垂体腺苷酸环化酶激活肽减轻大鼠缺血性脑水肿作用的实验研究

EXPERIMENTAL STUDY OF PITUITARY ADENYLATE CYCLASE ACTIVATING POLYPEPTIDE ON RELIEVING BRAIN EDEMA INDUCED BY ISCHEMIA IN RATS

目的 :研究垂体腺苷酸环化酶激活肽 (PACAP)在缺血性脑水肿中的作用及其可能的受体机制。方法 :采用大鼠四动脉结扎脑缺血模型 ,分别运用干湿重法和酶学法测定脑组织含水量及Na+ 、K+ 含量。结果 :大鼠四动脉结扎脑缺血 30min ,再灌流 1h ,脑组织含水量明显增加 ,Na+ 含量增高 ,而K+ 含量降低。缺血前经测脑室分别给予 1× 10 -9mol、1× 1110 mol及 1× 11-11mol的PACAP均能抑制脑组织含水量、Na+ 含量的增加和K+ 含量的降低。特异性PACAPⅠ型受体拮抗剂PACAP6 38能完全阻断PACAP的上述作用 ,而单纯给予PACAP6 38对脑缺血后脑组织含水量、Na+ 、K+ 含量无显著影响。结论 :外源性PACAP对缺血性脑水肿具有保护作用 ,该作用是由I型受体介导的。

Aim:In order to study the effects of pituitary adenylate cyclase activating polypeptide(PACAP) on brain edema induced by ischemia in rats and its underlying receptor mechanism.Methods:Brain ischemia model in rats was established by ligaturing four-vessels.The percentage ratio of wet over dry tissue weight、sodium and potassium contents of dry brain tissue were measured by weighing and enzymatic analysis methods.Results:The brain water contents significantly increased after rats exposed to 1 h of reperfusion following 30-minute ischemia.Furthermore,sodium contents in brain tissue increased and potassium contents decreased following perfusion. Changes of brain water contents, sodium and potassium contents were relieved by lateralventricular injection of PACAP in the concentration of 1×10 -9 ,1×10 -10 or 1×10 -11 mol respectively before ischemia.The effect of PACAP could be blocked by MCAP6-38(specific type Ⅰ PACAP receptor antagonist) lateral ventricular injection prior to PACAP administration.Conclusion: Exogenous PACAP may act as a protective effect in brain edema induced by ischemia in rats,which is mediated by type Ⅰ receptor.