Department of Physiology, Radboud University Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands.
Hypertension. 2010 Mar;55(3):636-43. doi: 10.1161/HYPERTENSIONAHA.109.147330. Epub 2010 Jan 25.
Autonomic dysreflexia is a hypertensive episode in spinal cord-injured individuals induced by exaggerated sympathetic activity and thought to be alpha-adrenergic mediated. alpha-Adrenoceptor antagonists have been a rational first choice; nevertheless, calcium channel blockers are primarily used in autonomic dysreflexia management. However, alpha-adrenoceptor blockade may leave a residual vasoconstrictor response to sympathetic nonadrenergic transmission unaffected. The aim was to assess the alpha-adrenergic contribution and, in addition, the role of supraspinal control to leg vasoconstriction during exaggerated sympathetic activity provoked by autonomic dysreflexia in spinal cord-injured individuals and by a cold pressure test in control individuals. Upper leg blood flow was measured using venous occlusion plethysmography during supine rest and during exaggerated sympathetic activity in 6 spinal cord-injured individuals and 7 able-bodied control individuals, without and with phentolamine (alpha-adrenoceptor antagonist) and nicardipine (calcium channel blocker) infusion into the right femoral artery. Leg vascular resistance was calculated. In spinal cord-injured individuals, phentolamine significantly reduced the leg vascular resistance increase during autonomic dysreflexia (8+/-5 versus 24+/-13 arbitrary units; P=0.04) in contrast to nicardipine (15+/-10 versus 24+/-13 arbitrary units; P=0.12). In controls, phentolamine completely abolished the leg vascular resistance increase during a cold pressure test (1+/-2 versus 18+/-14 arbitrary units; P=0.02). The norepinephrine increase during phentolamine infusion was larger (P=0.04) in control than in spinal cord-injured individuals. These results indicate that the leg vascular resistance increase during autonomic dysreflexia in spinal cord-injured individuals is not entirely alpha-adrenergic mediated and is partly explained by nonadrenergic transmission, which may, in healthy subjects, be suppressed by supraspinal control.
自主反射异常是一种由脊髓损伤个体交感神经活动过度引起的高血压发作，被认为是由α-肾上腺素能介导的。α-肾上腺素受体拮抗剂一直是合理的首选药物；然而，钙通道阻滞剂主要用于自主反射异常的管理。然而，α-肾上腺素受体阻断可能会使交感神经非肾上腺素能传递的残留血管收缩反应不受影响。目的是评估α-肾上腺素能的贡献，此外，还评估了中枢神经系统控制对脊髓损伤个体自主反射异常引起的过度交感神经活动和对照个体冷压力试验期间腿部血管收缩的作用。在 6 名脊髓损伤个体和 7 名健康对照个体中，使用静脉闭塞体积描记法在仰卧休息期间和过度交感神经活动期间测量大腿血流，在右股动脉中输注苯肾上腺素（α-肾上腺素受体拮抗剂）和尼卡地平（钙通道阻滞剂）时不进行输注。计算腿部血管阻力。在脊髓损伤个体中，与尼卡地平（15±10 对 24±13 任意单位；P=0.12）相比，苯肾上腺素显著降低了自主反射异常期间腿部血管阻力的增加（8±5 对 24±13 任意单位；P=0.04）。在对照组中，苯肾上腺素完全消除了冷压力试验期间腿部血管阻力的增加（1±2 对 18±14 任意单位；P=0.02）。苯肾上腺素输注期间去甲肾上腺素的增加在对照组中大于（P=0.04）在脊髓损伤个体中。这些结果表明，脊髓损伤个体自主反射异常期间腿部血管阻力的增加并非完全由α-肾上腺素能介导，部分由非肾上腺素能传递解释，在健康受试者中，这种传递可能受中枢神经系统控制的抑制。
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