Effect of nicotine on coagulation and fibrinolysis in intestinal ischemia-reperfusion injury rats
10.3969/j.issn.1673-9701.2024.14.010
- VernacularTitle:烟碱对肠缺血再灌注损伤大鼠凝血功能的影响
- Author:
Haisong WANG
1
;
Linmei XU
;
Zhenyi CHEN
;
Haiying GAO
;
Dongmiao CAI
Author Information
1. 厦门大学附属第一医院麻醉科,福建厦门 361003
- Keywords:
Intestinal ischemia-reperfusion injury;
Blood coagulation;
Nicotine
- From:
China Modern Doctor
2024;62(14):46-48,64
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of nicotine on coagulation in intestinal ischemia-reperfusion injury rats.Methods 32 male Sprague-dawley rats,weighing 250-300g,were randomly divided into 4 groups(n=8):sham operation group(S),intestinal ischemia-reperfusion(IR)group,nicotine(NIC)group,α7 nicotinic acetylcholine receptor(α7nAchR)antagonist group α-bungarotoxin(α-BGT)group.Intestinal IR was induced by clamping superior mesenteric artery for 45min and 120min of reperfusion.In group NIC nicotine 400μg/kg was injected intraperitoneally at 30min before superior mesenteric artery occlusion.In group α-BGT 1μg/kg was injected intraperitoneally at 15min before superior mesenteric artery occlusion.Plasma tumor necrosis factor-α(TNF-α),tissue factor(TF),antithrombin(AT),tissue plasminogen activator(tPA),fiber plasminogen activator inhibitor-1(PAI-1),D-dimer levels and platelet count(PLT)were measured after 120min reperfusion.Chiu's count was used to assess the changes in intestinal mucosal pathlolgical morphology.Results Compared with group S and group NIC,the plasma TNF-α,TF,tPA,PAI-1 and D-dimer levels were significantly increased,and plasma AT level and platelet count were significantly decreased,in group IR and group α-BGT(P<0.05),Chiu's scores were significantly increased(P<0.05).Conclusion Nicotine can inhibit the excessive activation of coagulation function in intestinal ischemia-reperfusion injury rats.Its mechanism may be related to activation of cholinergic antiinflammatory pathway,reducing the release of pro-inflammatory cytokines thereby reducing endothelial cell injury.