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Objective To study clinical efficacy of ulinastatin combined with naloxone in patients with cardiogenic shock(CS) after acute myocardial infarction (AMI).Methods Eighty patients with CS after AMI were randomly divided into routine treatment group (n =19),ulinastatin group (n =20),naloxone group (n =21) and ulinastatin combined with naloxone group (n =20).The levels of serum cardiac troponin I (cTnI),brain natriuretic peptide(BNP),tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6)were measured before and a week after treatment.In the meantime,recovery time of shock,the average hospitalization days and 28-day mortality rate were recorded.Results After the treatment,the levels of serum cTnI,BNP,TNF-α and IL-6decreased in all groups(P ＜ 0.01),and there was significant difference on the decreasing degree of cTnI,BNP,TNF-α and IL-6 in ulinastatin combined with naloxone group when compared with those in routine treatment group,ulinastatin group and naloxone group(cTnI:(1.04 ± 0.17) ng/L vs.(2.06 ± 0.15) ng/L,(1.59 ± 0.16)ng/L,(1.97 ± 0.14) ng/L; BNP:(143.21-56.94) ng/L vs.(261.07 ± 71.43) ng/L,(203.46 ± 65.73) ng/L,(252.96 ± 68.85) ng/L; TNF-α:(13.42 ± 8.93) ng/L vs.(31.21 ± 12.32) ng/L,(20.39 ± 11.08) ng/L,(28.98 ± 11.76) ng/L ; IL-6:(37.58 ± 11.14) ng/L vs.(80.46 ± 27.15) ng/L,(59.84 ± 20.72) ng/L,(76.15 ±26.45) ng/L; P ＜ 0.01).The recovery time of shock,the average hospitalization days and 28-day mortality rate in ulinastatin combined with naloxone group were significantly lower than those in routine treatment group,ulinastatin group and naloxone group(recovery time of shock:(7.16 ± 1.52) d vs.(11.43 ± 2.40) d,(8.05 ±1.81)d,(8.74 ± 1.98)d;the average hospitalization days:(15.03 ±3.23)d vs.(22.64 ±4.18)d,(18.93 ±3.97)d,(19.21 ±3.94)d ;28-day mortality rate:(41.62％ vs.61.20％,50.74％,52.31％ ; P ＜0.01)).Conclusion The application of ulinastatin combined with naloxone can effectively inhibit the cardiac injury and inflammatory response,promote the recovery of circulation function and improve prognosis in patients with CS after AMI.
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Objective To investigate the expression of CXCR6 in allograft rejection and effect of CXCL16/CXCR6 interaction on allograft survival Methods Intra-abdominal heterotopic heart transplantation was performed using wild type (WT) Balb/c mice (H-2d) (allogeneic) as donors or WT C57BL/6 mice (B6, H-2b) (syngeneic) as donors, and using WT B6 mice as recipients. The intragraft expression of CXCR6 and expression of CXCR6 in CD8+ T cells of the spleens from syngeneic and allogeneic recipients were examined. The allogeneic recipients were further divided into the experimental group (n = 5) and control group (n = 6) randomly. The experiment group and control group were injected with anti-CXCL16 mAb or control mAb respectively until rejection occurred. The cardiac allograft survival in experimental group and control group was evaluated. Results Rejected allografts showed higher expression of CXCR6 than syngeneic cardiac grafts. More importantly,expression of CXCR6 in CD8+ T cells was also up-regulated by allograft rejection. However, injection of anti-CXCL16 mAb could not inhibit cytotoxic activity of CD8+ T cells. Moreover, experimental group could not prolong the cardiac graft survival time as compared with control group. Conclusion Expression of CXCR6 in CD8+ T cells is up-regulated in allograft rejection.