A Case of Airway Constriction Caused by a Laryngeal Tumor

2020 ◽  
Vol 113 (8) ◽  
pp. 513-517
Author(s):  
Miwako Someya ◽  
Ryota Tomioka ◽  
Kiyoaki Tsukahara
Keyword(s):  
Laryngeal Tumor ◽  
Airway Constriction

Pattern and mechanism of airway response to hypocapnia in normal subjects

1979 ◽  
Vol 47 (1) ◽  
pp. 8-12 ◽  
Author(s):  
C. F. O'Cain ◽  
M. J. Hensley ◽  
E. R. McFadden ◽  
R. H. Ingram
Keyword(s):  
Vital Capacity ◽  
Normal Subjects ◽  
Oxygen Mixture ◽  
Flow Volume ◽  
Mixture Density ◽  
Lung Capacity ◽  
Airway Constriction ◽  
Maximal Expiratory Flow ◽  
Airway Response ◽  
Expiratory Flow

We examined the bronchoconstriction produced by airway hypocapnia in normal subjects. Maximal expiratory flow at 25% vital capacity on partial expiratory flow-volume (PEFV) curves fell during hypocapnia both on air and on an 80% helium- 20% oxygen mixture. Density dependence also fell, suggesting predominantly small airway constriction. The changes seen on PEFV curves were not found on maximal expiratory flow-volume curves, indicating the inhalation to total lung capacity substantially reversed the constriction. Pretreatment with a beta-sympathomimetic agent blocked the response, whereas atropine pretreatment did not, suggesting that hypocapnia affects airway smooth muscle directly, not via cholinergic efferents.

Atypical carcinoid (neuroendocrine carcinoma) of the gingiva: Counterpart of a laryngeal tumor

2004 ◽  
Vol 54 (2) ◽  
pp. 97-100 ◽  
Author(s):  
Yoshihiro Abiko ◽  
Ikuko Ogawa ◽  
Yufo Hattori ◽  
Kaoru Kusano ◽  
Michiko Nishimura ◽  
...  
Keyword(s):  
Neuroendocrine Carcinoma ◽  
Atypical Carcinoid ◽  
Laryngeal Tumor

Hypoxic airway constriction in infants of very low birth weight recovering from moderate to severe bronchopulmonary dysplasia

1989 ◽  
Vol 115 (3) ◽  
pp. 456-459 ◽  
Author(s):  
Jean S. Tay-Uyboco ◽  
Kim Kwiatkowski ◽  
Donald B. Cates ◽  
Linda Kavanagh ◽  
Henrique Rigatto
Keyword(s):  
Birth Weight ◽  
Low Birth Weight ◽  
Bronchopulmonary Dysplasia ◽  
Very Low Birth Weight ◽  
Airway Constriction

scholarly journals Individual canine Airway Response Variability to a Deep Inspiration

2011 ◽  
Vol 5 ◽  
pp. CCRPM.S6531
Author(s):  
Robert H. Brown ◽  
David W. Kaczka ◽  
Katherine Fallano ◽  
Steve Shapiro ◽  
Wayne Mitzner
Keyword(s):  
Temporal Variability ◽  
Variable Response ◽  
High Resolution Computed Tomography ◽  
Dose Rates ◽  
Beneficial Effects ◽  
Airway Constriction ◽  
Subsequent Response ◽  
Before And After ◽  
Airway Response ◽  
Airway Tone

In healthy individuals, a DI can reverse (bronchodilation) or prevent (bronchoprotection) induced airway constriction. For individuals with asthma or COPD, these effects may be attenuated or absent. Previous work showed that the size and duration of a DI affected the subsequent response of the airways. Also, increased airway tone lead to increased airway size variability. The present study examined how a DI affected the temporal variability in individual airway baseline size and after methacholine challenge in dogs using High-Resolution Computed Tomography. Dogs were anesthetized and ventilated, and on 4 separate days, HRCT scans were acquired before and after a DI at baseline and during a continuous intravenous infusion of methacholine (Mch) at 3 dose rates (17, 67, and 200 μg/mm). The Coefficient of Variation was used as an index of temporal variability in airway size. We found that at baseline and the lowest dose of Mch, variability decreased immediately and 5 minutes after the DI ( P < 0.0001). In contrast, with higher doses of Mch, the DI caused a variable response. At a rate of 67 μg/min of Mch, the temporal variability increased after 5 minutes, while at a rate of 200 μg/min of Mch, the temporal variability increased immediately after the DI. Increased airway temporal variability has been shown to be associated with asthma. Although the mechanisms underlying this temporal variability are poorly understood, the beneficial effects of a DI to decrease airway temporal variability was eliminated when airway tone was increased. If this effect is absent in asthmatics, this may suggest a possible mechanism for the loss of bronchoprotective and bronchodilatory effects after a DI in asthma.

scholarly journals Interaction between airway edema and lung inflation on responsiveness of individual airways in vivo

1997 ◽  
Vol 83 (2) ◽  
pp. 366-370 ◽  
Author(s):  
Robert H. Brown ◽  
Wayne Mitzner ◽  
Elizabeth M. Wagner
Keyword(s):  
Dose Response ◽  
Lung Volume ◽  
Bronchial Artery ◽  
Wall Thickening ◽  
Airway Wall ◽  
Lung Inflation ◽  
Wall Area ◽  
Airway Edema ◽  
Airway Constriction

Brown, Robert H., Wayne Mitzner, and Elizabeth M. Wagner.Interaction between airway edema and lung inflation on responsiveness of individual airways in vivo. J. Appl. Physiol. 83(2): 366–370, 1997.—Inflammatory changes and airway wall thickening are suggested to cause increased airway responsiveness in patients with asthma. In five sheep, the dose-response relationships of individual airways were measured at different lung volumes to methacholine (MCh) before and after wall thickening caused by the inflammatory mediator bradykinin via the bronchial artery. At 4 cmH2O transpulmonary pressure (Ptp), 5 μg/ml MCh constricted the airways to a maximum of 18 ± 3%. At 30 cmH2O Ptp, MCh resulted in less constriction (to 31 ± 5%). Bradykinin increased airway wall area at 4 and 30 cmH2O Ptp (159 ± 6 and 152 ± 4%, respectively; P < 0.0001). At 4 cmH2O Ptp, bradykinin decreased airway luminal area (13 ± 2%; P< 0.01), and the dose-response curve was significantly lower ( P = 0.02). At 30 cmH2O, postbradykinin, the maximal airway narrowing was not significantly different (26 ± 5%; P = 0.76). Bradykinin produced substantial airway wall thickening and slight potentiation of the MCh-induced airway constriction at low lung volume. At high lung volume, bradykinin increased wall thickness but had no effect on the MCh-induced airway constriction. We conclude that inflammatory fluid leakage in the airways cannot be a primary cause of airway hyperresponsiveness.

Hypocapnia-induced constriction of the canine peripheral airways exhibits tachyphylaxis

1987 ◽  
Vol 63 (2) ◽  
pp. 497-504 ◽  
Author(s):  
J. Kolbe ◽  
S. R. Kleeberger ◽  
H. A. Menkes ◽  
E. W. Spannhake
Keyword(s):  
Prolonged Exposure ◽  
Atropine Sulfate ◽  
Chlorpheniramine Maleate ◽  
Mechanically Ventilated ◽  
Peripheral Airways ◽  
Airway Constriction ◽  
Peripheral Lung ◽  
Histamine H1 Receptors ◽  
Constrictor Response ◽  
Compensatory Effect

Hypocapnia-induced constriction of peripheral airways may be important in regulating the distribution of ventilation in pathological conditions. We studied the response of the peripheral lung to hypocapnia in anesthetized, paralyzed, mechanically ventilated dogs using the wedged bronchoscope technique to measure resistance of the collateral system (Rcs). A 5-min hypocapnic challenge produced a 161 +/- 19% (mean +/- SE) increase in Rcs. The magnitude of this response was not diminished with repeated challenge or by atropine sulfate (1 mg base/kg iv), chlorpheniramine maleate (5 mg base/kg iv), or indomethacin (5 mg/kg iv). The response was reduced by 75% by isoproterenol (5 micrograms/kg iv) (P less than 0.01) and reduced by 80% by nifedipine (20 micrograms/kg iv) (P less than 0.05). During 30-min exposure to hypocapnia the maximum constrictor response occurred at 4–5 min, after which the response attenuated to approximately 50% of the maximum response (mean = 53%, range 34–69%). Further 30-min challenges with hypocapnia resulted in significantly decreased peak responses, the third response being 50% of the first (P less than 0.001). The inability of indomethacin or propranolol to affect the tachyphylaxis or attenuation of the response suggests that neither cyclooxygenase products nor beta-adrenergic activity was involved. Hence, hypocapnia caused a prompt and marked constrictor response in the peripheral lung not associated with cholinergic mechanisms or those involving histamine H1-receptors or prostaglandins. With prolonged exposure to hypocapnia there was gradual attentuation of the constrictor response with continued exposure and tachyphylaxis to repeated exposure both of which would tend to diminish any compensatory effect of hypocapnic airway constriction on the distribution of ventilation.

scholarly journals Effects of inhaled aminophylline on airway constriction and inflammation in ovalbumin-sensitized guinea pigs

Drug Delivery ◽  
2013 ◽  
Vol 21 (5) ◽  
pp. 321-327 ◽  
Author(s):  
Masato Muraki ◽  
Shota Wada ◽  
Takeshi Ohno ◽  
Souichirou Hanada ◽  
Hirochiyo Sawaguchi ◽  
...  
Keyword(s):  
Guinea Pigs ◽  
Airway Constriction

scholarly journals Probing airway conditions governing ventilation defects in asthma via hyperpolarized MRI image functional modeling

2009 ◽  
Vol 106 (4) ◽  
pp. 1293-1300 ◽  
Author(s):  
Lisa Campana ◽  
Jennifer Kenyon ◽  
Sanaz Zhalehdoust-Sani ◽  
Yang-Sheng Tzeng ◽  
Yanping Sun ◽  
...  
Keyword(s):  
Computational Models ◽  
Maximum Size ◽  
Measured Data ◽  
Lung Imaging ◽  
Small Airways ◽  
Functional Modeling ◽  
Airway Constriction ◽  
The Mean ◽  
Hyperpolarized Mri ◽  
Central Airway

Image functional modeling (IFM) has been introduced as a method to simultaneously synthesize imaging and mechanical data with computational models to determine the degree and location of airway constriction in asthma. Using lung imaging provided by hyperpolarized 3He MRI, we advanced our IFM method to require matching not only to ventilation defect location but to specific ventilation throughout the lung. Imaging and mechanical data were acquired for four healthy and four asthmatic subjects pre- and postbronchial challenge. After provocation, we first identified maximum-size airways leading exclusively to ventilation defects and highly constricted them. Constriction patterns were then found for the remaining airways to match mechanical data. Ventilation images were predicted for each pattern, and visual and statistical comparisons were done with measured data. Results showed that matching of ventilation defects requires severe constriction of small airways. The mean constriction of such airways leading to the ventilation defects needed to be 70–80% rather than fully closed. Also, central airway constriction alone could not account for dysfunction seen in asthma, so small airways must be involved.

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