摘要
应用家兔失血性休克模型观察肾小球的超微结构改变并探讨其在发病学的上意义。结果发现①内皮细胞肿胀,胞浆向管腔内伸出众多树枝状突起,内皮窗孔少而且口径缩小。②脏层上皮细胞增生肿大,胞体及其主要大突起膨大伸长形成厚板状包壳包绕毛细血管袢,足突间隙变窄及融合。③系膜旁区增生扩大。④基底膜不规则增厚,部分地区与内皮和上皮剥离。⑤毛细血管腔内充塞内皮碎片,纤维素条块,髓鞘样物质及变形红细胞。这些改变导致肾小球阻塞,血流量减少,滤过率下降,从而构成了休克时肾功能不全的超微结构基础。
The model of hemorrhagic shock of rabbits was established to observe ultrastructural changes of glomeruli. The results showed: ① Endothelial cells were swollen with the protruding of cytoplasm into the lumens of capillaries in finger—like or nodular patternThe number of endothelial fenestration was decreased with reduced calibre. ② The podocytes proliferated. The cytoplasm and major processes of podocytes were expanded to form thick plate—like shells encapsulating capillary loops. Foot process slits were narrowed and coalesced in some areas. ③ The mesangium was extended. ④ Irregulat thickening of the basement membrane occured with focal detachment of endothelium and epithelium ⑤ The lumens of capillaries contained a large amount of cellular dehrisfibrin masses, myelin figures and deformed RBC. These alterations led to glomerular obstruction,reduction of blood flow and diminished filtration rate,and therefore constituted the ultrastructural basis of ARF in hemorrhagic shock.
出处
《临床与实验病理学杂志》
CAS
CSCD
北大核心
1992年第A08期48-50,共3页
Chinese Journal of Clinical and Experimental Pathology
关键词
失血性休克
肾功能衰竭
超微结构
hemorrhagic shock
acut renal failure
ultrastruture
rabbits
