0.039) different for the Nocturnal and non-Nocturnal Asthma groups. Circulating eosinophil numbers were greater in subjects who had more frequent episodes of Nocturnal Asthma, a...
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relationship of plasma epinephrine and circulating eosinophils to Nocturnal Asthma
The American review of respiratory disease, 1994Co-Authors: Mary Ellen Bates, William J Calhoun, Nizar N. Jarjour, T Schultz, J Sedgwick, Lara M. Schrader, Murray K. Clayton, Kristen M. Geiger, Cheri A. Swenson, William W. BusseAbstract:The mechanisms of nighttime airway obstruction are not fully established, but include circadian fluctuations in epinephrine and cortisol. To evaluate the relationship of circadian patterns in epinephrine and cortisol to nighttime airflow obstruction, 10 young adult Asthma patients (ages 19 to 25 yr) were admitted to a hospital clinical research unit for a 3-day study during which plasma concentrations of epinephrine, cortisol, and histamine were determined along with white blood cell and eosinophil counts every 6 h (1600, 2200, 0400, and 1000 h). Six of the 10 patients experienced at least one episode of Nocturnal Asthma (defined by more than a 15% decrease in antemeridian (A.M.) to postmeridian (P.M.) FEV 1 values)
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Enhanced Production of Oxygen Radicals in Nocturnal Asthma
The American review of respiratory disease, 1992Co-Authors: Nizar N. Jarjour, William W. Busse, William J CalhounAbstract:Although the mechanisms of Nocturnal worsening of pulmonary function in Asthmatics have not been entirely established, airway inflammation is felt to be a major factor in disease severity. Consequently, to determine whether changes in branchoalveolar lavage (BAL) fluid cellular components and their functions are related to Nocturnal airway obstruction, we performed BAL at 4:00 a.m. and at 4:00 p.m. in Asthma subjects with (n = 5) and without (n = 10) Nocturnal Asthma. No significant changes were observed from 4:00 p.m. to 4:00 a.m. in the concentration of total cells or the percentage or concentration of eosinophils or neutrophils in BAL fluid from subjects with or without Nocturnal Asthma. However, superoxide anion generation by air-space cells from subjects with Nocturnal Asthma was significantly greater at 4:00 a.m. than at 4:00 p.m. (6.9 ± 1.7 versus 1.8 ± 0.5 nmol/500K cells/h, p < 0.05). Moreover, superoxide production at 4:00 a.m. was greater in subjects with than in those without Nocturnal Asthma ...
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Characteristics of Peripheral Blood Eosinophils in Patients with Nocturnal Asthma
The American review of respiratory disease, 1992Co-Authors: William J Calhoun, Mary Ellen Bates, Lara M. Schrader, Julie B. Sedgwick, William W. BusseAbstract:A number of mechanisms have been proposed to explain Nocturnal exacerbations of Asthma including circadian patterns in circulating cortisol and catecholamines. These factors may influence airway smooth muscle tone and circulating eosinophil characteristics and function. Because recent evidence has indicated that eosinophils contribute to airway inflammation and the severity of Asthma, we evaluated the relationship among peripheral blood eosinophils, their density distribution, and the appearance of Nocturnal Asthma. Fifteen patients with Asthma were evaluated. Spirometry (FEV1 and FVC) was determined at 0400 and 1600, and the number and density distribution of peripheral blood eosinophils were determined. Five patients had Nocturnal Asthma, defined as a 15% or greater fall In FEV1 at 0400 versus 1600. The patients with Nocturnal Asthma had greater numbers of eosinophils (cells × 106/ml) at 0400 (0.845 ± 0.13 versus 0.351 ± 0.03) and 1600 (0.651 ± 0.18 versus 0.319 ± 0.07) and a greater circadian variation...