Arthroscopic suture anchor capsulorrhaphy versus labral-based suture capsulorrhaphy in a cadaveric model.

PURPOSE: The purpose of this study was to establish whether suture anchor capsulorrhaphy (SAC) is biomechanically superior to suture capsulorrhaphy (SC) in the management of recurrent anterior shoulder instability without a labral avulsion. METHODS: Twelve matched pairs of shoulders were randomized to either SC or SAC. Specimens were mounted in 60° of abduction and 90° of external rotation. Testing was conducted on an MTS servohydraulic load testing device (MTS, Eden Prairie, MN). A compressive load of 22 N was applied, followed by a 2-N anterior and posterior force to establish a 0 point. Translation with 10-N anterior and posterior loads was recorded for baseline laxity measurement. Arthroscopic capsulorrhaphy was performed with either 3 solitary sutures or 3 suture anchors. Specimens were remounted and returned to the 0 point. Translation was measured with 10-N anterior and posterior loads to determine reduction in translation. Specimens were then loaded to failure to the 0 point at a rate of 0.1 mm/s. RESULTS: Load to failure was significantly greater (P = .02) in the SC group (13.6 ± 1.0 N) versus the SAC group (20.5 ± 2.8 N). No differences were found between SC (2.7 ± 0.7 mm) and SAC (2.3 ± 0.6 mm) when we compared reduction of anterior translation with a 10-N load. The percent reduction of anterior displacement with a 10-N load was similar for the SC (49.9%) and SAC (49.6%) groups. The dominant mode of failure in the study was suture pull-through of the capsular tissue. CONCLUSIONS: Our study indicates that labral-based SC and SAC similarly reduce anterior glenohumeral translation at low loading conditions. Load-to-failure studies indicate that SAC exhibits significantly greater resistance to translation at higher loading conditions. Our study suggests that the use of a suture anchor when one is performing a capsulorrhaphy may provide biomechanical advantage at high loading conditions. CLINICAL RELEVANCE: Our study suggests that when one is performing capsulorrhaphy, the use of a suture anchor may provide biomechanical advantages at high loading conditions.

Lung protective ventilation strategies: have we applied them in trauma patients at risk for acute lung injury and acute respiratory distress syndrome?

Lung protective ventilation strategies for patients with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are well documented, and many medical centers fail to apply these strategies in ALI/ARDS. The objective of this study was to determine if we apply these strategies in trauma patients at risk for ALI/ARDS. We undertook a retrospective review of trauma patients mechanically ventilated for > or = 4 days with an ICD-9 for traumatic pneumothorax, hemothorax, lung contusion, and/or fractured ribs admitted from May 1, 1999 through April 30, 2000 (Group 1), the pre-ARDS Network study, and from May 1, 2003 through April 30, 2004 (Group 2), the post-ARDS Network study. Tidal volume (VT)/kg admission body weight, VT/kg ideal body weight (IBW), and plateau and peak pressures were analyzed with respect to mortality. VT/Kg admission body weight and IBW were significantly reduced when comparing Group 1 with Group 2 (9.27 to 8.03 and 11.67 to 10.04, respectively). VT/kg IBW was greater (P < 0.01) for patients who died in Group 1 (13.81) compared with patients who lived (10.29) or died (9.89) in Group 2. Peak and plateau pressures were greater (P < 0.01) in patients who died in Group 1 than patients who lived or died in Group 2. A strict ARDS Network ventilation strategy (VT < 6 mL/kg) is not followed, rather a low plateau/peak pressure strategy is used, which is a form of lung protective ventilation.

Regulation of apoptosis in eicosapentaenoic acid-treated HL-60 cells.

BACKGROUND: Neutrophil apoptosis is an important physiological process in the resolution of pulmonary inflammation. Previous studies have shown that eicosapentaenoic acid (EPA; 20:5n-3) increases the rate of apoptosis in a concentration- and time-dependent manner in HL-60 cells. However, it is not known if the EPA-induced apoptosis involves the lipoxygenase (LO) and cyclooxygenase (COX) enzymes or the downstream metabolic products of these enzymes. Thus, the objective of this study was to determine the effects of inhibitors LO and COX enzymes on apoptosis, viability, and necrosis in EPA-treated HL-60 cells. MATERIALS AND METHODS: Cells were incubated with 50 mum EPA in the presence of an enzyme inhibitor (1-10 microm) for 12 h. Compounds were used to inhibit COX 1 and 2 (ibuprofen), 5-, 12-, 15-LO (NDGA), 12-LO (baicalein), 5-LO (AA-861), and 5-LO activating protein (MK-886). Eicosanoid (0.001-1.0 mum) add-back experiments were also conducted; LTB(4) and 5-HETE with 5-LO inhibition and 12-HETE with 12-LO inhibition. Flow cytometry was used to assess apoptosis. RESULTS: Inhibition of COX 1 and 2 had no effect on apoptosis. Inhibition of 5-LO and 12-LO significantly increased apoptosis in EPA-treated HL-60 cells. Addition of LTB(4) reduced apoptosis to levels significantly lower than in HL-60 cells treated with EPA alone; 5-HETE and 12-HETE also lowered apoptosis to control levels. CONCLUSIONS: These data indicate that inhibition of LO, particularly 5-LO, increased apoptosis in EPA-treated HL-60 cells. Furthermore, this study demonstrated that the products of the LO enzymes, particularly LTB(4), are critical in the regulation of apoptosis in EPA-treated HL-60 cells.

Inhibition of 5-lipoxygenase induces cell death in anti-inflammatory fatty acid-treated HL-60 cells.

BACKGROUND: Enteral nutrition containing eicosapentaenoic (20:5 omega-3) and gamma-linolenic acid (18:3 omega-6) decreases leukotriene B4 levels and neutrophils in bronchoalveolar lavage fluid of patients and animals with acute respiratory distress syndrome. Reduction in pulmonary inflammation may be caused by decreased neutrophil migration or survival. We showed that apoptosis increases in eicosapentaenoic/gamma-linolenic acid-treated HL-60 cells. We hypothesize that eicosapentaenoic/gamma-linolenic acid-induced apoptosis involves downstream metabolic products of lipoxygenase and cyclooxygenase enzymes. This study determined the effects of inhibitors of lipoxygenase and cyclooxygenase enzymes on eicosapentaenoic/gamma-linolenic acid-treated HL-60 cells. METHODS: Cells were incubated with 50 microM eicosapentaenoic/20 microM gamma-linolenic acid in the presence of an enzyme inhibitor (1-10 microM) for 12 hours. Compounds were used to inhibit cyclooxygenase (ibuprofen), 12-lipoxygenase (baicalein), or 5-lipoxygenase (AA-861). Flow cytometry assessed viability, apoptosis, and necrosis. RESULTS: 5-Lipoxygenase inhibition decreased cell viability and increased cell death (apoptosis + necrosis) in eicosapentaenoic/gamma-linolenic acid-treated HL-60 cells. Inhibition of cyclooxygenase 1 and 2 and 12-lipoxygenase had no significant effect on cellular viability and death in eicosapentaenoic/gamma-linolenic acid-treated HL-60 cells. Adding leukotriene B4 counteracted the effect of 5-lipoxygenase inhibition on apoptosis in eicosapentaenoic/gamma-linolenic acid-treated HL-60 cells. CONCLUSIONS: These data suggest that the processing of eicosapentaenoic and gamma-linolenic acid by 5-lipoxygenase is critical to HL-60 cell survival.

Role of downstream metabolic processing of proinflammatory fatty acids by 5-lipoxygenase in HL-60 cell apoptosis.

BACKGROUND: Proinflammatory eicosanoids formed from arachidonic acid (AA) by lipoxygenase (LO) and cyclooxygenase (COX) pathways have been shown to inhibit apoptosis in certain cell types. This study determined whether inhibition of LO and COX increased apoptosis in AA-treated HL-60 cells in vitro. METHODS: HL-60 cells were incubated with 50 micromol/L AA and an enzyme inhibitor (1-10 micromol/L) for COX, LO, 12-LO, and 5-LO for 12 hours. Flow cytometry was used to assess viability, apoptosis, and necrosis. Apoptosis was further assessed using terminal dUTP nick end-labeling and DNA fragmentation. RESULTS: The highest concentration of LO inhibitors, but not COX inhibitors, decreased viability and increased apoptosis and necrosis in the presence of exogenous AA. CONCLUSION: These results suggest that disruption of the metabolism of AA by LO, in particular 5-LO, decreases cell survival and increases apoptosis. Thus, downstream metabolic processing of AA by LO but not COX plays a critical role in the regulation of HL-60 cell apoptosis.