International Collaboration on Repair Discoveries (ICORD), University of British Columbia, Blusson Spinal Cord Centre, Vancouver, British Columbia, Canada.
Spine J. 2010 Dec;10(12):1108-17. doi: 10.1016/j.spinee.2010.09.018.
Individuals with high spinal cord injury (SCI) are prone to significant fluctuation in blood pressure with episodes of very high and low blood pressure during autonomic dysreflexia (AD) and orthostatic hypotension, respectively. We do not know how such blood pressure lability affects the vasculature.
We used a well-characterized animal model of AD to determine whether increasing the frequency of AD during recovery from SCI would exacerbate injury-induced dysfunction in resistance vessels.
STUDY DESIGN/SETTING: Experimental animal study. International Collaboration On Repair Discoveries (ICORD), University of British Columbia, Canada.
Complete transection of the T3 spinal cord was performed in male Wistar rats. For 14 days after injury, AD was induced via colorectal distension (CRD; 30 minutes per day) in the experimental group (SCI-CRD). One month after SCI, baseline cardiovascular parameters and severity of CRD-induced AD were assessed in SCI-CRD animals and SCI-only controls. Mesenteric arteries were harvested for in vitro myography to characterize vasoactive responses to phenylephrine (PE) and acetylcholine (ACh).
Mesenteric arteries from SCI-CRD animals exhibited larger maximal responses to PE than arteries from SCI-only controls. Hyperresponsiveness to PE was not a product of endothelial dysfunction because mesenteric arteries from both groups had similar vasodilator responses to ACh. Both SCI-only controls and SCI-CRD animals exhibited CRD-evoked AD 1 month after SCI; however, CRD-induced hypertension was less pronounced in animals that were previously exposed to CRD.
Injury-induced changes within the vasculature may contribute to the development of AD after SCI. Here, we provide evidence that AD itself has significant and long-lasting effects on vascular function. This finding has implications for the medical management of AD and provides an impetus for maintaining stable blood pressure.
患有高脊髓损伤（SCI）的个体在自主反射障碍（AD）和直立性低血压期间分别出现非常高和低血压的情况下，血压波动很大。我们不知道这种血压不稳定性如何影响血管。
我们使用 AD 的一种经过充分表征的动物模型来确定在 SCI 恢复期间增加 AD 的频率是否会加剧损伤引起的阻力血管功能障碍。
研究设计/设置：实验动物研究。加拿大英属哥伦比亚大学国际修复发现合作组织（ICORD）。
雄性 Wistar 大鼠的 T3 脊髓完全横断。在损伤后 14 天内，实验组（SCI-CRD）通过直肠扩张（CRD；每天 30 分钟）诱导 AD。在 SCI 后 1 个月，评估 SCI-CRD 动物和 SCI 对照组的基线心血管参数和 CRD 诱导 AD 的严重程度。收获肠系膜动脉进行离体血管环研究，以表征对苯肾上腺素（PE）和乙酰胆碱（ACh）的血管活性反应。
与 SCI 对照组相比，SCI-CRD 动物的肠系膜动脉对 PE 的最大反应更大。对 PE 的高反应不是内皮功能障碍的产物，因为两组的肠系膜动脉对 ACh 均具有相似的血管舒张反应。SCI 对照组和 SCI-CRD 动物在 SCI 后 1 个月均表现出 CRD 诱发的 AD；然而，先前暴露于 CRD 的动物的 CRD 诱导性高血压不那么明显。
血管内的损伤诱导变化可能导致 SCI 后 AD 的发展。在这里，我们提供的证据表明 AD 本身对血管功能具有重大且持久的影响。这一发现对 AD 的医疗管理具有重要意义，并为维持稳定的血压提供了动力。
