Nakase H, Kempski O S, Heimann A, Takeshima T, Tintera J
Institute for Neurosurgical Pathophysiology, Johannes Gutenberg-University of Mainz, Germany.
J Neurosurg. 1997 Aug;87(2):307-14. doi: 10.3171/jns.1997.87.2.0307.
Research on cerebral venous circulation disturbances (CVCDs) has been limited partly by the paucity of animal models that produce consistent venous infarction. Occlusion of two adjacent cortical veins in rats by means of a photochemical thrombotic technique provides a minimally invasive, clinically relevant, and reproducible model suited to study the pathophysiology of CVCDs. In this study, the effects of venous occlusion on regional cortical blood flow and the brain damage that ensues were evaluated. Cortical vein occlusion was induced by photoactivation of rose bengal via 100-microm fiberoptic illumination. The cerebral venous flow pattern was examined using fluorescence angiography until 90 minutes after venous occlusion, and regional cerebral blood flow (rCBF) was determined at 48 locations by using laser Doppler scanning. Histological damage was assessed 48 hours after vein occlusion. Occlusion of two cortical veins (Group T; seven animals) was compared with single-vein occlusion and its ensuing brain damage (Group S; five animals) and with sham-operated control (five animals). An rCBF reduction occurred 30 minutes after occlusion in Group T and was more extensive than the decrease in Group S after 60 minutes. Observation frequency histograms based on local CBF data obtained in Group T demonstrated that local CBF at some sites decreased to a level below the ischemic threshold within 90 minutes. Six of the seven rats in Group T had a growing venous thrombus with extravasation of fluorescein. The resulting infarction was significantly larger in Group T (9.8 +/- 4.5% of the hemispheric area) than in Group S (only 3 +/- 1.5% of the hemispheric area). In conclusion, microcirculation perturbations occur early after venous occlusion and result in the formation of a venous thrombus accompanied by local ischemia and severe venous infarction. The extent of vein occlusion determines the resulting brain damage. Based on the results of this study, the authors conclude that CVCDs may be attenuated by prevention of venous thrombus progression together with the use of protective measures against the consequences of ischemia.
脑静脉循环障碍（CVCDs）的研究部分受到能产生一致静脉梗死的动物模型匮乏的限制。通过光化学血栓形成技术闭塞大鼠两条相邻的皮质静脉，可提供一种微创、临床相关且可重复的模型，适合用于研究CVCDs的病理生理学。在本研究中，评估了静脉闭塞对局部皮质血流及随之发生的脑损伤的影响。通过100微米光纤照明光激活孟加拉玫瑰红诱导皮质静脉闭塞。在静脉闭塞后90分钟内使用荧光血管造影检查脑静脉血流模式，并使用激光多普勒扫描在48个位置测定局部脑血流（rCBF）。在静脉闭塞48小时后评估组织学损伤。将两条皮质静脉闭塞组（T组；7只动物）与单静脉闭塞及其随后的脑损伤组（S组；5只动物）以及假手术对照组（5只动物）进行比较。T组在闭塞后30分钟出现rCBF降低，且比60分钟后S组的降低更广泛。基于T组获得的局部CBF数据的观察频率直方图显示，T组某些部位的局部CBF在90分钟内降至缺血阈值以下。T组7只大鼠中有6只出现不断增大的静脉血栓伴荧光素外渗。T组产生的梗死灶（占半球面积的9.8±4.5%）明显大于S组（仅占半球面积的3±1.5%）。总之，静脉闭塞后早期会出现微循环紊乱，并导致伴有局部缺血和严重静脉梗死的静脉血栓形成。静脉闭塞的程度决定了由此产生的脑损伤。基于本研究结果，作者得出结论，通过预防静脉血栓进展以及采取针对缺血后果的保护措施，可能会减轻CVCDs。
