Recurrent autonomic dysreflexia exacerbates vascular dysfunction after spinal cord injury

Peripheral vascular function in spinal cord injury: a systematic review

“…94 The peripheral mechanism responsible for the enhanced pressor response does not appear to be endothelial dysfunction, as acetylcholine (endothelium-dependent)-induced vasorelaxation is normal following T3 SCI in rodents. 16 Instead, others have suggested that impaired neuronal re-uptake of NE and PE, 92,95 and/or increased reactivity of the vascular smooth muscle 93 may be responsible for the enhanced pressor response to PE. However, it is also likely that other explanations for such hypersensitivity must exist as PE is metabolized in the liver by phase I and phase II enzyme systems (mainly monoamine oxidase) and is, therefore, not a substrate for neuronal re-uptake.…”

“…On the contrary, it has been reported that daily induction of a 30 min bout of AD via colorectal distension caused aadrenoceptor hypersensitivity, but this was accompanied by a less severe pressor response to a single bout of colorectal distension (that is, reduced severity of AD). 16 Thus, future studies are required to determine whether a-adrenoceptor hypersensitivity occurs after SCI and the potential effect of such hypersensitivity on the cardiovascular system.…”

“…104,112 In the only study to examine the effect of episodic hypertension per se on vascular endothelial function in SCI, it was reported that 2 weeks of repetitively induced AD in rodents with T3 SCI exacerbates injury-induced hypersensitivity to PE in superior mesenteric arteries (Figure 3), but does not appear to alter endothelial function. 16 That study, however, only assessed hypersensitivity following a relatively short time span of induced AD; thus, the long-term effects of such blood pressure oscillations in SCI remain unknown. There are several lines of evidence from other pathological states that suggest chronic blood pressure oscillations damage the vascular endothelium.…”

“…[13][14][15] This is somewhat surprising: as we will describe in this review, SCI induces vascular deconditioning below the level of injury and disrupts supraspinal control of the spinal sympathetic circuits that ultimately innervate the adventitial-media layer of blood vessels, both of which lead to a multitude of vascular abnormalities that may contribute to elevated CVD risk. 16 It is highly likely, therefore, that adaptations in the peripheral vasculature after SCI are of equal, if not greater, clinical importance than the wellrecognized central cardiovascular adaptations that occur in this population. Accordingly, the aim of this review is threefold: (1) to provide an overview of the autonomic nervous system and blood vessel structure and function; (2) to describe changes thereof following SCI; and (3) to discuss the effects that loss of sympathetic neural control and physical deconditioning has on the peripheral vasculature in the SCI population.…”

Atypical autonomic dysreflexia during robotic-assisted body weight supported treadmill training in an individual with motor incomplete spinal cord injury

“…[3][4][5] AD can be precipitated by various afferent irritants from below the level of the injury particularly novel stimuli such as electrical stimulation and body weight supported exercise. 6 Alan et al 6 reported that injury-induced vasculature changes may contribute to AD occurrence via circulatory changes and the altered ability to tolerate novel sensory input.…”