Xiong C, Hu H, Wei W, Chen X, Wu Z
Department of General Surgery, First Affiliated Hospital, Hubei Medical University, Wuhan, China.
Zhonghua Wai Ke Za Zhi. 2000 Apr;38(4):297-9, 17.
To observe the damage to liver sinusoidal endothelial cells during normothermic ischemia and reperfusion.
The afferent vessels of rat liver were clamped for 20, 40, 60 and 90 min respectively. The blood flow to the liver then was restored by removing the clamp. Ultrastructural changes in the sinusoidal endothelial cells in various periods were observed.
After 20 or 40 min ischemia, fenestrations of the endothelial cells were enlarged and became mesh-like, but reperfusion for 120 min, led to recovery. After 60 or 90 min ischemia, the sieve plates and cytoplasmic processes of the endothelial cells were destroyed and the perikaryon tended to be desquamated. Reperfusion for 120 min led to no recovery, but resulted in the aggravation of injury and irreversible damage. The liver sinusoids were filled with numerous blood cells and blebs derived from hepatocytes, resulting in circulatory disturbance.
Warm ischemia results in severe endothelial cell destruction. Endothelial cell damages may have unfavorable effects on the microcirculation of the reperfusion liver after prolonged ischemia.
观察常温下肝脏缺血再灌注过程中肝窦内皮细胞的损伤情况。
分别夹闭大鼠肝脏的输入血管20、40、60和90分钟。然后松开夹子恢复肝脏血流。观察不同时期肝窦内皮细胞的超微结构变化。
缺血20或40分钟后,内皮细胞窗孔扩大并呈网状,但再灌注120分钟后可恢复。缺血60或90分钟后,内皮细胞筛板和细胞质突起被破坏,核周趋于脱落。再灌注120分钟未能恢复,反而导致损伤加重和不可逆损害。肝窦内充满大量血细胞和来自肝细胞的小泡,导致循环障碍。
热缺血导致严重的内皮细胞破坏。长时间缺血后内皮细胞损伤可能对再灌注肝脏的微循环产生不利影响。