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급성 척수손상 고양이에서 Nimodipine투여가 척수혈류와 척수기능 회복에 미치는 효과

Other Titles
 (The) effect of nimodipine on spinal cord blood flow and neuronal function in acute spinal cord injured cat 
Issue Date
1992
Description
의학과/박사
Abstract
[한글] 척수 손상은 수상 직후부터 신경장애를 초래하며 일생동안 마비의 상태로서 임상적인 증상의 호전을 기대하기 힘들며 이에 대한 치료가 미미한 상태이다. 이러한 신경손상에 대한 기전규명 및 치료에 대하여 많은 연구가 있었으나 확실히 밝혀진 바 없다. 척수손상 후 신경장애는 일차적인 물리적 손상과 이차적인 신경 손상에 의하여 나타나는데, 이중 이차적인 신경 손상의 기전으로서 척수울혈의 확산, 생화학적인 변화, 혈관계 변화, 염증반응에 의한 변화등 여러가지 가설이 제시되고 있으나 그중 혈관계의 변화에 의한 척수혈류 감소, 척수 허혈 상태가 가장 유력시 되고 있다. 척수 허혈시 나타나는 신경 손상의 기전으로 칼슘 이온의 세포내 유입이 신경 세포의 기능 장해와 세포사에 중요한 요인으로 밝혀짐에 따라, 칼슘길항제가 임상적으로 척수혈류의 증가 및 손상된 신경기 능 회복에 효과적일 것으로 생각되었다. 칼슘길항제중 nimodipine이 중추 신경계에 가장 선택적으로 작용을 하며, 이를 지주막하 출혈에 의한 혈관 연축이나 뇌경색에 투여하면 뇌빈혈 부위에 작용하여 혈류 증가를 유도한다고 밝혀졌다. 그러나 nimodipine 투여가 척수 손상에 미치는 영향에 대하여는 아직 명확히 밝혀진바 없다. 본 연구에서는 척수 손상 고양이에서 칼슘 통로 차단제인 nimodipine을 투여하여 척수 손상에 미치는 영향을 연구하였으며, 고양이 18마리에서 투여 약물의 종류에 따라 4군으로 나누고 척수 손상을 준후 시간 경과에 따라 각 군에서의 척수혈류 및 체성감각 유발전 위의 변화를 관찰하여 다음과 같은 결론을 얻었다. 1. 실험동물에서 급성 척수손상후 척수혈류는 급격히 감소하였으며 시간이 경과함에 따라 더욱 하강하였다. 척수혈류의 감소는 손상 인접부위에서 원위부에 비하여 더욱 현저하였다. 2. 척수 손상후 nimodipine을 투여한 군에서 평균동맥압의 감소에도 불구하고 척수혈류의 증가를 보였으며 이는 nimodipine의 혈관 확장 작용이 말초 혈관보다 척수 혈관에 더욱 영향을 미쳐 증가한 것으로 생각된다. 3. Adrenaline을 투여하여 평균동맥압을 유지하면서 nimodipine을 투여한 군에서 nimodipine을 단독으로 투여한 군에 비하여 더욱 현저한 혈류 증가가 있었으며, 이 혈류 증가의 효과가 더욱 오랫동안 지속되었다. 이는 adrenaline에 의한 심박동수 및 심박출량의 증가가 nimodipine의 말초 혈관 확장에 의한 혈압강하를 방지함으로서 생긴 현상으로 생각되어 nimodipine 투여시 평균 동맥압을 유지하는 것이 중요하다고 판단된다. 4. 체성감각 유발전위의 회복은 혈류 증가가 가장 현저한 nimodipine과 adrenaline을 투여한군에서 더욱 뚜렷이 나타나, 척수 손상 후 신경기능의 회복은 척수혈류의 증가에 의한 것으로 생각된다. 이상의 연구결과로 칼슘 통로 차단제인 nimodipine은 평균동맥압을 적정수준 유지한 상태에서 투여하면 말초 혈관보다 척수 혈관에 더 큰 영향을 미쳐 척수 손상으로 인한 허혈 상태에서 척수혈류를 증가시키며, 이로 인하여 신경기능 회복에 효과가 있는 것으로 생각된다. The effect of nimodipine on spinal card blood flow and neuronal function in acute spinal ford injured cat Yong Eun Cho Department of Medical Science The Graduate School, Yonsei University (Directed by Professor Young Soo Kim) Spinal cord injury causes immediate neuronal dysfuction and remained paralysis in life without clinical improvement. The spinal cord injury is caused by initial mechanical damage and secondary neuronal damage. The exact mechanisms of secondary neuronal damage are still unknown and their treatmet is obscure even though many studies about them. The vascular chance after injury is supported widely as a mechanism of secondary neuronal damage which causes decreased microcirculation and cord ischemia. There is considerable evidence that Ca**++ ion plays a key role in the pathogenesis of posttraumatic ischemia and Ca**++ ion influx promotes cellular dysfuction and cell death. So calcium antagonist is considered that it can improve spinal cord blood flow and restore impaired neuronal function. In this report, the effects of calcium channel blocker, nimodipine on spinal cord blood flow and spinal somatosensory evoked potential were measured and those were compared with vehicle group in 400g-cm cord injured cat. And the effects of nimodipine were compared between nimodipine and adrenaline treated group of which mean arterial blood pressure was maintained above 100 mmHg and nimodipine only treated group. Spinal cord blood flow was measured at T^^6 (injury level), T^^4 , T^^12 by the hydrogen clearance technique and spinal somatosensory evoked Potential was recorded at T^^4 , T^^12 after injury at T^^6 level. The results of this study are summarized as follows: 1. The spinal cord blood flow was decreased abruptly just after spinal cord injury and after that it decreased progressively. 2. In nimodipine treated group, there was a improvement of spinal cord blood flow inspite of decreased mean arterial blood pressure. It might be thought that the vasodilatory effect of nimodipine was more potent in spinal vasculature than in systemic peripheral vessels. 3. The increased spinal cord blood flow was more prominant and prolonged in nimodipine and adrenaline treated group than nimodipine only treated group. It was thought that increased heart beat and cardiac contractility by adrenaline counteracted systemic hypotension which resulted from vasodilatory effect of nimodipine. It suggests that maintenance of mean arterial pressure is important during nimodipine therapy in spinal cord injury. 4. The improvements of spinal somatosensory evoked potential were more evident in nimodipine and adrenaline treated group. It might be caused by spinal cord blood flow improvement. From the above result it is speculated that the calcium channel blocker, nimodipine can improve spinal blood flow and impaird neuronal function in spinal cord injury.
[영문] Spinal cord injury causes immediate neuronal dysfuction and remained paralysis in life without clinical improvement. The spinal cord injury is caused by initial mechanical damage and secondary neuronal damage. The exact mechanisms of secondary neuronal damage are still unknown and their treatmet is obscure even though many studies about them. The vascular chance after injury is supported widely as a mechanism of secondary neuronal damage which causes decreased microcirculation and cord ischemia. There is considerable evidence that Ca**++ ion plays a key role in the pathogenesis of posttraumatic ischemia and Ca**++ ion influx promotes cellular dysfuction and cell death. So calcium antagonist is considered that it can improve spinal cord blood flow and restore impaired neuronal function. In this report, the effects of calcium channel blocker, nimodipine on spinal cord blood flow and spinal somatosensory evoked potential were measured and those were compared with vehicle group in 400g-cm cord injured cat. And the effects of nimodipine were compared between nimodipine and adrenaline treated group of which mean arterial blood pressure was maintained above 100 mmHg and nimodipine only treated group. Spinal cord blood flow was measured at T^^6 (injury level), T^^4 ,T^^12 by the hydrogen clearance technique and spinal somatosensory evoked Potential was recorded at T^^4 , T^^12 after injury at T^^6 level. The results of this study are summarized as follows: 1. The spinal cord blood flow was decreased abruptly just after spinal cord injury and after that it decreased progressively. 2. In nimodipine treated group, there was a improvement of spinal cord blood flow inspite of decreased mean arterial blood pressure. It might be thought that the vasodilatory effect of nimodipine was more potent in spinal vasculature than in systemic peripheral vessels. 3. The increased spinal cord blood flow was more prominant and prolonged in nimodipine and adrenaline treated group than nimodipine only treated group. It was thought that increased heart beat and cardiac contractility by adrenaline counteracted systemic hypotension which resulted from vasodilatory effect of nimodipine. It suggests that maintenance of mean arterial pressure is important during nimodipine therapy in spinal cord injury. 4. The improvements of spinal somatosensory evoked potential were more evident in nimodipine and adrenaline treated group. It might be caused by spinal cord blood flow improvement. From the above result it is speculated that the calcium channel blocker, nimodipine can improve spinal blood flow and impaird neuronal function in spinal cord injury.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/117050
Appears in Collections:
2. 학위논문 > 1. College of Medicine (의과대학) > 박사
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