Shutka B V, Mel'man E P
Biull Eksp Biol Med. 1986 Jan;101(1):94-8.
Resetting of arterial and arteriolar wall structural components have been studied in the white rat kidney glomeruli after experimental ischemia (30 min, 1-3 h) without blood flow recovery and with the following recirculation for 3-30 days. The experiments have established that acute renal ischemia caused by the vascular leg ligation for 30-60 min without the following blood flow recovery results in slight microstructural alterations of arterial and arteriolar wall elements. With increased ischemia duration (2-3 h) pathological changes become more prominent and separation of vascular endothelial cells and defibering of the internal elastic membrane take place. In transitory (30-60 min) ischemia of the remaining kidney (one kidney is removed) three days later desquamation of endothelial cells occurs in some arteries. Thinning of arterial walls and overstrain of internal elastic membrane are observed. However, later on (in 30 days) short-term ischemia (30 min) is followed by complete recovery of structural components of arterial and arteriolar walls. In more durable ischemia (2-3 h) of the remaining kidney the recovered blood flow causes marked destructive life-threatening changes in vascular walls.
在实验性缺血(30分钟、1 - 3小时)后,未恢复血流且随后再灌注3 - 30天的情况下,对白大鼠肾肾小球动脉和小动脉壁结构成分的重置进行了研究。实验证实,通过结扎血管腿部30 - 60分钟导致急性肾缺血且随后不恢复血流,会引起动脉和小动脉壁成分轻微的微观结构改变。随着缺血持续时间增加(2 - 3小时),病理变化变得更加显著,血管内皮细胞分离且内弹性膜纤维松解。在剩余肾脏(切除一个肾脏)短暂缺血(30 - 60分钟)三天后,一些动脉出现内皮细胞脱落。观察到动脉壁变薄和内弹性膜过度伸展。然而,随后(30天后),短期缺血(30分钟)后动脉和小动脉壁结构成分完全恢复。在剩余肾脏更持久的缺血(2 - 3小时)中,恢复的血流会导致血管壁出现明显的、危及生命的破坏性变化。