Control of the mucosal microcirculation in the upper respiratory tract

Timothy Smith, J. Prazma, C. C. Coleman, A. F. Drake, R. C. Boucher

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

This study was designed to investigate the regulatory mechanisms of the mucosal microvascular network in the upper respiratory tract. Tracheal mucosal circulation was observed using a specially constructed chamber that allowed direct microscopic visualization of mucosal arterioles. Solutions of increasing hypertonicity (500 and 900 mOsm) applied to the tracheal epithelium resulted in increasing dilation of the underlying mucosal arterioles (p <0.001). N(omega)-nitro-L-arginine methyl ester (L-NAME, 1 mmol/L), a specific inhibitor of nitric oxide synthesis, added to a hypertonic solution inhibited dilation of mucosal arterioles (p <0.001). Addition of the substrate for nitric oxide synthesis, L-arginine (0.6 mmol/L) to the hypertonic solution containing L-NAME resulted in dilation of mucosal arterioles once again. These data demonstrate that nitric oxide is a crucial mediator in the response of mucosal arterioles to the hypertonic stimulus presented to the epithelial surface of the trachea. Further elucidation of the control of the mucosal microcirculation in the upper respiratory tract could be implemented in new treatment for pathologic processes of the upper respiratory tract such as mucosal congestion and edema.

Original languageEnglish (US)
Pages (from-to)646-652
Number of pages7
JournalOtolaryngology - Head and Neck Surgery
Volume109
Issue number4
StatePublished - 1993
Externally publishedYes

Fingerprint

Arterioles
Microcirculation
Respiratory System
NG-Nitroarginine Methyl Ester
Hypertonic Solutions
Dilatation
Nitric Oxide
Pathologic Processes
Microvessels
Trachea
Arginine
Edema
Epithelium

ASJC Scopus subject areas

  • Otorhinolaryngology

Cite this

Smith, T., Prazma, J., Coleman, C. C., Drake, A. F., & Boucher, R. C. (1993). Control of the mucosal microcirculation in the upper respiratory tract. Otolaryngology - Head and Neck Surgery, 109(4), 646-652.

Control of the mucosal microcirculation in the upper respiratory tract. / Smith, Timothy; Prazma, J.; Coleman, C. C.; Drake, A. F.; Boucher, R. C.

In: Otolaryngology - Head and Neck Surgery, Vol. 109, No. 4, 1993, p. 646-652.

Research output: Contribution to journalArticle

Smith, T, Prazma, J, Coleman, CC, Drake, AF & Boucher, RC 1993, 'Control of the mucosal microcirculation in the upper respiratory tract', Otolaryngology - Head and Neck Surgery, vol. 109, no. 4, pp. 646-652.
Smith, Timothy ; Prazma, J. ; Coleman, C. C. ; Drake, A. F. ; Boucher, R. C. / Control of the mucosal microcirculation in the upper respiratory tract. In: Otolaryngology - Head and Neck Surgery. 1993 ; Vol. 109, No. 4. pp. 646-652.
@article{e1ac410bcd2242239ffe78fc61bdbd1f,
title = "Control of the mucosal microcirculation in the upper respiratory tract",
abstract = "This study was designed to investigate the regulatory mechanisms of the mucosal microvascular network in the upper respiratory tract. Tracheal mucosal circulation was observed using a specially constructed chamber that allowed direct microscopic visualization of mucosal arterioles. Solutions of increasing hypertonicity (500 and 900 mOsm) applied to the tracheal epithelium resulted in increasing dilation of the underlying mucosal arterioles (p <0.001). N(omega)-nitro-L-arginine methyl ester (L-NAME, 1 mmol/L), a specific inhibitor of nitric oxide synthesis, added to a hypertonic solution inhibited dilation of mucosal arterioles (p <0.001). Addition of the substrate for nitric oxide synthesis, L-arginine (0.6 mmol/L) to the hypertonic solution containing L-NAME resulted in dilation of mucosal arterioles once again. These data demonstrate that nitric oxide is a crucial mediator in the response of mucosal arterioles to the hypertonic stimulus presented to the epithelial surface of the trachea. Further elucidation of the control of the mucosal microcirculation in the upper respiratory tract could be implemented in new treatment for pathologic processes of the upper respiratory tract such as mucosal congestion and edema.",
author = "Timothy Smith and J. Prazma and Coleman, {C. C.} and Drake, {A. F.} and Boucher, {R. C.}",
year = "1993",
language = "English (US)",
volume = "109",
pages = "646--652",
journal = "Otolaryngology - Head and Neck Surgery (United States)",
issn = "0194-5998",
publisher = "Mosby Inc.",
number = "4",

}

TY - JOUR

T1 - Control of the mucosal microcirculation in the upper respiratory tract

AU - Smith, Timothy

AU - Prazma, J.

AU - Coleman, C. C.

AU - Drake, A. F.

AU - Boucher, R. C.

PY - 1993

Y1 - 1993

N2 - This study was designed to investigate the regulatory mechanisms of the mucosal microvascular network in the upper respiratory tract. Tracheal mucosal circulation was observed using a specially constructed chamber that allowed direct microscopic visualization of mucosal arterioles. Solutions of increasing hypertonicity (500 and 900 mOsm) applied to the tracheal epithelium resulted in increasing dilation of the underlying mucosal arterioles (p <0.001). N(omega)-nitro-L-arginine methyl ester (L-NAME, 1 mmol/L), a specific inhibitor of nitric oxide synthesis, added to a hypertonic solution inhibited dilation of mucosal arterioles (p <0.001). Addition of the substrate for nitric oxide synthesis, L-arginine (0.6 mmol/L) to the hypertonic solution containing L-NAME resulted in dilation of mucosal arterioles once again. These data demonstrate that nitric oxide is a crucial mediator in the response of mucosal arterioles to the hypertonic stimulus presented to the epithelial surface of the trachea. Further elucidation of the control of the mucosal microcirculation in the upper respiratory tract could be implemented in new treatment for pathologic processes of the upper respiratory tract such as mucosal congestion and edema.

AB - This study was designed to investigate the regulatory mechanisms of the mucosal microvascular network in the upper respiratory tract. Tracheal mucosal circulation was observed using a specially constructed chamber that allowed direct microscopic visualization of mucosal arterioles. Solutions of increasing hypertonicity (500 and 900 mOsm) applied to the tracheal epithelium resulted in increasing dilation of the underlying mucosal arterioles (p <0.001). N(omega)-nitro-L-arginine methyl ester (L-NAME, 1 mmol/L), a specific inhibitor of nitric oxide synthesis, added to a hypertonic solution inhibited dilation of mucosal arterioles (p <0.001). Addition of the substrate for nitric oxide synthesis, L-arginine (0.6 mmol/L) to the hypertonic solution containing L-NAME resulted in dilation of mucosal arterioles once again. These data demonstrate that nitric oxide is a crucial mediator in the response of mucosal arterioles to the hypertonic stimulus presented to the epithelial surface of the trachea. Further elucidation of the control of the mucosal microcirculation in the upper respiratory tract could be implemented in new treatment for pathologic processes of the upper respiratory tract such as mucosal congestion and edema.

UR - http://www.scopus.com/inward/record.url?scp=0027362191&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027362191&partnerID=8YFLogxK

M3 - Article

C2 - 8233499

AN - SCOPUS:0027362191

VL - 109

SP - 646

EP - 652

JO - Otolaryngology - Head and Neck Surgery (United States)

JF - Otolaryngology - Head and Neck Surgery (United States)

SN - 0194-5998

IS - 4

ER -