&NA;To determine the influence of systemic arterial blood pressure upon the pathogenesis of spinal cord injury, we eliminated the increase in systemic blood pressure normally observed after trauma to the spinal cord with the ganglionic blocker chlorisondamine. Blockade of the pressure response did not influence the development of hemorrhagic necrosis in the spinal cord. We conclude that the transient pressure response accompanying spinal cord injury is probably not a major factor in the pathogenesis of hemorrhagic necrosis at the site of the spinal cord injury.