Systemic microcirculation dysfunction after low thoracic spinal cord injury in mice

Spinal cord injury (SCI) disturbs the autonomic nervous system and induces dysfunction or failure of multiple organs. The systemic microcirculation disturbance that contributes to the complications associated with SCI remains to be clarified.

We used male mice (29-32 g) and modified weight-drop injury at T10 to evaluate the systemic microcirculation dysfunction during the first 2 weeks after SCI. We determined permeability and microvascular blood flow in several organs and evaluated their vasomotor function. We also measured circulating endothelial cells (CECs), circulating endothelial progenitor cells (CEPCs), circulating pericyte progenitor cells (CPPCs), and serum proinflammatory cytokines.

The endothelial permeability of almost all organs increased after SCI. Microvascular blood flow decreased in the bladder and kidney and increased in the spleen and was accompanied by endothelial vasomotor dysfunction. SCI also induced an increase in CECs, CEPCs, and CPPCs in peripheral blood. Finally, we confirmed changes in a systemic cytokine profile (interleukin [IL]-3, IL-6, IL-10, IL-13, granulocyte colony-stimulating factor, and regulated on activation normal T cell expressed and secreted) after SCI.

These data indicate that a systemic microcirculation disturbance occurs after SCI. This information may play a key role in the development of effective therapeutic strategies for SCI.