摘要
目的研究重型颅脑外伤后脑脊液中ET-1、NO浓度变化与脑血管痉挛的关系。方法重型脑外伤病人30例,人院时GCS小于8分。入院后24h及3、5、7d进行双侧大脑中动脉,颈内动脉颅外段脑血流速度检测及脑脊液ET-1、NO浓度测定。结果13例(43%)发生脑血管痉挛,重度2例,中度5例,轻度6例。伤后痉挛组与非痉挛组病人脑脊液中ET-1浓度均高于正常组,NO浓度均低于正常组。痉挛组病人ET-1及NO浓度变化过程同痉挛组的经颅多普勒检查表现相符,ET-1、NO浓度与非痉挛组存在明显差异,而且中重度痉挛组与轻度痉挛组之间存在明显差异。结论颅脑外伤后脑血管痉挛发生率高,是颅脑外伤后基本病理过程之一;脑血管痉挛发生的机制可能与脑脊液ET升高,NO抑制,导致血管收缩舒张平衡破坏有关。
Objective This study was designed to elucidate the potential role of ET and NO in the pathogenesis of posttraumatic cerebra vasospasm (CVS). Methods Thirty patients admitted after suffering severe head injuries, with Glasgow Coma Scale Scores ranging from 3 to 8, were evaluated with transcranial doppler (TCD). Blood flow velocities were determined in bileteral MCA and extracranial portion of ICA. Cerebrospinal fluid concentrations of endothelin and nitric oxide were measured serially for 1 week after head injury and compared with those in normal volunteers. Results Vasospasm, defined as MCA velocity greater than 120cm/s and epsilateral Lindergaard index greater than 3, was found in 13 patients. In patients with severe head injury, the levels of ET-1 in CSF increased above those of normal volunteer's, meanwhile the levels of NO were lower in patients with head injury than in normal volunteers; The levels of ET-1 and NO in patients with and without CVS were significantly different. Conclusion CVS is a frequent complication of head injury; The increase of ET-1 and decrease of NO in CSF, caused by multiple facts after head injury, may destroy the balance of vasoconstriction and vasodilation, and induce CVS.
出处
《上海第二医科大学学报》
CSCD
2000年第1期55-58,共4页
Acta Universitatis Medicinalis Secondae Shanghai