Hemocoagulase atrox reduces vascular modeling in rabbit carotid artery adventitia.
OBJECTIVE
This study aimed to compare the effects of hemocoagulase atrox and cauterization hemostasis on intimal hyperplasia and explore the effect of hemocoagulase atrox on vascular modeling in rabbit carotid artery adventitia.


METHODS
A total of 27 rabbits were randomly divided into 3 groups (0d, 14d, 28d). They were anaesthetized using an intramuscular injection of phenobarbital sodium (1 ml/kg). The left and right common carotid arteries were exposed and capillary hemorrhaged after blunt dissection of the adventitia layers of common carotid arteries. Nine rabbits in each group were again randomly divided into 3 groups, in which animals were respectively treated with hemocoagulase (2 U/ml), cauterization (power = 40 w) and saline (as control). Groups of animals were euthanized at 0, 14 and 28 days after surgery. The samples were equally divided in the middle of the adventitia removal section to obtain equal parts for histologic, immunohistochemical and molecular biologic analysis. The vascular repair after adventitial stripping was observed by HE staining, Masson staining and transmission electron microscopy. The expression of carotid MCP-1, PCNA, TGF-β1, α-SMA and VEGF were measured at different time points by RT-PCR and immunohistochemical staining.


RESULTS
HE staining and Masson staining showed that hemocoagulase atrox had a significantly stronger effect on reducing intimal hyperplasia than the cauterization after 14 and 28 days. The results of RT-PCR showed that the expression of MCP-1, TGF-β1, α-SMA and VEGF in hemocoagulase atrox-treated animals were lower than that of cauterization-treated animals.


CONCLUSIONS
Our results suggested that hemocoagulase atrox as a topical hemostatic is safety and efficiently and it can accelerate adventitia restoration and decrease intimal proliferation.
Department of Vascular Surgery, The Second Affiliated Hospital of Anhui Medical University Hefei, Anhui 230601, PR China.
Sheng-Yun
SY
Wan
Yuan-Cheng
YC
Hu
Yan-Qing
YQ
Zhan
Dan-Dan
DD
Qin
Yang
Y
Ding
D000199:Actins / Q000378:metabolism; D000287:Administration, Topical; D063194:Adventitia / Q000187:drug effects* / Q000378:metabolism / Q000601:surgery / Q000648:ultrastructure; D000818:Animals; D012103:Batroxobin / Q000008:administration & dosage / Q000494:pharmacology*; D020212:Carotid Artery Injuries / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D017536:Carotid Artery, Common / Q000187:drug effects* / Q000378:metabolism / Q000601:surgery / Q000648:ultrastructure; D002425:Cautery; D018932:Chemokine CCL2 / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D006470:Hemorrhage / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D006489:Hemostatic Techniques; D006490:Hemostatics / Q000008:administration & dosage / Q000494:pharmacology*; D006965:Hyperplasia; D008297:Male; D058426:Neointima; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D011817:Rabbits; D013997:Time Factors; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
D000199:Actins; D018932:Chemokine CCL2; D006490:Hemostatics; D018809:Proliferating Cell Nuclear Antigen; D053773:Transforming Growth Factor beta1; D042461:Vascular Endothelial Growth Factor A; D012103:Batroxobin
Adventitia; cauterization; hemocoagulase; hemostasis; vascular remodeling