RESUMEN
【Objective】 To explore the feasibility of tirofiban, a platelet surface glycoprotein (GP)Ⅱb/Ⅲa receptor antagonist intervene in transfusion-related acute lung injury (TRALI), by inhibiting platelet activation and by preventing platelet and neutrophil binding to form aggregates. 【Methods】 1) Fifty wild-type male Balb/c mice, aged 8 to 10 weeks, were randomly divided into TRALI, normal, tirofiban TRALI intervention, isotype control and tirofiban normal intervention groups. In the TRALI model, tirofiban TRALI intervention and isotype control groups, each mouse was injected intraperitoneally with lipopolysaccharide (LPS) 0.1 mg/kg, and after 18 h with 4.5 mg/kg anti-MHC-I or IgG2a isotype control antibody, in which 0.5 μg/g tirofiban was injected 30 min before anti-MHC-I injection, and was labeled as tirofiban TRALI intervention. The group without any treatment was set as normal group. The tirofiban normal intervention group was injected with only 0.5 μg/g tirofiban into the tail vein, 30 min before the injection of anti-MHC-I. 2) After antibody injection, the mice were observed for 2 h, then executed with their lungs removed, and the extent of lung injury and the intervention effect of tirofiban were analyzed by comparing the differences in lung dry to wet ratio, total protein, myeloperoxidase (MPO), inflammatory factors and quantitative results of HE staining. The platelet activation level in whole blood and immunofluorescence (IF) quantification of platelet and neutrophil fluorescence were detected by flow cytometry to analyze the mechanism of tirofiban on TRALI. 【Results】 1) The indexes of lung injury in the tirofiban TRALI intervention group and TRALI model group for HE staining were 0.663 3±0.141 9 vs. 0.173 3±0.120 4 (P<0.05), respectively; 2) Platelet activation levels(%)in whole blood in the TRALI group, normal group and tirofiban TRALI intervention group were 22.87±9.943 vs 5.070±2.234 vs 5.767±3.224(P<0.05), respectively. 3) The mean fluorescence density of platelet neutrophil aggregates for IF detection in the tirofiban intervention group and TRALI model group was 21.89±3.536 vs. 32.77±0.9624 (P<0.05). 【Conclusion】 The platelet GP Ⅱ b/Ⅲa-specific inhibitor tirofiban inhibited platelet-neutrophil binding in mice, thus could possibly intervene in TRALI.
RESUMEN
Objective To investigate the effect of tirofiban on myocardial necrosis biomarker after percutaneous coronary interventions(PCI)in patients with aspirin resistance(AR).Methods 374 consecutive patients with aspirin 100 mg≥1 week,receiving no other antiplatelet therapy,scheduled for PCI were enrolled.all patients were given an loading dose of 300 mg clopidogrel at least 12 hours before PCI and an 75 mg maintenance dose per day.Patients were randomized into tirofiban group(n=38)and control group(n=45)after PCI.The levels of CKMB,TnI at 8,12,and 24 hours after PCI were measured in all patients;if the CK-MB,TnI value was above normal upper limitation,it was considered elevated.Results 83 patients were AR(22.2%)and 54.2%of them are females.The frequencies of CK-MB elevation were 15(39.5%)in tirofiban group and 19(42.2%)in control group,and TnI elevation was 18(47.4%)and 23(51.1%)in the two groups respectively.Conclusion Tirofiban can not decrease the elevation level of CK-MB and TnI in patients with AR after PCI.