The Nasal Respiratory Handicap of Expiratory Airflow Disease: The Response to Bronchodilator Aerosols

Bm, Cohen

doi:10.1159/000192697

Cited by 13 publications

(4 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Hiley, Wilson & Yates (1978) reported that /J2-adrenoceptors were present in the feline capacitance vessels. In man, topical administration of isoprenaline or terbutaline results in either a variable response (McLean, Mathews, Ciarkowski, Brayton & Solomon, 1976), an increase in airway pressure (Grobler, 1966) or no effect (Cohen, 1970;Svensson, Hegardt & Lofkvist, 1980). Our results suggest that ,,-and fl2-adrenoceptors are present in the nose of the dog.…”

Section: Nasal Airway Resistancementioning

confidence: 62%

Control of nasal vasculature and airflow resistance in the dog.

Lung¹,

Phipps²,

Wang³

et al. 1984

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. Nasal vascular and airflow resistances have been measured in dogs, simultaneously on both sides separately.2. Vascular resistance was measured either by constant flow perfusion of the terminal branch of the maxillary artery (which supplies, via the sphenopalatine artery, the nasal septum, most of the turbinates and the nasal sinuses) or by measuring blood flow through this artery, maintained by the dog's own blood pressure.3. Airflowresistancewasassessedbyinsertingballoon-tippedendotrachealcatheters into the back of each nasal cavity via the nasopharynx, and measuring transnasal pressure at constant airflow through each side of the nose simultaneously.4. Preliminary experiments indicated that there was 5-10 % collateral anastomosis between the two sides.5. Close-arterial injection of drugs showed different patterns of response. 6. Adrenaline, phenylephrine, chlorpheniramine and low doses of prostaglandin F2a increased vascular resistance and lowered airway resistance.7. Salbutamol, methacholine and histamine lowered vascular resistance and increased airway resistance.8. Dobutamine decreased airway resistance with a small increase in vascular resistance.9. Prostaglandins E1, E2 and F2a (high dose) decreased both vascular and airway resistances.10. Substance P, eledoisin-related peptide and vasoactive intestinal polypeptide lowered vascular resistance with little change in airway resistance.11. The results are interpreted in terms of possible drug actions on precapillary resistance vessels, sinusoids and venules, and arteriovenous anastomoses. It is concluded that nasal airway resistance cannot be correlated with vascular resistance or blood flow, since the latter has a complex and ill-defined relationship with nasal vascular blood volume. M. A. LUNG AND OTHERS

show abstract

Section: Nasal Airway Resistancementioning

confidence: 62%

Control of nasal vasculature and airflow resistance in the dog.

Lung¹,

Phipps²,

Wang³

et al. 1984

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…These differences were not unexpected in view of the central location of the subepithelial receptors responsible for cough and for reflex bronchoconstriction [38], The same determinations (R", [R" + R J, and Cl) appeared most useful in reflect ing meaningful differences among the various treatment formulations, among a single formulation and its components, and between active drug mixtures and a matched placebo. The trends of total and lower airway re- sistance changes again suggest that consideration of nasal and lower tract flow resistances, obtained in concert, is more helpful and precise than re liance upon R;i-based indices alone in defining the site and total activity of respiratory medications, implementing our earlier conclusions from aerosol trials [39,40],…”

Section: Discussionmentioning

confidence: 66%

Respiratory and Cough Mechanics in Antitussive Trials

Cohen¹

1975

Respiration

View full text Add to dashboard Cite

The relative responsitivy of nine expirographic and airway indices to antitussive therapy was studied in a randomized double-blind trial in which 60 adults without bronchopulmonary disorders, but suffering from common colds, were given oral doses of five drug formulations placebo during their initial 48 h of symptoms. Thoracic gas volume (V_tg), nasal (R_n), lower (R_a), total ([R_n + R_a]) and specific (sR_a) airway resistances were determined plethysmographically; forced vital capacity (FVC), forced expiratory volume for the first second (FEV_1.0) and maximal mid-expiratory flow rate (MMEFR) were recorded spirometrically. Cough pressure at peak flow furnished an index of cough (CI). The measurements were made at baseline and for 4 h after drug; medication was continued for two additional doses and the indices determined again the following morning. Abnormal control means were noted for R_n and [R_n + R_a] (90.8%), cough resistance (83.3%), MMEFR (58.3%), R_a and sR_a (30.0%), but less often for FEV_1.0, V_tg and FVC (6.6, 5.1 and 0.0%, respectively). Nasal and total airways flow resistance means were as sensitive to active therapy and in discriminating the relative worth of medication as direct CI values, R_a and sR_a were less reliable, and the three spirometric functions were the least responsive. This ranking was consistent with the common central airways location of subepithelial receptors responsible for cough and the associated reflex bronchoconstriction. The greatest changes in cough resistance followed treatment with the most significant activity in the nasal, as well as the lower tract, component of total airway resistance.

show abstract

“…Grobler [10] and McLean et al [18] observed a swelling of the nasal mucosa after isoproterenol spraying, but this was de nied by Cohen [9]. Borum and Mygind [6] and Schumacker [21] detected a slight but statistically significant swelling of the nasal mucosa when it was sprayed with fenoterol, a Pj-receptor agonist.…”

Section: Discussionmentioning

confidence: 99%

Responses of Resistance and Capacitance Vessels in Human Nasal Mucosa to β-Receptor Agonists

Konno¹,

Terada²,

Okamoto³

1987

ORL

View full text Add to dashboard Cite

To investigate the responses of nasal vessels, divided into resistance and capacitance vessels, to a β-receptor agonist in human, mucosal blood flow of the inferior turbinate and nasal airway resistance were measured when 1.5 mg terbutaline was applied topically. Mucosal blood flow was measured by the hydrogen clearance method just beneath the site where terbutaline in physiological saline (0.02 ml) was applied on an extremely localized area of the nasal mucosa. Nasal airway resistance of the ipsilateral and contralateral nasal cavities was measured separately by anterior rhinomanometry when terbutaline in normal saline (0.1 ml) was sprayed in the unilateral nasal cavity. Topical application of terbutaline elicited neither a significant increase of mucosal blood flow of the inferior turbinate nor an increase of nasal airway resistance. β-Receptors seem not to be as densely distributed both in the resistance vessels and in the capacitance vessels as to cause vasodilatation by their activation in the nasal mucosa.

show abstract

The Nasal Respiratory Handicap of Expiratory Airflow Disease: The Response to Bronchodilator Aerosols

Cited by 13 publications

References 14 publications

Control of nasal vasculature and airflow resistance in the dog.

Control of nasal vasculature and airflow resistance in the dog.

Respiratory and Cough Mechanics in Antitussive Trials

Responses of Resistance and Capacitance Vessels in Human Nasal Mucosa to β-Receptor Agonists

Contact Info

Product

Resources

About