{Reference Type}: Journal Article
{Title}: A 72-h sedated porcine model of traumatic spinal cord injury.
{Author}: Thygesen MM;Entezari S;Houlind N;Nielsen TH;Olsen NØ;Nielsen TD;Skov M;Borgstedt-Bendixen J;Tankisi A;Rasmussen M;Einarsson HB;Agger P;Orlowski D;Dyrskog SE;Thorup L;Pedersen M;Rasmussen MM;
{Journal}: Brain Spine
{Volume}: 4
{Issue}: 0
{Year}: 2024
暂无{DOI}: 10.1016/j.bas.2024.102813
{Abstract}: UNASSIGNED: There is an increasing focus on the prevention of secondary injuries following traumatic spinal cord injury (TSCI), especially through improvement of spinal cord perfusion and immunological modulation. Such therapeutic strategies require translational and controlled animal models of disease progression of the acute phases of human TSCI.
UNASSIGNED: Is it possible to establish a 72-h sedated porcine model of incomplete thoracic TSCI, enabling controlled use of continuous, invasive, and non-invasive modalities during the entire sub-acute phase of TSCI?
UNASSIGNED: A sham-controlled trial was conducted to establish the model, and 10 animals were assigned to either sham or TSCI. All animals underwent a laminectomy, and animals in the TSCI group were subjected to a weight-drop injury. Animals were then kept sedated for 72 h. The amount of injury was assessed by ex-vivo measures MRI-based fiber tractography, histology and immunohistochemistry.
UNASSIGNED: In all animals, we were successful in maintaining sedation for 72 h without comprising vital physiological parameters. The MRI-based fiber tractography showed that all TSCI animals revealed a break in the integrity of spinal neurons, whereas histology demonstrated no transversal sections of the spine with complete injury. Notably, some animals displayed signs of secondary ischemic tissue in the cranial and caudal sections.
UNASSIGNED: This study succeeded in producing a porcine model of incomplete TSCI, which was physiologically stable up to 72 h. We believe that this TSCI model will constitute a potential translational model to study the pathophysiology secondary to TSCI in humans.