摘要
本实验动态测定了肾性高血压大鼠（ＲＨＲ）不同时期下丘脑和血浆ＥＴ和ＣＧＲＰ水平的变化以及局部脑缺血后不同时期的改变，并与正常血压的ｗｉｓｔａｒ鼠对比。结果发现，形成稳定高血压的３月龄ＲＨＲ和７月龄ＲＨＲ其下丘脑和血浆中的ＥＴ含量均明显高于同龄Ｗｉｓｔａｒ鼠，而ＣＧＲＰ含量无显著差异。局部脑缺血后２４小时，无论ＲＨＲ还是Ｗｉｓｔａｒ鼠，其下丘脑和血浆ＥＴ和ＣＧＲＰ均比缺血前明显增高（Ｐ＜０．０１），以ＲＨＲ更加明显。缺血持续７天时，ＥＴ和ＣＧＲＰ在Ｗｉｓｔａｒ鼠全部恢复至缺血前水平，而在ＲＨＲ下丘脑和血浆中ＣＧＲＰ含量恢复至缺血前水平，ＥＴ含量仍明高于缺血前水平。结果提示，高水平的ＥＴ含量可能参与了ＲＨＲ高血压的形成和发展，而局部脑缺血后，ＲＨＲ中枢和外周ＥＴ大量持续释放不利于缺血区域侧支循环血管的开放，此可能是高血压性脑梗塞恢复慢，疗效差的原因之一．
In this study,ET and CGRP levels in hypothalamus and plasma of renal hypertensive rats(RHR) and it with focal cerebral ischemia were dynamic measured by radioimmunoassay.The results showed that ET contents in hypothalamus and plasma of 3 months and 7 months RHR were higher remarkably than that of Wistar rats with same ages(P<0.01).The ET levels in hypothalamus and plasma of 7 months RHR were increased significantly as compare with that of 3 months RHR.The CGRP contents in hypothalamus and plasma of both ages RHR had no changes.When focal cerebral ischemia for 24 hours in RHR and Wistar rats, both ET and CGRP levels in hypothalamus and plasma were increased remarkably than that of unischemia RHR and Wista rats.When focal cerebral ischemia for 7 days,ET and CGRP levels in hypothalamus and plasma of Wistar rats and CGRP levels in RHR hypothalamus and plasma were all recovered to the levels of that before ischemia,but ET levels in hypothalamus and plasma of RHR were still keep higher levels than that before ischemia (P<0.01 and P<0.05).The results suggested that high levels ET concents in central nervous system and peripheral plasma of RHR may be play an important role in the forming, maintenance and development of hypertension.After focal cerebral ischemia, ET persistent high level releasing would be harmful to collateral circulative blood vessels opening,which was one of reason in clinical patients with hypertensive focal cerebral infarct recovery slowly and curative effect unsatisfvingly.
出处
《脑与神经疾病杂志》
1996年第3期129-132,共4页
Journal of Brain and Nervous Diseases
关键词
高血压
脑缺血
内皮素
降钙素基因
相关肽
Endothelin
Calcitonin gene-related peptide
Hypertension
cerebral ischemia
