The influence of rotator cuff tear type and weight bearing on shoulder biomechanics in an ex vivo simulator experiment.

Glenohumeral biomechanics after rotator cuff (RC) tears have not been fully elucidated. This study aimed to investigate the muscle compensatory mechanism in weight-bearing shoulders with RC tears and asses the induced pathomechanics (i.e., glenohumeral translation, joint instability, center of force (CoF), joint reaction force). An experimental, glenohumeral simulator with muscle-mimicking cable system was used to simulate 30° scaption motion. Eight fresh-frozen shoulders were prepared and mounted in the simulator. Specimen-specific scapular anthropometry was used to test six RC tear types, with intact RC serving as the control, and three weight-bearing loads, with the non-weight-bearing condition serving as the control. Glenohumeral translation was calculated using instantaneous helical axis. CoF, muscle forces, and joint reaction forces were measured using force sensors integrated into the simulator. Linear mixed effects models (RC tear type and weight-bearing) with random effects (specimen and sex) were used to assess differences in glenohumeral biomechanics. RC tears did not change the glenohumeral translation (p > 0.05) but shifted the CoF superiorly (p ≤ 0.005). Glenohumeral translation and joint reaction forces increased with increasing weight bearing (p < 0.001). RC and deltoid muscle forces increased with the presence of RC tears (p ≤ 0.046) and increased weight bearing (p ≤ 0.042). The synergistic muscles compensated for the torn RC tendons, and the glenohumeral translation remained comparable to that for the intact RC tendons. However, in RC tears, the more superior CoF was close to where glenoid erosion occurs in RC tear patients with secondary osteoarthritis. These findings underscore the importance of early detection and precise management of RC tears.

Perioperative diclofenac application during video-assisted thoracic surgery pleurodesis modulates early inflammatory and fibrinolytic processes in an experimental model.

BACKGROUND/PURPOSE: It has been substantiated that the quality of pleurodesis is reduced when non-steroidal anti-inflammatory drugs (NSAIDs) are used perioperatively. The effects of NSAID administration on the early inflammatory and fibrinolytic processes after mechanical pleurodesis were investigated in an established pig model. METHODS: Left-sided mechanical pleural abrasion was performed on 24 pigs assigned to either an NSAID or a control group. Pleural fluid and blood samples were analysed over a 24-hour period. Histological evaluation of neutrophil influx at the site of pleural abrasion was performed. RESULTS: The volume of pleural effusion was significantly decreased in the diclofenac group at 10 and 24 h, and the protein content was significantly lower. The diclofenac group at 24 h had a diminished total number of white blood cells and a reduced content of transforming growth factor-ß. Moreover, the diclofenac group had a reduced percentage of neutrophils at 6 h. Significantly increased levels of D-dimers and tissue plasminogen activator were measured at 6 h and of interleukin-10 at 24 h. Neutrophils at the site of pleural abrasion were significantly reduced. CONCLUSIONS: Systemic application of diclofenac led to a local enhancement of fibrinolysis and attenuation of pro-inflammatory and fibrotic processes necessary for adhesion formation in our model.

The effect of organ-specific CD26/DPP IV enzymatic activity inhibitor-preconditioning on acute pulmonary allograft rejection.

BACKGROUND: Systemic inhibition of serum CD26/dipeptidylpeptidase (DPP IV) enzymatic activity abrogated acute rejection of pulmonary allografts, whereas organ-specific inhibition ameliorated ischemia/reperfusion injury in syngeneic transplants. Here, we analyze the effect of allograft-specific inhibitor preconditioning on acute rejection in the presence of cyclosporine-based immunosuppressive therapy. METHODS: Orthotopic left single lung transplantation (Tx) in rats (LBNF1 to LEWIS). Control (n=5) grafts were flushed with Perfadex alone, whereas treated (n=5) transplants were perfused with Perfadex and AB192, a specific inhibitor of CD26/DPP IV enzymatic activity. All recipients were treated with 2.5 mg of cyclosporine A/kg per day subcutaneously after Tx. Recipients were sacrificed at day 5 after Tx, and oxygenation capacity was measured. In addition, staining for vasoactive intestinal peptide (VIP) and proliferating cell nuclear antigen (PCNA) at explantation (VIP) and at day 5 (VIP, PCNA) was performed with determination of protein levels for PCNA and mRNA for VIP. RESULTS: Grafts from treated versus controls showed significantly increased oxygenation capacity (P<.008), correlating with significantly less acute rejection (P<.02). PCNA staining and protein expression were significantly lower in perivascular and bronchial epithelial cells (P=.001) in treated versus controls. There was significantly higher staining for VIP at the time of Tx in alveolar macrophages in treated versus controls (P=.001), which was seen up to day 5 post-Tx in both macrophages and respiratory epithelium (P=.001) with elevated mRNA expression for VIP in treated animals. CONCLUSION: Perfusion with a specific inhibitor of CD26/DPP IV enzymatic activity was associated with sustained preservation of pulmonary VIP levels, correlating with an amelioration of the acute rejection cascade.