Hossman K A, Blöink M
Stroke. 1981 Mar-Apr;12(2):211-7. doi: 10.1161/01.str.12.2.211.
In 27 pentobarbital-anesthetized cats cerebral blood flow and regulation of cerebral blood flow was measured one to 3 weeks following stereotactical xenotransplantation of a rat glioma clone into the internal capsula. Tumor growth was accompanied by severe vasogenic peritumoral edema in the white matter of the tumor-bearing hemisphere. White matter water content in the vicinity of the tumor increased from 69.1 +/- 0.9 to 0.5 +/- 0.7 ml/100 g wet weight (means +/- SE) which corresponds to an increase in tissue volume of about 60%. Intracranial pressure after 3 weeks was 12 +/- 2.6 mm Hg. Blood flow in the peritumoral white matter decreased from 32.2 +/- 5.6 to 18.6 +/- 1.9 ml/100/g/min but it did not change in the peritumoral grey matter or the opposite hemisphere. The decrease in blood flow was due to the volume expansion of the swollen edematous tissue and not to a compression of the microcirculation because neither flow nor vascular resistance changed when referred to dry rather than to wet weight of the edematous tissue. Flow regulation in the peritumoral edematous white matter was disturbed. CO2 reactivity of blood flow was 5.4% mm Hg change in aPCO2 (non-edematous contralateral white matter 6.4%/mm Hg), and the autoregulatory capacity between 40 and 170 mm Hg was 0.7%/mm Hg (non-edematous white matter 1.0% mm Hg). It is concluded that in the absence of significant intracranial hypertension, even severe degrees of vasogenic peritumoral edema do not interfere with blood flow and flow regulation. This is in contrast to the cytotoxic type of edema, and indicates that microcirculatory compression by edema, when present, is the consequence of pericapillary glial hydrops and not of an accumulation of extravasated edema fluid.
在27只戊巴比妥麻醉的猫中,于大鼠胶质瘤克隆立体定向异种移植至内囊后1至3周,测量脑血流量及脑血流量调节情况。肿瘤生长伴随着荷瘤半球白质中严重的血管源性瘤周水肿。肿瘤附近白质的含水量从69.1±0.9增加至80.5±0.7毫升/100克湿重(均值±标准误),这相当于组织体积增加约60%。3周后的颅内压为12±2.6毫米汞柱。瘤周白质的血流量从32.2±5.6降至18.6±1.9毫升/100克/分钟,但瘤周灰质或对侧半球的血流量未发生变化。血流量的减少是由于肿胀水肿组织的体积增大,而非微循环受压,因为以水肿组织的干重而非湿重计算时,血流量和血管阻力均未改变。瘤周水肿白质中的血流调节受到干扰。血流量的二氧化碳反应性为动脉血二氧化碳分压每变化1毫米汞柱时变化5.4%(对侧非水肿白质为6.4%/毫米汞柱),40至170毫米汞柱之间的自动调节能力为0.7%/毫米汞柱(非水肿白质为1.0%/毫米汞柱)。得出的结论是,在无明显颅内高压的情况下,即使是严重程度血管源性瘤周水肿也不会干扰血流及血流调节。这与细胞毒性水肿类型不同,表明若存在水肿对微循环的压迫,是毛细血管周围胶质积水的结果,而非外渗水肿液积聚的结果。