Hemodynamic alterations and myocardial mitochondrial respiration in diabetic spinal cord injured rats

Abstract

Spinal cord injured (SCI) individuals are at high risk for cardiovascular disease (CVD). The more severe a spinal cord injury, the greater risk of all CVD. In addition, SCI also increases the prevalence of disorders such as type II diabetes due to metabolic abnormalities. While higher risk of both diabetes and CVD may be associated with the immobility and increased sympathetic activation of patients with SCI, mitochondrial function may be affected by these factors thereby playing a role in decreasing cardiac efficiency. Mitochondrial function has been found to decrease in the spinal cord after SCI, but mitochondrial function in the heart is unknown due to limited research in cardiac dysfunction after SCI. We will use a rat model of spinal cord injury and type II diabetes to examine changes in CVD function. We expect to see decreased mitochondrial function that could explain the altered hemodynamics in the damaged heart of SCI diabetic animals. Not only will this study serve to assess the unique physiologic characteristics of the heart in chronic SCI individuals, but it will provide a different SCI model that incorporates diabetes for the purpose of exacerbating the onset of cardiovascular disease.