OBJECTIVE To identify the degree of left arytenoid cartilage (LAC) abduction that allows laryngeal airflow similar to that in galloping horses, assess 2-D and 3-D biomechanical effects of prosthetic laryngoplasty on LAC movement and airflow, and determine the influence of suture position through the muscular process of the arytenoid cartilage (MPA) on these variables. SAMPLE 7 equine cadaver larynges. PROCEDURES With the right arytenoid cartilage maximally abducted and inspiratory airflow simulated by vacuum, laryngeal airflow and translaryngeal pressure and impedance were measured at 12 incremental LAC abduction forces (0% to 100% [maximum abduction]) applied through laryngoplasty sutures passed caudocranially or mediolaterally through the left MPA. Cross-sectional area of the rima glottis and left-to-right angle quotient were determined from photographs at each abduction force; CT images were obtained at alternate forces. Arytenoid and cricoid cartilage markers allowed calculation of LAC roll, pitch, and yaw through use of Euler angles on 3-D reconstructed CT images. RESULTS Translaryngeal pressure and impedance decreased, and airflow increased rapidly at low abduction forces, then slowed until a plateau was reached at approximately 50% of maximum abduction force. The greatest LAC motion was rocking (pitch). Suture position through the left MPA did not significantly affect airflow data. Approximately 50% of maximum abduction force, corresponding to a left arytenoid angle of approximately 30° and left-to-right angle quotient of 0.79 to 0.84, allowed airflow of approximately 61 ± 6.5 L/s. CONCLUSIONS AND CLINICAL RELEVANCE Ex vivo modeling results suggested little benefit to LAC abduction forces > 50%, which allowed airflow similar to that reported elsewhere for galloping horses.

A glutamic acid to lysine (E40K) residue substitution in superoxide dismutase 1 (SOD1) is associated with canine degenerative myelopathy: the only naturally occurring large animal model of amyotrophic lateral sclerosis (ALS). The E40 residue is highly conserved across mammals, except the horse, which naturally carries the (dog mutant) K40 residue. Here we hypothesized that in vitro expression of mutant dog SOD1 would recapitulate features of human ALS (ie, SOD1 protein aggregation, reduced cell viability, perturbations in mitochondrial morphology and membrane potential, reduced ATP production, and increased superoxide ion levels); further, we hypothesized that an equivalent equine SOD1 variant would share similar perturbations in vitro, thereby explain horses' susceptibility to certain neurodegenerative diseases. As in human ALS, expression of mutant dog SOD1 was associated with statistically significant increased aggregate formation, raised superoxide levels (ROS), and altered mitochondrial morphology (increased branching (form factor)), when compared to wild-type dog SOD1-expressing cells. Similar deficits were not detected in cells expressing the equivalent horse SOD1 variant. Our data helps explain the ALS-associated cellular phenotype of dogs expressing the mutant SOD1 protein and reveals that species-specific sequence conservation does not necessarily predict pathogenicity. The work improves understanding of the etiopathogenesis of canine degenerative myelopathy.