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  Vol. 133 No. 4, April 2007 TABLE OF CONTENTS
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Graded Carbon Dioxide Laser–Induced Subglottic Injury in the Rabbit Model

J. Brett Chafin, MD; Vlad C. Sandulache, PhD; Joshua L. Dunklebarger, MD; Todd D. Otteson, MD; Paul A. Hoffmann, BS; Patricia A. Hebda, PhD; Joseph E. Dohar, MD, MS

Arch Otolaryngol Head Neck Surg. 2007;133(4):358-364.

Objective  To conduct an endoscopic and histologic analysis of the subglottic effects of various carbon dioxide laser–induced injuries in the rabbit model.

Design  Animals were assigned to either a control (cricothyroidotomy only) group or 4 (cricothyroidotomy and posterior subglottic laser) groups that were injured using varying systematically controlled carbon dioxide laser power exposures (5 W, 8 W, and 12 W), with durations of 2 or 4 seconds, and surface area exposures (25% or 40%).

Subjects  Twenty-seven New Zealand white rabbits.

Interventions  The subglottis was approached via cricothyroidotomy. Control airways were immediately closed, while injured airways were subjected to graded carbon dioxide laser exposures prior to closure. Airways were endoscopically monitored preoperatively, immediately postoperatively, and on postoperative days 1, 7, 14, and 21, after which the animals were humanely killed and subglottic tissue harvested for histological evaluation.

Results  Clinical observation revealed no significantly obstructive (acute) stenosis during the duration of the study. Endoscopic visualization revealed the formation of posterior subglottic scarring. Histological analysis of the mucosa revealed that use of carbon dioxide laser resulted in a statistically significant (unpaired, 2-tailed t test, P<.05) proportional thickening of the lamina propria layer, without significant changes in the epithelial and cartilaginous layers. In addition, mucosal blood vessel size increased proportional to the power of the laser delivered to the area (P<.05).

Conclusions  Carbon dioxide laser–induced injury to the subglottis caused localized scarring, lamina propria thickening, and increased vascularity, which resolved with time and was not associated with significant airway obstruction. This model describes a systematic, controlled, and reproducible method of investigating subglottic injury.


Author Affiliations: Department of Pediatric Otolaryngology, Children's Hospital of Pittsburgh (Drs Chafin, Sandulache, Dunklebarger, Otteson, Hebda, and Dohar and Mr Hoffmann), and Departments of Otolaryngology (Drs Chafin, Sandulache, Dunklebarger, Otteson, Hebda, and Dohar), Cell Biology and Physiology (Dr Hebda), Cellular and Molecular Pathology Program (Drs Sandulache and Hebda) University of Pittsburgh School of Medicine, Department of Speech and Communication Disorders, University of Pittsburgh School of Health and Rehabilitation Sciences (Dr Hebda and Dohar), and the McGowan Institute for Regenerative Medicine (Drs Sandulache, Hebda, and Dohar), Pittsburgh, Pa.



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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

A Novel Murine Model for the Examination of Experimental Subglottic Stenosis
Richter et al.
Arch Otolaryngol Head Neck Surg 2009;135:45-52.
ABSTRACT | FULL TEXT  

Acute and Chronic Changes in the Subglottis Induced by Graded Carbon Dioxide Laser Injury in the Rabbit Airway
Otteson et al.
Arch Otolaryngol Head Neck Surg 2008;134:694-702.
ABSTRACT | FULL TEXT  





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