已知缓激肽通过影响各种组织的反应,如扩张外周血管,增加血管的通透性来影响炎症反应的进程。缓激肽参与凝血,花生四烯酸的产生以及补体、儿茶酚胺和肾素-血管紧张素-醛固酮系统。脑缺血时,活化的缓激肽可改变脑血管的通透性,因而能影响缺血性脑水肿的进程。但是,缓激肽在缺血性脑水肿病因上的作用还不清楚。最近有文献报道,在血管原性离水肿中激肽酶-激肽系统被激活。 参与脑水肿进程的激肽酶-激肽系统在脑缺血时也同样被活化。为了研究这个问题,作者用自发性高血压大鼠经受3h脑缺血后再灌注,以确定缺血性脑水肿进程与内原性缓激肽的关系。为进一步评价内原性产生的缓激肽对缺血性脑水肿进程的影响, Bradykinin is known to affect the course of inflammatory responses by affecting the response of various tissues, such as expanding peripheral blood vessels and increasing the permeability of blood vessels. Bradykinin is involved in coagulation, arachidonic acid production, and complement, catecholamine, and renin-angiotensin-aldosterone systems. In cerebral ischemia, activated bradykinin can change the permeability of cerebral blood vessels, which can affect the process of ischemic brain edema. However, the role of bradykinin in the etiology of ischemic brain edema is unclear. Recently, it has been reported in the literature that kallikrein-kinin system is activated during hemangiogenesis. The kinin-kinin system involved in brain edema processes is also activated during cerebral ischemia. To study this problem, the authors underwent spontaneous hypertensive rats 3h after cerebral ischemia reperfusion to determine the relationship between ischemic brain edema process and endogenous bradykinin. In order to further evaluate the effect of endogenous bradykinin on the process of ischemic brain edema,