S18.3 Adaptations of the vasculature following spinal cord injury

Abstract

In rats, spinal cord injury (SCI) produces a marked increase in the strength of neurovascular transmission in arterial vessels located bellow the level of the lesion [1]. Data from humans with SCI indicates that this change is also present and that it contributes to generating episodes of high blood pressure (autonomic dysreflexia) triggered by bladder distension and other sensory stimuli [2]. In humans, it is suggested that the decrease in ongoing sympathetic nerve activity following SCI produces an increase in vascular smooth muscle sensitivity to noradrenaline (NA) and that this change accounts for the augmentation of neurovascular transmission. This suggestion is based on animal experiments where short-term (up to 2 weeks) interruption of sympathetic nerve activity or denervation results in vascular smooth muscle becoming ‘supersensitive’ to NA. However, we have recently demonstrated that this change is transient and is not present in arteries where sympathetic nerve traffic has been interrupted for 7–8 weeks. These findings accord with our demonstration that SCI-induced augmentation of neurovascular transmission in rats cannot be explained by an increased reactivity of the vascular smooth muscle to NA [1].