Retrospective Evaluation of the Use and Complications of Small-Bore Wire-Guided Thoracostomy Tubes in Dogs and Cats: 156 Cases (2007-2019).

Background: Small-bore wire-guided thoracostomy tubes (SBWGTT) are commonly used in small animals for management of pleural space disease. We aimed to evaluate the indications, placement locations, types of complications, and complication rate of small-bore wire-guided thoracostomy tube placements in dogs and cats in a university setting. Methods: Electronic medical records of patients that underwent SBWGTT placement were reviewed. Signalment, disease, outcome, indication for thoracostomy tube, placement location, number of attempts, diagnostic imaging, number, and type (insertional, technical, and infectious) of complications were recorded. Logistic regression analysis was performed to determine risk factors for complications. Results: A hundred fifty-six cases were identified between 2007 and 2019. Traumatic pneumothorax (33%), pyothorax (25%), and spontaneous pneumothorax (16%) were the most common indications for placement of a SBWGTT. Complications developed in 50 cases (32%). Technical and insertional complications accounted for 21.7% and 14.1% of all cases. Infectious complications were rare with 3.1% of all cases. Pneumothorax (19%), soft tissue swelling at insertion site (14%), and kinking of the chest tube (13%) were most common. Accidental lung perforation was reported in 5/50 complications (7%). Multiple chest tube placement attempts were associated with complications (OR = 6.01 CI: 2.13 to 16.93 p = 0.0007). Conclusions: Complications of SBWGTT placement occurred in one third of cases. Serious complications such as accidental lung perforation was reported in two cases. Complications were associated with number of attempts.

14-3-3-zeta mediates GLP-1 receptor agonist action to alter α cell proglucagon processing.

Recent studies demonstrate that α cells contribute to glucose-stimulated insulin secretion (GSIS). Glucagon-like peptide-1 receptor (GLP-1R) agonists potently potentiate GSIS, making these drugs useful for diabetes treatment. However, the role of α and ß cell paracrine interactions in the effects of GLP-1R agonists is undefined. We previously found that increased ß cell GLP-1R signaling activates α cell GLP-1 expression. Here, we characterized the bidirectional paracrine cross-talk by which α and ß cells communicate to mediate the effects of the GLP-1R agonist, liraglutide. We find that the effect of liraglutide to enhance GSIS is blunted by α cell ablation in male mice. Furthermore, the effect of ß cell GLP-1R signaling to activate α cell GLP-1 is mediated by a secreted protein factor that is regulated by the signaling protein, 14-3-3-zeta, in mouse and human islets. These data refine our understanding of GLP-1 pharmacology and identify 14-3-3-zeta as a potential target to enhance α cell GLP-1 production.