摘要
本文探讨了精氨酸加压素(AVP)对急性缺血性脑水肿的作用及其作用机理。结果表明,侧脑室注射AVP后,缺血性皮层水肿显著加重,且这一作用不能被钙通道拮抗剂所阻断。侧脑室注射AVP抗血清、V_2及V_1/V_2型AVP受体拮抗剂均显著减轻缺血性皮层水肿。此外,侧脑室注射AVP后,缺血皮屋Na^+-K^+ATP酶活力显著降低;皮层等脑区cAMP含量显著升高,下丘脑和纹状体cGMP含量亦显著升高。提示AVP可能是通过cAMP、cGMP介导的AVP受体的作用,产生抑制脑细胞膜Na^+-K^+ATP酶活力的效应,从而促进缺血性脑水肿的形成。
The purpose of this experiments is to study the role of arginine vasopressin (AVP)iu acute ischemic brain edema and its mechanism. The results showde that intracerebroventricular injection ( ICV ) of AVP exacerbated the ischemic corticalc edema,and the calcium entry Mocker couldn' t block this role of AVP in ischemi brain edema. ICV of AVP antiserum,m V2 and V1/V2 receptor antagonist respectively decreased significantly the ischemic cortical edema. In addition, the Na + -K+ATPase activity of ischemic cortex was significantly decreased, and the contents of cAMP in cortex, hy pothalamus, staiatumand pons-medulla were markedly increased, and the contents of cGMP in hypothalamus and staiatum alsoincreased after ICV of AVP. These suggested that AVP was involved in the pa-thophysiologic process of acute ischemic brain edema, and its mechanism mightbe the effect of AVP on AVP receptor mediated by cAMP, cGMP, and that in turn inhibited the Na+-K+ ATPase activity of brain cell membrane,then exaggerated the formation of ischemic brain edema
出处
《基础医学与临床》
CSCD
1992年第3期43-47,共5页
Basic and Clinical Medicine
关键词
精氨酸加压素
缺血性
脑水肿
arginine vasopressin (AVP)ischemic brain edema second messengervasopressiu receptors Na+-K+ATPase
