Brain microvessels: factors altering their patency after the occlusion of a middle cerebral artery (Wistar rat).
Brain microvessels: factors altering their patency after the occlusion of a middle cerebral artery (Wistar rat).
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发表时间：
1994-09
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通讯作者：
Julio H. Garcia;Kaiyin Liu;Y. Yoshida;Song Chen;J. Lian
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作者：
Julio H. Garcia;Kaiyin Liu;Y. Yoshida;Song Chen;J. Lian
大动脉闭塞数小时后，大鼠脑中发生缺血性损伤至全坏死的进展，部分原因可能是微血管循环恶化。本研究的目的是定量选择的结构变化，涉及星形胶质细胞和内皮细胞的局灶性脑缺血区域内的大脑中动脉闭塞。这些结构变化的幅度与通过位于闭塞动脉区域内的微血管（直径≤ 15 μ）的循环大分子的开放性变化相关。185只成年雄性Wistar大鼠在将尼龙单丝穿过颈外动脉后闭塞右侧大脑中动脉。在动脉闭塞后30分钟至7天的时间间隔内，通过心血管灌注或断头和浸泡固定来终止实验。从每个实验亚组中随机选择的动物在死亡前约20分钟静脉注射辣根过氧化物酶（分子量44 kd）。在由充满辣根过氧化物酶的血管组成的面积分数的逐渐下降之前，在30至60分钟，内皮细胞（细胞核和细胞质）占据的表面积（在微血管的横截面上）增加。其次是星形胶质细胞核的平均直径增加了23.7%，微血管的管腔表面减少了约35%。这些观察结果表明，大的脑动脉闭塞导致内皮细胞和星形胶质细胞迅速肿胀;这两种早期生物反应可能会干扰红细胞循环和氧气输送，这（动脉闭塞后）完全依赖于侧支动脉连接提供的循环。通过其干扰微血管通畅性和氧气输送，细胞肿胀可能会影响神经元坏死的速度。在该脑梗塞模型中，坏死神经元的数量在大脑中动脉闭塞后约72小时达到峰值。（摘要截短至400字）
The progression from ischemic injury to pannecrosis that occurs in the rat brain several hours after occluding a large artery may be partly attributable to a worsening of the circulation through the microvessels. The objective of this study was to quantitate selected structural changes involving astrocytes and endothelial cells within an area of focal brain ischemia created by the occlusion of a middle cerebral artery. The magnitude of these structural changes was correlated with alterations in the patency to a circulating macromolecule through the microvessels (< or = 15 mu in diameter) located within the territory of the occluded artery. One hundred eighty-five adult male Wistar rats had the right middle cerebral artery occluded after threading a nylon monofilament through the external carotid artery. Experiments were terminated by either cardiovascular perfusion or decapitation and immersion fixation at intervals ranging between 30 minutes and 7 days after the arterial occlusion. Randomly selected animals from each experimental subgroup were injected intravenously with horseradish peroxidase (molecular weight 44 kd) approximately 20 minutes before death. The progressive decline in the area fraction comprised by the vessels filled with horseradish peroxidase was preceded at 30 to 60 minutes by an increase in the surface area occupied (on a cross-section of a microvessel) by endothelial cells (both nucleus and cytoplasm). This was followed by an increase of 23.7% in the mean diameter of astrocytes nuclei and a decrease of approximately 35% in lumenal surface of the microvessels. These observations suggest that the occlusion of a large cerebral artery causes prompt swelling of endothelial cells and astrocytes; both of these early biological responses may interfere with erythrocyte circulation and oxygen delivery, which (after the arterial occlusion) are entirely dependent on the circulation provided by the collateral arterial connections. Through its interference with microvascular patency and oxygen delivery, cell swelling may influence the rate at which neurons become necrotic. In this model of brain infarct the number of necrotic neurons peaks approximately 72 hours after middle cerebral artery occlusion.(ABSTRACT TRUNCATED AT 400 WORDS)