Effect of intracoronary tirofiban on platelet alpha-granule membrane protein and myocardial perfusion level during emergency percutaneous coronary intervention.

This study aimed to investigate the effect of intracoronary application of tirofiban on platelet alpha-granule membrane protein (GMP-140) and myocardial perfusion levels during emergency percutaneous coronary intervention (PCI). A total of 70 patients who accepted emergency PCI treatment were randomly divided into tirofiban and control groups. We determined GMP-140 and troponin I (cTnI) levels before and 12 h after surgery, as well as N-terminal pro-brain natriuretic peptide levels 1 and 7 days after surgery in the two groups. The results showed that GMP-140 and cTnI levels were significantly (P < 0.01) lower in the tirofiban group than in the control group 12 h after operation (17.99 ± 1.01 vs 24.56 ± 1.96 µg/L and 50.96 ± 2.20 vs 58.69 ± 2.34 ng/mL, respectively). The D-value of the N-terminal pro-brain natriuretic peptide levels between 1 and 7 days after operation was significantly higher in the tirofiban group than in the control group (894.19 ± 90.91 vs 829.50 ± 84.18 pg/mL; P < 0.01). The intracoronary application of tirofiban during emergency PCI clearly reduced the GMP-140 level, inhibited the activation function of platelets, improved myocardial perfusion, and helped recover cardiac function in patients.

Effects of thrombin on the secondary cerebral injury of perihematomal tissues of rats after intracerebral hemorrhage.

This study aimed to investigate the effects of thrombin released in hematoma after intracerebral hemorrhage (ICH) on the cerebral injury of perihematomal tissues and to evaluate the protection effect of hirudin on the cerebral injury after ICH. We used the autologous uncoagulated blood injection method to prepare the ICH rat model, and all rats were randomly divided into a normal group, an ICH group, or a hirudin group. At different time points, rat heads were cut to harvest brain sections. Immunohistochemical staining, histochemical staining, and hematoxylin and eosin staining were conducted for CD34, microglia, and neutrocytes. CD34-positive microvessels were most abundant in brain tissues of the sham-operation group. At 12 h after ICH, CD34 expression reduced and reached the minimum level at 72 h (P<0.01). At 6 h after ICH, microglia expression was visible and reached a peak at 48 h (P<0.01). At 12 h after ICH, neutrocyte infiltration was visible and the number was greatest at 48 h (P<0.01). The early application of hirudin after ICH could significantly reduce microglia and neutrocyte expression and could significantly slow down the CD34 decrease trend (P<0.01). However, hirudin application in the edematization stage after ICH did not significantly increase CD34- positive microvessel abundance (P>0.05). A thrombin-mediated inflammatory reaction is involved in the cerebral injury after ICH, and the early application of hirudin has a protective effect.