Effects of hydrogen sulfide on coagulation dysfunction in rats with intestinal ischemia-reperfusion injury
LU Genlin1, WU Aibing2, WANG Hongbin3.
1.The First Department of General Surgery, Yiwu Central Hospital, Jinhua, 322000; 2.Oncology Center, the Affiliated Hospital of Guangdong Medical College, Zhanjiang, 523808; 3.Department of Hepatopancreatobiliary Surgery, the Affiliated Hospital of Qinghai University, Xining, 810001
LU Genlin,WU Aibing,WANG Hongbin.. Effects of hydrogen sulfide on coagulation dysfunction in rats with intestinal ischemia-reperfusion injury[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2016, 46(5): 344-347.
Abstract：Objective: To study the effects of hydrogen sulfide on coagulation dysfunction in rats with intestinal ischemia-reperfusion injury and its mechanism. Methods: Twenty-four male Wistar rats were randomly divided into three groups (8 in each group): sham operation group (group A), ischemia-reperfusion group (group B), ischemia-reperfusion and sodium hydrosulfide group (group C). The animal model of intestinal ischemia-reperfusion was established. Rats in Group C were received sodium hydrosulfide (100 μmol/kg bolus+1 mg·kg-1·h-1 infusion) 10 min prior to the onset of reperfusion. Expressions of PAR-1 and PAR-3 were detected by RT-PCR and flow cytometry. Serum H2S was tested by sensitive sulfide electrode. Serum TF, TNF-α, t-PA, PAI-1 were determined by ELISA. PLG:A, FVIII:C, vWF, AT:A, platelet were measured. Results: PAR-1, PAR-1 mRNA, TF, TNF-α, FVIII:C, vWF, t-PA, PAI-1 in group C were significantly higher than those in group A, predominantly lower than those in group B (P<0.01). H2S, PLG:A, AT:A in group C were sharply higher than those in group B, strikingly lower than those in group A (P<0.01). H2S negatively correlated with PAR-1, PAR-1 mRNA, TF, TNF-α, FVIII:C, vWF, t-PA, PAI-1 (r=-0.58, -0.68, -0.62, -0.64, -0.73, -0.55, -0.57, -0.64, P<0.01), positively correlating with PLG:A, AT:A (r=0.57, 0.61, P<0.01). Conclusion: H2S attenuates coagulation dysfunction in rats with intestinal ischemia-reperfusion injury by down-regulating PAR-1, TF, TNF-α.
