Mchedlishvili G, Kapuściński A, Nikolaishvili L
Stroke. 1976 Jul-Aug;7(4):410-6. doi: 10.1161/01.str.7.4.410.
Controlled cerebral ischemia was produced in rabbits by bilateral occlusion of the common carotid arteries and restriction of collateral blood flow by a decrease of the systemic arterial pressure to a desirable level (by hemorrhage into a pressurized reservior system). The following circulatory parameters were simultaneously monitored: systemic arterial pressure (SAP), pressure in the circle of Willis (Pcw), systemic venous pressure (SVP), and pressure in the sagittal venous sinus of brain (Pvs). The cerebral blood flow (CBF) was measured by means of the H2-clearance method, and the brain volume (BrV) changes were evaluated with a mechanical system of the sterotaxic device. It has been concluded that the pre-edematous changes in the brain tissue arise during deep ischemis but an important factor in the brain edema development is the recovery of the CBF with and increase of the intravascular pressure closely related to the brain blood volume augmentation. The latter may be pronouced because of diminution of the blood outflow from the brain when the SVP is increased. The compensation for the BrV increase (caused either by brain blood volume augmentation or by brain edema) is obtained by Pcw decrease probably due to resistance rise in the internal carotid and vertebral arteries. The brain edema may be additionally compensated by an active decrease of the systemic arterial pressure.
通过双侧颈总动脉闭塞以及通过将体循环动脉压降至理想水平（通过向加压储液器系统内放血）来限制侧支血流，在兔身上制造可控性脑缺血。同时监测以下循环参数：体循环动脉压（SAP）、 Willis 环压力（Pcw）、体循环静脉压（SVP）以及脑矢状窦压力（Pvs）。采用氢气清除法测量脑血流量（CBF），并使用立体定向装置的机械系统评估脑体积（BrV）变化。得出的结论是，脑组织的水肿前期变化出现在深度缺血期间，但脑水肿发展的一个重要因素是脑血流量的恢复以及与脑血容量增加密切相关的血管内压力升高。当 SVP 升高时，由于脑血流流出减少，后者可能会更加明显。BrV 增加（由脑血容量增加或脑水肿引起）的代偿可能是由于颈内动脉和椎动脉阻力增加导致 Pcw 降低。脑水肿可能还会通过体循环动脉压的主动降低得到额外代偿。
