Acoustic rhinometry compared with posterior rhinomanometry in the measurement of histamine‐ and bradykinin‐induced changes in nasal airway patency.

1 The effects of inhibitors of nitric oxide synthase and local anaesthetics were studied on changes in human nasal airway patency and albumin extravasation in response to bradykinin and histamine, in vivo. 2 Compared with the action of the vasoconstrictor, ephedrine, 2.5 ,umol, N0-nitro-L-arginine methyl ester (L-NAME), 1 pmol alone, did not change the resting value of the minimal cross-sectional area (A min) of the human nasal airway. L-NAME, 0.1 to 10 ymol, produced a dose-related inhibition of the reduction in A min caused by bradykinin, 300 pig. NG-monomethyl-L-arginine (L-NMMA), 1 pimol, similarly reduced the effect of bradykinin, 300 ,ug, on A min, but NG-nitro-D-arginine methyl ester (D-NAME), had no effect. L-NAME, 0.1 to 10 pmol, or L-NMMA, 10 imol, failed to inhibit the effect of histamine, 300 pg on A min. 3 The inhibition by L-NAME, 1 ,umol of the action of bradykinin, 300 pg on A min was maximal between 15 and 30 min after pretreatment with L-NAME.4 L-NAME, 1 and 10 pimol, inhibited the extravasation of albumin into the nasal cavity induced by bradykinin, 300 pug, and also by histamine, 300 pug. D-NAME, 1 and 10 ,umol had no effect on the extravasation of albumin in response to bradykinin or histamine. 5 L-Arginine, 30 pmol, reversed the effect of L-NAME, 1 Mmol, on the bradykinin-and histamineinduced albumin extravasation into the nasal airway. 6 Local anaesthesia of the nasal airway with lignocaine, 10 mg, or benzocaine, 10 mg, failed to inhibit the reduction in A min or the albumin extravasation induced by either bradykinin, 300 mig, and histamine, 300 Mig. 7 We conclude that the extravasation of plasma albumin caused by bradykinin and by histamine involves the generation of nitric oxide. The nasal blockage induced by bradykinin involves nitric oxide generation but the nasal blockage induced by histamine does not.

Section: Resultsmentioning

confidence: 76%

“…Nasal patency (cross-sectional area of the nasal cavity) was determined by the method of acoustic rhinometry as previously described (Austin & Foreman, 1994b). The parameter used to assess nasal patency was the minimal cross-sectional area (A min) of the nasal airway.…”

Section: Measurement Of Nasal Patencymentioning

confidence: 99%

Attenuation of human nasal airway responses to bradykinin and histamine by inhibitors of nitric oxide synthase

Dear

Ghali

Foreman

1996

“…Minimum nasal cross-sectional area (A min) was determined by acoustic rhinometry as previously described (Austin & Foreman, 1994b).…”

mentioning

confidence: 99%

Reduction by Hoe 140, the B₂ kinin receptor antagonist, of antigen‐induced nasal blockage

Austin

Foreman

1994

In subjects with allergic rhinitis to house-dust mite (HDM), antigen challenge produced a significant increase in nasal blockage but had no effect on nasal vascular permeability. The B2 kinin receptor antagonist, [D-Arg0,Hyp3,Thi5,D-Tic7,Oic8]-bradykinin (Hoe 140), 200 Lg administered by intranasal aerosol 2 min prior to challenge with HDM, 500 u significantly reduced nasal blockage induced by the antigen challenge. The data are compatible with a role for B2 kinin receptors in the nasal response to challenge with antigen which is responsible for nasal blockage.

“…Acoustic rhinometry is an established research technique for objectively measuring nasal blockage (Austin & Foreman, 1994;Fisher et al, 1994). The acoustic rhinometer, supplied by GM instruments (Kilwinning, U.K.), produces a sound pulse that travels up a hollow tube, through a 6 cm sterile plastic nose piece, and into the subject's nasal cavity.…”

Section: Measurement Of Nasal Patencymentioning

confidence: 99%

Histamine receptors that influence blockage of the normal human nasal airway

Taylor‐Clark

Sodha

Warner

et al. 2005

The aim of this study was to investigate the mechanisms by which histamine causes nasal blockage. Histamine, 40–800 μg, intranasally into each nostril, induced significant blockage of the nasal airway in normal human subjects, as measured by acoustic rhinometry. Oral pretreatment with cetirizine, 5–30 mg, the H1 antagonist, failed to reverse completely the nasal blockage induced by histamine, 400 μg. Dimaprit, 50–200 μg, the H2 agonist, intranasally, caused nasal blockage, which was reversed by oral pretreatment with ranitidine, 75 mg, the H2 antagonist. A combination of cetirizine, 20 mg, and ranitidine, 75 mg, caused greater inhibition of the nasal blockage caused by histamine, 400 μg, than cetirizine alone. In the presence of both antagonists, there was residual histamine‐induced nasal blockage. R‐α‐methylhistamine (R‐α‐MeH), 100–600 μg, the H3 agonist, intranasally, caused nasal blockage, which was not inhibited by either cetirizine or ranitidine. Thioperamide, 700 μg, the H3 antagonist, intranasally, reversed the R‐α‐MeH‐induced nasal blockage. Thioperamide alone had no significant action on the nasal blockage induced by histamine, 400 and 1000 μg, but, in the presence of cetirizine, 20 mg, thioperamide further reduced the histamine‐induced nasal blockage. Corynanthine, 2 mg, the α1‐adrenoceptor antagonist, administered intranasally, caused nasal blockage. Corynanthine produced a greater increase in nasal blockage when in combination with bradykinin compared to its combination with R‐α‐MeH. There appears to be a contribution of H1, H2 and H3 receptors to histamine‐induced nasal blockage in normal human subjects. The sympathetic nervous system actively maintains nasal patency and we suggest that activation of nasal H3 receptors may downregulate sympathetic activity. British Journal of Pharmacology (2005) 144, 867–874. doi:10.1038/sj.bjp.0706118