A Biomechanical Comparison of an Open Repair and 3 Minimally Invasive Percutaneous Achilles Tendon Repair Techniques During a Simulated, Progressive Rehabilitation Protocol.

BACKGROUND: While the nonoperative management of Achilles tendon ruptures is a viable option, surgical repair is preferred in healthy and active populations. Recently, minimally invasive percutaneous repair methods with assistive devices have been developed. HYPOTHESIS/PURPOSE: The purpose of this study was to biomechanically analyze 3 commercially available, minimally invasive percutaneous techniques compared with an open Achilles repair during a simulated, progressive rehabilitation program. It was hypothesized that no significant biomechanical differences would exist between repair techniques. STUDY DESIGN: Controlled laboratory study. METHODS: A simulated, midsubstance Achilles rupture was created 6 cm proximal to the calcaneal insertion in 33 fresh-frozen cadaveric ankles. Specimens were then randomly allocated to 1 of 4 different Achilles repair techniques: (1) open repair, (2) the Achillon Achilles Tendon Suture System, (3) the PARS Achilles Jig System, or (4) an Achilles Midsubstance SpeedBridge Repair variation. Repairs were subjected to a cyclic loading protocol representative of progressive postoperative rehabilitation: 250 cycles at 1 Hz for each loading range: 20-100 N, 20-200 N, 20-300 N, and 20-400 N. RESULTS: The open repair technique demonstrated significantly less elongation (5.2 ± 1.1 mm) when compared with all minimally invasive percutaneous repair methods after 250 cycles (P < .05). No significant differences were observed after 250 cycles between the Achillon, PARS, or SpeedBridge repairs, with mean displacements of 9.9 ± 2.2 mm, 12.2 ± 4.4 mm, and 10.0 ± 3.9 mm, respectively. When examined over smaller cyclic intervals, the majority of elongation, regardless of repair, occurred within the first 10 cycles. Within the first 10 cycles, open repairs achieved 71.2% of the total elongation observed after 250 cycles. Corresponding values for the Achillon, PARS, and SpeedBridge repairs were 81.8%, 77.9%, and 69.0%, respectively. No significant differences were observed in the total number of cycles to failure between minimally invasive percutaneous repairs and open repairs. Minor differences in the mechanism of failure were noted; however, the majority of all repairs failed at the suture-tendon interface. CONCLUSION: Minimally invasive percutaneous repair techniques demonstrated a susceptibility to significant early repair elongation when compared with open repairs. However, the ultimate strengths of repairs (cycles to failure) were comparable across all techniques. CLINICAL RELEVANCE: The reduced early elongation of open repairs suggests that patients treated with this technique may be able to progress through an earlier and/or more aggressive postoperative rehabilitation protocol with a lower risk of early irrevocable repair elongation or gapping about the repair site. However, in cases where cosmesis or wound-healing complications are of significant concern, minimally invasive percutaneous techniques provide a biomechanically reasonable alternative based on their repair strengths (cycles to failure). These repairs may need to be protected longer postoperatively to allow for biological healing and avoid early repair elongation and potential gapping between the healing tendon ends.

Tumor necrosis factor-alpha-induced hypertension in pregnant rats results in decreased renal neuronal nitric oxide synthase expression.

BACKGROUND: Preeclampsia is associated with increases in plasma levels of tumor necrosis factor-alpha (TNF-alpha), a cytokine known to contribute to endothelial dysfunction. We recently reported that a twofold elevation in plasma TNF-alpha produces significant reductions in renal function and hypertension in pregnant rats. The purpose of this study was to determine the role of the nitric oxide (NO) system in TNF-alpha-induced hypertension in pregnant rats. METHODS: Tumor necrosis factor-alpha (50 ng/day) was chronically infused starting at day 14 of gestation. Mean arterial pressure, 24-h urinary nitrite/nitrate excretion, and renal nitric oxide synthase (NOS) protein expression by Western blot analysis was measured at day 19 of gestation. RESULTS: A twofold increase in plasma TNF-alpha levels in pregnant rats resulted in a significant increase in arterial pressure (97 +/- 3.6 v 116 +/- 2.1 mm Hg, pregnant versus TNF-alpha pregnant, respectively, P < .05), but no significant change in urinary nitrite/nitrate excretion (22.0 +/- 1.9 v 20.8 +/- 2.5 micromol/24 h, pregnant versus TNF-alpha pregnant, respectively), a measure of whole body NO production. As abnormalities in renal production of NO would not be reflected in the measure of whole body NO production, changes in renal NOS protein levels were determined. The protein expression of both neuronal (nNOS) and inducible (iNOS) nitric oxide synthase were significantly decreased in the medulla of TNF-alpha pregnant rats (nNOS: 10.6 +/- 0.7 v 8.2 +/- 0.8 densitometric units, P < .05; and iNOS: 19.2 +/- 0.9 v 15.4 +/- 0.8 densitometric units, P < .05, pregnant versus TNF-alpha pregnant, respectively). CONCLUSION: The hypertension associated with a chronic twofold increase in TNF-alpha in pregnant rats is associated with significant decreases in renal nNOS and iNOS protein production.