Barry D I, Jarden J O, Paulson O B, Graham D I, Strandgaard S
J Hypertens. 1984 Dec;2(6):589-97. doi: 10.1097/00004872-198412000-00003.
The cerebrovascular effects of converting enzyme inhibition were examined in normotensive and hypertensive rats. Cerebral blood flow was measured using the intracarotid 133xenon injection method in halothane/nitrous oxide anaesthetized animals. The main finding was that following intravenous administration of captopril (10 mg/kg), cerebral blood flow autoregulation was markedly altered. Although cerebral blood flow was unchanged from baseline levels, both the lower and upper limits of autoregulation were reset to lower mean arterial pressure and the autoregulatory plateau shortened. The lower limit was shifted 20-30 mmHg, the upper limit 50-60 mmHg, and the plateau shortened by 20-40 mmHg. The effect was interpreted as being a consequence of compensatory autoregulatory constriction of small resistance vessels in the brain following captopril-induced dilatation of large resistance vessels. It was inferred that locally produced angiotensin II might play a role in the resistance of large cerebral arteries.
在正常血压和高血压大鼠中研究了转换酶抑制的脑血管效应。在氟烷/一氧化二氮麻醉的动物中,使用颈内注射133氙的方法测量脑血流量。主要发现是,静脉注射卡托普利(10mg/kg)后,脑血流量自动调节明显改变。尽管脑血流量与基线水平无变化,但自动调节的下限和上限均重新设定为较低的平均动脉压,且自动调节平台缩短。下限下移20 - 30 mmHg,上限下移50 - 60 mmHg,平台缩短20 - 40 mmHg。该效应被解释为卡托普利诱导大阻力血管扩张后,脑内小阻力血管代偿性自动调节性收缩的结果。据推测,局部产生的血管紧张素II可能在大脑大动脉的阻力中起作用。