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Some cervical dislocation injuries may be acutely treated with traction via Gardner-Wells tongs, which are attached to the skull via two pins. While a variety of techniques have been proposed and utilized in the literature and clinical practice to use the tongs, these techniques have not been methodically studied to confirm how they transmit loads to the cervical spine. The current study investigated the mechanical effect of different traction techniques in a laboratory setting. A 50th male Hybrid anthropomorphic test device was used as a human surrogate to represent an average male in height and weight was modified to represent a patient with a unilateral facet dislocation injury. Electronic sensors at the atlanto-occipital joint recorded the loading delivered to the superior cervical spine by traction loading. Combinations of the following variables were evaluated as traction loads were progressively increased to one-third of body weight: tong pin position in the skull (anterior-posterior and superior-inferior to the recommended neutral position), traction cable angle in the sagittal plane (elevated, horizontal, declined), and presence or absence of an occipital support. Analysis of the cervical axial traction loads showed that the only significant predictor of cervical tension was the magnitude of the traction load. Anterior-posterior changes in the pin positions in the skull significantly influenced the cervical flexion-extension moment and anterior-posterior (AP) shear. The data show that a combined cervical tension, flexion moment, and anterior shear force can be achieved with posteriorly biased pins and a bolster behind the head. Increasing the angle of traction cable increased the cervical flexion moment and anterior shear force. The following variables should be carefully considered when applying cervical traction since they significantly affect cervical loading: magnitude of the hanging traction load, anterior-posterior pin position, use of an occipital bolster, and traction load angle. [ABSTRACT FROM AUTHOR]

Hyperfiltration subjects podocytes to increased tensile stress and fluid flow shear stress (FFSS). We showed a 1.5- to 2.0-fold increase in FFSS in uninephrectomized animals and altered podocyte actin cytoskeleton and increased synthesis of prostaglandin E2 (PGE2) following in vitro application of FFSS. We hypothesized that increased FFSS mediates cellular changes through specific receptors of PGE2. Presently, we studied the effect of FFSS on cultured podocytes and decapsulated isolated glomeruli in vitro, and on solitary kidney in uninephrectomized sv129 mice. In cultured podocytes, FFSS resulted in increased gene and protein expression of cyclooxygenase (COX)-2 but not COX-1, prostanoid receptor EP2 but not EP4, and increased synthesis and secretion of PGE2, which were effectively blocked by indomethacin. Next, we developed a special flow chamber for applying FFSS to isolated glomeruli to determine its effect on an intact glomerular filtration barrier by measuring change in Palbumin permeability (PPalb) in vitro. FFSS caused an increase in PPalb that was blocked by indomethacin (P < 0.001). Finally, we show that unilateral nephrectomy in sv129 mice resulted in glomerular hypertrophy (P = 0.006), increased glomerular expression of COX-2 (P < 0.001) and EP2 (P = 0.039), and increased urinary Palbumin excretion (P = 0.001). Activation of the COX-2-PGE2-EP2 axis appears to be a specific response to FFSS in podocytes and provides a mechanistic basis for alteration in podocyte structure and the glomerular filtration barrier, leading to Palbuminuria in hyperfiltration-mediated kidney injury. The COX-2-PGE2-EP2 axis is a potential target for developing specific interventions to ameliorate the effects of hyperfiltration-mediated kidney injury in the progression of chronic kidney disease. [ABSTRACT FROM AUTHOR]

Hyperfiltration subjects podocytes to increased tensile stress and fluid flow shear stress (FFSS). We showed a 1.5- to 2.0-fold increase in FFSS in uninephrectomized animals and altered podocyte actin cytoskeleton and increased synthesis of prostaglandin E2 (PGE2) following in vitro application of FFSS. We hypothesized that increased FFSS mediates cellular changes through specific receptors of PGE2. Presently, we studied the effect of FFSS on cultured podocytes and decapsulated isolated glomeruli in vitro, and on solitary kidney in uninephrectomized sv129 mice. In cultured podocytes, FFSS resulted in increased gene and protein expression of cyclooxygenase (COX)-2 but not COX-1, prostanoid receptor EP2 but not EP4, and increased synthesis and secretion of PGE2, which were effectively blocked by indomethacin. Next, we developed a special flow chamber for applying FFSS to isolated glomeruli to determine its effect on an intact glomerular filtration barrier by measuring change in albumin permeability (Palb) in vitro. FFSS caused an increase in Palb that was blocked by indomethacin (P < 0.001). Finally, we show that unilateral nephrectomy in sv129 mice resulted in glomerular hypertrophy (P = 0.006), increased glomerular expression of COX-2 (P < 0.001) and EP2 (P = 0.039), and increased urinary albumin excretion (P = 0.001). Activation of the COX-2-PGE2-EP2 axis appears to be a specific response to FFSS in podocytes and provides a mechanistic basis for alteration in podocyte structure and the glomerular filtration barrier, leading to albuminuria in hyperfiltration-mediated kidney injury. The COX-2-PGE2-EP2 axis is a potential target for developing specific interventions to ameliorate the effects of hyperfiltration-mediated kidney injury in the progression of chronic kidney disease.