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- Publisher Website: 10.1113/jphysiol.1984.sp015172
- Scopus: eid_2-s2.0-0021286865
- PMID: 6204040
- WOS: WOS:A1984SN11700035
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Article: Control of nasal vasculature and airflow resistance in the dog
Title | Control of nasal vasculature and airflow resistance in the dog |
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Authors | |
Issue Date | 1984 |
Publisher | Wiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751 |
Citation | Journal Of Physiology, 1984, v. VOL. 349, p. 535-551 How to Cite? |
Abstract | Nasal vascular and airflow resistances have been measured in dogs, simultaneously on both sides separately. 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. Airflow resistance was assessed by inserting balloon-tipped endotracheal catheters into the back of each nasal cavity via the nasopharynx, and measuring transnasal pressure at constant airflow through each side of the nose simultaneously. Preliminary experiments indicated that there was 5-10% collateral anastomosis between the two sides. Close-arterial injection of drugs showed different patterns of response. Adrenaline, phenylephrine, chlorpheniramine and low doses of prostaglandin F(2α) increased vascular resistance and lowered airway resistance. Salbutamol, methacholine and histamine lowered vascular resistance and increased airway resistance. Dubutamine decreased airway resistance with a small increase in vascular resistance. Prostaglandins E1, E2 and F(2α) (high dose) decreased both vascular and airway resistances. Substance P, eledoisin-related peptide and vasoactive intestinal polypeptide lowered vascular resistance with little change in airway resistance. 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. |
Persistent Identifier | http://hdl.handle.net/10722/171486 |
ISSN | 2023 Impact Factor: 4.7 2023 SCImago Journal Rankings: 1.708 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lung, MA | en_US |
dc.contributor.author | Phipps, RJ | en_US |
dc.contributor.author | Wang, JCC | en_US |
dc.contributor.author | Widdicombe, JG | en_US |
dc.date.accessioned | 2012-10-30T06:15:24Z | - |
dc.date.available | 2012-10-30T06:15:24Z | - |
dc.date.issued | 1984 | en_US |
dc.identifier.citation | Journal Of Physiology, 1984, v. VOL. 349, p. 535-551 | en_US |
dc.identifier.issn | 0022-3751 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171486 | - |
dc.description.abstract | Nasal vascular and airflow resistances have been measured in dogs, simultaneously on both sides separately. 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. Airflow resistance was assessed by inserting balloon-tipped endotracheal catheters into the back of each nasal cavity via the nasopharynx, and measuring transnasal pressure at constant airflow through each side of the nose simultaneously. Preliminary experiments indicated that there was 5-10% collateral anastomosis between the two sides. Close-arterial injection of drugs showed different patterns of response. Adrenaline, phenylephrine, chlorpheniramine and low doses of prostaglandin F(2α) increased vascular resistance and lowered airway resistance. Salbutamol, methacholine and histamine lowered vascular resistance and increased airway resistance. Dubutamine decreased airway resistance with a small increase in vascular resistance. Prostaglandins E1, E2 and F(2α) (high dose) decreased both vascular and airway resistances. Substance P, eledoisin-related peptide and vasoactive intestinal polypeptide lowered vascular resistance with little change in airway resistance. 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. | en_US |
dc.language | eng | en_US |
dc.publisher | Wiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751 | en_US |
dc.relation.ispartof | Journal of Physiology | en_US |
dc.subject.mesh | Adrenergic Agonists - Pharmacology | en_US |
dc.subject.mesh | Airway Resistance - Drug Effects | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Dogs | en_US |
dc.subject.mesh | Eledoisin - Analogs & Derivatives - Pharmacology | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Histamine Antagonists - Pharmacology | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Methacholine Chloride | en_US |
dc.subject.mesh | Methacholine Compounds - Pharmacology | en_US |
dc.subject.mesh | Nose - Blood Supply - Drug Effects - Physiology | en_US |
dc.subject.mesh | Prostaglandins - Pharmacology | en_US |
dc.subject.mesh | Substance P - Pharmacology | en_US |
dc.subject.mesh | Vascular Resistance - Drug Effects | en_US |
dc.subject.mesh | Vasoactive Intestinal Peptide - Pharmacology | en_US |
dc.title | Control of nasal vasculature and airflow resistance in the dog | en_US |
dc.type | Article | en_US |
dc.identifier.email | Lung, MA:makylung@hkucc.hku.hk | en_US |
dc.identifier.authority | Lung, MA=rp00319 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1113/jphysiol.1984.sp015172 | - |
dc.identifier.pmid | 6204040 | - |
dc.identifier.scopus | eid_2-s2.0-0021286865 | en_US |
dc.identifier.volume | VOL. 349 | en_US |
dc.identifier.spage | 535 | en_US |
dc.identifier.epage | 551 | en_US |
dc.identifier.isi | WOS:A1984SN11700035 | - |
dc.publisher.place | United Kingdom | en_US |
dc.identifier.scopusauthorid | Lung, MA=7006411781 | en_US |
dc.identifier.scopusauthorid | Phipps, RJ=7103320669 | en_US |
dc.identifier.scopusauthorid | Wang, JCC=7701314571 | en_US |
dc.identifier.scopusauthorid | Widdicombe, JG=7102473701 | en_US |
dc.identifier.issnl | 0022-3751 | - |