Sharma H S
Neuropharmacology. 1987 Jan;26(1):85-92. doi: 10.1016/0028-3908(87)90049-9.
Intracarotid (10 mg/kg), intracerebroventricular (100, 200 micrograms) or topical application (0.8 M) of captopril (a converting enzyme inhibitor) increased the permeability of the blood-brain barrier to Evans blue albumin (EBA) and [131I]sodium in anesthetized normotensive rats. The permeability of the blood-brain barrier to albumen in 6 and to [131I]sodium in 10 out of 14 regions of the brain was increased in the perfused hemisphere after infusion of captopril into the right carotid artery. These regions of the brain were associated with a 54-107% increase in regional cerebral blood flow (CBF). Pretreatment with indomethacin and aprotinin prevented both the increased regional permeability of the blood-brain barrier along with regional cerebral blood flow. Pretreatment with vinblastine prevented only the regional increase in permeability of the blood-brain barrier. The regional cerebral blood flow continued to remain high. The probable mechanism(s) underlying the increased cerebral blood flow and permeability of the blood-brain barrier after infusion of captopril is discussed.
在麻醉的正常血压大鼠中,颈动脉内注射(10毫克/千克)、脑室内注射(100、200微克)或局部应用(0.8摩尔)卡托普利(一种转化酶抑制剂)可增加血脑屏障对伊文思蓝白蛋白(EBA)和[131I]钠的通透性。向右侧颈动脉注入卡托普利后,灌注半球的14个脑区中有6个脑区的血脑屏障对白蛋白的通透性以及10个脑区对[131I]钠的通透性增加。这些脑区的局部脑血流量(CBF)增加了54 - 107%。用吲哚美辛和抑肽酶预处理可防止血脑屏障局部通透性增加以及局部脑血流量增加。用长春碱预处理仅能防止血脑屏障局部通透性增加。局部脑血流量仍持续保持较高水平。本文讨论了注入卡托普利后脑血流量增加和血脑屏障通透性增加的可能机制。