Paulson O B, Vorstrup S, Andersen A R, Smith J, Godtfredsen J
Department of Neurology, Rigshospitalet, Copenhagen, Denmark.
J Hypertens Suppl. 1985 Dec;3(3):S487-8.
The cerebrovascular effect of converting enzyme inhibition was investigated in normal volunteers, in hypertensive patients and in patients with severe chronic heart failure. Cerebral blood flow (CBF) was measured by single photon emission tomography of the uptake and wash-out of inhaled xenon-133. In some of the patients, CBF was also monitored by repeated determinations of the cerebral arterio-venous oxygen difference. In the normal volunteers and the hypertensive patients captopril (50 mg) caused a downward shift of the lower limit of CBF autoregulation of 10-15 mmHg. In some of the patients with chronic heart failure, captopril (6.25 mg) induced a marked decrease of the arterial blood pressure. Regional and average CBF, however, remained constant. These findings indicate that captopril treatment may protect the brain against ischaemia during sudden decreases of the blood pressure by a shift of the lower limit of CBF autoregulation.
在正常志愿者、高血压患者和重度慢性心力衰竭患者中研究了转换酶抑制的脑血管效应。通过吸入氙 - 133的摄取和洗脱的单光子发射断层扫描测量脑血流量(CBF)。在一些患者中,还通过重复测定脑动静脉氧差来监测CBF。在正常志愿者和高血压患者中,卡托普利(50毫克)使CBF自动调节下限下移10 - 15毫米汞柱。在一些慢性心力衰竭患者中,卡托普利(6.25毫克)导致动脉血压明显下降。然而,局部和平均CBF保持不变。这些发现表明,卡托普利治疗可能通过CBF自动调节下限的下移,在血压突然下降期间保护大脑免受缺血影响。