[Change of vWF, PAl-1 and t-PA in rats with hyperlipemia and its significance].
OBJECTIVE
To establish the hyperlipoidemia model and observe its effect on the expression of plasma vWF, PAl-1 and t-PA after endothelial cell injury caused by the model at different time in rats.


METHODS
Sixty male Sprague-Dawley rats weighing (200+/-20)g were randomly divided into 6 groups (n=10 in each): high flat composition for 7 weeks (Group A7), 8 weeks (Group A8)and 9 weeks(Group A9), common bait vessel feeding for 7 weeks(Group C7), 8 weeks(Group C8) and 9 weeks (Group C9). When it reached the setting time, the rats were put to death and the serum was separated to detect the blood-fat immediately. Meanwhile, the pathological sections of the rat aorta were made to observe the endothelial injury. The blood plasma was separated and the content of the blood plasma PAl-1, t-PA and vWF was detected by ELISA assay.


RESULTS
(1)TG, TC and LDL of the rats intragastrically administrated high flat composition were higher than those of the control group,and HDL increased with time at first, but lowered when longer than 9 weeks. (2) There were no lesions in the aortic endothelium in all rats of Group C through optical microscope,while different lesions in the aortic endothelium in all rats of Group A were observed. (3)In the 3 groups A, the plasma vWF and PAI-1 were gradually increasing with time while t-PA gradually decreased. (4) There was no significant difference of vWF between Group A7 and Group A8. PAI-I increased gradually with the aggravation of endotheliocytes in Group A; and t-PA decreased gradually with the aggravation of endothelium in Group A.


CONCLUSIONS
(1) As intragastric administration prolongs, the plasma lipid of rats keeps increasing with the aggravation of the endodermis injury. (2) PAI-1, t-PA and vWF are the molecular markers of vascular endothelial cell injury in rats. (3) PAI-l and t-PA are more sensitive than vWF in reflecting the endothelial cell injury in hyperlipemia early metaphase.
Jiang
Hai-he
HH
Department of Cardiopulmonary Surgery, Xiangya Hospital, Central South University, Changshaa, China.
Liu
Yi
Y
Lin
Guo-qiang
GQ
Li
Ying-qiu
YQ
D000818:Animals; D001011:Aorta / Q000473:pathology; D042783:Endothelial Cells / Q000473:pathology*; D006949:Hyperlipidemias / Q000097:blood* / Q000473:pathology; D008297:Male; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D010959:Tissue Plasminogen Activator / Q000097:blood*; D014841:von Willebrand Factor / Q000378:metabolism*
D017395:Plasminogen Activator Inhibitor 1; D014841:von Willebrand Factor; D010959:Tissue Plasminogen Activator