在我们的整个生命过程中，脑血管中会形成微小的血栓或“微栓子”。很多这种血栓会被血液流动的力量清除，而其他的则会被“纤维蛋白溶解”过程消化。现在，第三种栓塞清除机制已被发现，它被称之为“栓塞溢出”。
对活的小鼠所做的高分辨率固定组织显微镜及双光子成像研究表明，很多“微栓子”不会被血液或“纤维蛋白溶解”过程溶解，而是在一个星期内被包裹“栓子”的内皮细胞主动清除的，因为发挥这种功能的内皮细胞会被重塑而生成一个未被堵塞的血管。
这个过程在老年小鼠中所需时间较长，说明血栓清除是中风之后康复的患者的一个可能的治疗目标，也是与年龄相关的认知疾病的一个可能的治疗目标。 （生物谷Bioon.com）
生物谷推荐原文出处：
Nature doi:10.1038/nature09001
Embolus extravasation is an alternative mechanism for cerebral microvascular recanalization
Carson K. Lam,Taehwan Yoo,Bennett Hiner,Zhiqiang Liu& Jaime Grutzendler
Cerebral microvascular occlusion is a common phenomenon throughout life1, 2 that might require greater recognition as a mechanism of brain pathology. Failure to recanalize microvessels promptly may lead to the disruption of brain circuits and significant functional deficits3. Haemodynamic forces and the fibrinolytic system4 are considered to be the principal mechanisms responsible for recanalization of occluded cerebral capillaries and terminal arterioles. Here we identify a previously unrecognized cellular mechanism that may also be critical for this recanalization. By using high-resolution fixed-tissue microscopy and two-photon imaging in living mice we observed that a large fraction of microemboli infused through the internal carotid artery failed to be lysed or washed out within 48?h. Instead, emboli were found to translocate outside the vessel lumen within 2–7 days, leading to complete re-establishment of blood flow and sparing of the vessel. Recanalization occurred by a previously unknown mechanism of microvascular plasticity involving the rapid envelopment of emboli by endothelial membrane projections that subsequently form a new vessel wall. This was followed by the formation of an endothelial opening through which emboli translocated into the perivascular parenchyma. The rate of embolus extravasation was significantly decreased by pharmacological inhibition of matrix metalloproteinase 2/9 activity. In aged mice, extravasation was markedly delayed, resulting in persistent tissue hypoxia, synaptic damage and cell death. Alterations in the efficiency of the protective mechanism that we have identified may have important implications in microvascular pathology, stroke recovery and age-related cognitive decline.
