在我們的整個(gè)生命過程中,，腦血管中會(huì)形成微小的血栓或“微栓子”。很多這種血栓會(huì)被血液流動(dòng)的力量清除,，而其他的則會(huì)被“纖維蛋白溶解”過程消化。現(xiàn)在，第三種栓塞清除機(jī)制已被發(fā)現(xiàn),，它被稱之為“栓塞溢出”。
對(duì)活的小鼠所做的高分辨率固定組織顯微鏡及雙光子成像研究表明,，很多“微栓子”不會(huì)被血液或“纖維蛋白溶解”過程溶解,，而是在一個(gè)星期內(nèi)被包裹“栓子”的內(nèi)皮細(xì)胞主動(dòng)清除的，因?yàn)榘l(fā)揮這種功能的內(nèi)皮細(xì)胞會(huì)被重塑而生成一個(gè)未被堵塞的血管,。
這個(gè)過程在老年小鼠中所需時(shí)間較長(zhǎng),，說明血栓清除是中風(fēng)之后康復(fù)的患者的一個(gè)可能的治療目標(biāo)，也是與年齡相關(guān)的認(rèn)知疾病的一個(gè)可能的治療目標(biāo),。 （生物谷Bioon.com）
生物谷推薦原文出處：
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.
