Yamaguchi S, Kobayashi S, Yamashita K, Kitani M
Third Division of Internal Medicine, Shimane Medical University, Izumo, Japan.
J Cereb Blood Flow Metab. 1989 Oct;9(5):597-602. doi: 10.1038/jcbfm.1989.85.
The effect of pial arterial pressure (PAP) on brain edema was examined in cats with middle cerebral artery (MCA) occlusion. Measurements of PAP and regional CBF (rCBF) were collected in the central core and the peripheral margin of the MCA territory over 180 min post MCA occlusion. Brain water content in each region was determined at the end of the experiment. MCA occlusion resulted in decreased PAP and rCBF in both the core (PAP = 13 mm Hg, rCBF = 9 ml/100 g/min) and the peripheral region (PAP = 15 mm Hg, rCBF = 18 ml/100 g/min). Brain edema developed in both the core and the peripheral region. Brain water content was correlated inversely with PAP in the core region and positively in the peripheral region. The results indicate that decreased blood flow contributes to cytotoxic edema in the core, and a hydrostatic pressure gradient preferentially enhances edema formation in the peripheral region. Maintenance of high perfusion pressure early after ischemia onset may suppress brain edema in the core region.
在大脑中动脉(MCA)闭塞的猫中,研究了软脑膜动脉压(PAP)对脑水肿的影响。在MCA闭塞后180分钟内,测量MCA区域中心核心区和周边边缘区的PAP和局部脑血流量(rCBF)。实验结束时测定每个区域的脑含水量。MCA闭塞导致核心区(PAP = 13 mmHg,rCBF = 9 ml/100 g/min)和周边区(PAP = 15 mmHg,rCBF = 18 ml/100 g/min)的PAP和rCBF均降低。核心区和周边区均出现脑水肿。核心区脑含水量与PAP呈负相关,周边区呈正相关。结果表明,血流量减少导致核心区细胞毒性水肿,静水压梯度优先增强周边区水肿形成。缺血发作后早期维持高灌注压可能抑制核心区脑水肿。