Study on Pathological Process of Cerebral Venous Circulation Disturbance

脑静脉循环障碍(CVCD)的研究在一定程度上受到缺乏产生持续性静脉梗塞的动物模型的限制。我们已经报道，光化学血栓技术闭塞大鼠皮质静脉是一种侵袭性较小、临床相关和可重复性较好的模型。实验1：通过荧光血管造影术评价脑静脉血流模式的变化，用现代激光多普勒“扫描”技术评价局部脑血流量(RCBF)和脑血容量(CBV)，用光化学血栓形成技术评价大鼠皮质静脉阻塞模型的脑损伤。荧光血管造影结果可将动物分为3组：(1)A组，闭塞后静脉血流模式改变(n=12)；(2)B组，血流中断和/或静脉血栓形成(n=5)；(3)C组：S…更多的火腿手术动物(n=5)。B组以荧光素外渗、局部脑血流量显著降低、脑血流量短时升高和局部脑损伤为典型表现。脑皮质血流量图显示B组为短暂高灌注区，周围为低灌注区，周围充血。实验2：比较双侧皮质静脉闭塞组(T；n=7)与单静脉闭塞合并脑损伤组(S，n=5)的结果。缺血30min后，T组局部脑血流量下降早于S组，60min后下降幅度大于T组。T组数据直方图显示局部脑血流量在90min内降至缺血阈值以下。T组7只大鼠中有6只出现血栓生长，伴有荧光渗出和脑损伤，且梗塞面积大于S组。结论静脉阻断后早期出现微循环扰动，导致静脉血栓形成，伴有局部严重缺血和严重静脉梗塞。静脉闭塞的程度直接反映了脑损伤的程度。根据这项研究的结果，CVCD的治疗应包括预防持续静脉血栓和缺血的形成。较少

Research on cerebral venous circulation disturbances (CVCD) has been limited partly by the lack of animal models that produce consistent venous infarction. We have reported that raty cortical vein occlusion by a photochemical thrombotic technique is a less invasite, clinically relevant and reproducible model. We here investigated microcirculation after venous occlusion and subsequent brain damage in this model.Experiment-1 : We evaluated changes of the cerebral venous flow pattern by fluorescence angiography, regional cerebral blood flow (rCBF) and cerebral blood volume (CBV) assessed by a modem laser Doppler "scanning" technique, and brain damage histologically in a rat cortical vein occlusion model using a photochemical thrombotic technique. Fluorescence angiographic findings could classify animals into 3 groups : (1)Group A,with a changed venous flow pattern after occlusion (n=12) ; (2)Group B,With an interruption of blood flow and/or a growing venous thrombus (n=5) ; (3)Group C : s … More ham-operated animals (n=5). Extravasation of fluorescein, a massive decrease of rCBF,a short-lasting increase of CBVF and regional brain damage were typical for group B.Cortical CBF mapping revealed a transient hyperperfusion zone with hyperemia surrounding a hypoperfused ischemic core in group B.Experiment-2 : We compared the results of two cortical veins occlusion group (T ; n=7) with those of the single vein occlusion with brain damage group (S ; n=5). rCBF reduction observed in group T,which occurred from 30 min post occlusion, was earlier and greater than decrese in group S from 60 min. Histogram obtained from data of group T demonstrated that local CBF of some locations decreased to a level below the ischemic threshold within 90 min. Six among 7 rats in group T had growing venous thrombus with extravasation of fluorescence and brain damage, and infarction size was bigger in group T than in group S.In conclusion, microciruclation perturbation appears very early following venous occlusion to result in the formation of venous thrombus accompanied by local critical ischemia and severe venous infarction. The extent of vein occlusion reflects the brain damage directly. Based on the results of this study, therapy for CVCD should include the prevention of formation of ongoing venous thrombus and ischemia. Less