F Jahshan1, O Ertracht2, A Abu Ammar3, O Ronen4, S Srouji5, L Apel-Sarid6, N Eisenbach1, S Atar5, E Sela4, M Gruber7. 1. Translational Otolaryngology Research Lab, Department of Otolaryngology, Galilee Medical Center, Nahariya, Israel. 2. Eliachar Research Laboratory, Galilee Medical Center, Nahariya, Israel. 3. Department of Pharmaceutical Engineering, Azrieli College of Engineering, Jerusalem, 9103501, Israel. 4. Translational Otolaryngology Research Lab, Department of Otolaryngology, Galilee Medical Center, Nahariya, Israel; Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel. 5. Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel. 6. Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel; Department of Pathology, Galilee Medical Center, Nahariya, Israel. 7. Translational Otolaryngology Research Lab, Department of Otolaryngology, Galilee Medical Center, Nahariya, Israel; Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel. Electronic address: maayan_gr@yahoo.com.
Abstract
OBJECTIVE: Laryngotracheal damage is a well-described complication of endotracheal intubation and animal models are essential for studying the underlying cellular injury cascade. This novel rat model is based on transoral intubation and aims to simulate the common clinical scenario of tube-related airway damage. METHODS: Prospective randomized control pilot study. 28 male Sprague-Dawley were randomly assigned into three groups: control, 3-h' intubation and 6-h' intubation. The animals were then euthanized and their laryngotracheal complexes sent for histological analysis. Epithelial damage, mucosal thickness and mucosal gland hypertrophy were reviewed. RESULTS: Total of 13 control animals and 15 intubated animals. 10 intubated animals survived the study protocol. Loss of epithelial surface architecture including damage to the microscopic ciliary mechanism was a common feature amongst all intubated animals. Average mucosal thickness of the larynx (including vocal cords and subglottic area) was 143 ± 88 μm for control rats, 315 ± 101 μm for rats intubated 3 h and 574 ± 174 μm for rats intubated 6 h .This was a statistically significant difference. Average mucosal gland hypertrophy in the laryngeal subsite was 0.41 ± 0.5 in control rats, 1.4 ± 0.5 in rats intubated 3 h and 2.0 ± 0.0 for rats intubated 6 h (statistically significant difference). There was a clear difference between three and 6 h of intubation with poorer mucosal injury parameters for longer intubation. CONCLUSIONS: We describe a novel rat-based animal model for simulating airway mucosal damage following transoral intubation. This animal model is easy to carry out, reproducible and involves containable animal mortality rates.
OBJECTIVE: Laryngotracheal damage is a well-described complication of endotracheal intubation and animal models are essential for studying the underlying cellular injury cascade. This novel rat model is based on transoral intubation and aims to simulate the common clinical scenario of tube-related airway damage. METHODS: Prospective randomized control pilot study. 28 male Sprague-Dawley were randomly assigned into three groups: control, 3-h' intubation and 6-h' intubation. The animals were then euthanized and their laryngotracheal complexes sent for histological analysis. Epithelial damage, mucosal thickness and mucosal gland hypertrophy were reviewed. RESULTS: Total of 13 control animals and 15 intubated animals. 10 intubated animals survived the study protocol. Loss of epithelial surface architecture including damage to the microscopic ciliary mechanism was a common feature amongst all intubated animals. Average mucosal thickness of the larynx (including vocal cords and subglottic area) was 143 ± 88 μm for control rats, 315 ± 101 μm for rats intubated 3 h and 574 ± 174 μm for rats intubated 6 h .This was a statistically significant difference. Average mucosal gland hypertrophy in the laryngeal subsite was 0.41 ± 0.5 in control rats, 1.4 ± 0.5 in rats intubated 3 h and 2.0 ± 0.0 for rats intubated 6 h (statistically significant difference). There was a clear difference between three and 6 h of intubation with poorer mucosal injury parameters for longer intubation. CONCLUSIONS: We describe a novel rat-based animal model for simulating airway mucosal damage following transoral intubation. This animal model is easy to carry out, reproducible and involves containable animal mortality rates.