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本实验用人工合成的纤维蛋白(原)降解产物——肽6A(P6A)灌流离体大鼠心脏,发现冠脉流量(CPF)呈剂量依赖性增加。5×10~(-5)mol/L P6A增加CPF的幅度与10~(-6)mol/L前列环素(PGl_2)的作用相似(分别增加49.7±3.4%和60.7±8.1%);用该浓度的P6A灌流使心脏6—keto—PGF_(1α)的释放增加65.7%(10.6±1.9 vs.对照6.8±1.9ng/g wet;wt心肌,P<0.01)。用消炎痛预处理心脏以阻止PGl_2合成,能显著抑制但不能全消除P6A的扩冠作用,提示促进内源性PGl_2释放是P6A扩冠作用的重要(非唯一)机制。静脉滴注或血栓局部应用P6A,能明显抑制大鼠静脉血栓模型的血栓形成,血栓重量分别较对照减少36.9%和53.9%(P<0.01)。实验表明,P6A有扩张冠脉和抑制血栓形成的作用,推测P6A作为冠脉再通治疗的辅助剂,有临床应用前景。
In this study, isolated rat heart was perfused with peptide 6A (P6A), a synthetic degradation product of fibrin, and found that coronary flow (CPF) increased in a dose-dependent manner. The amplitude of CPF increased with the concentration of 5 × 10-5 mol / L P6A was similar to that of 10 -6 mol / L prostacyclin (49.7 ± 3.4% and 60.7 ± 8.1%, respectively) This concentration of P6A perfusion increased the release of 6-keto-PGF_ (1α) in the heart by 65.7% (10.6 ± 1.9 vs. 6.8 ± 1.9 ng / g wet; wt myocardium, P <0.01). The pretreatment of heart with indomethacin to prevent the synthesis of PGl_2 could significantly inhibit but not completely eliminate the crown-expanding effect of P6A, suggesting that the promotion of endogenous PGl 2 release is an important (non-unique) mechanism of P6A crown expansion. Intravenous drip or topical thrombosis P6A significantly inhibited thrombosis in rat venous thrombosis model, and the thrombus weight decreased by 36.9% and 53.9% (P <0.01) compared with the control. Experiments show that, P6A can dilate coronary artery and inhibit the role of thrombosis, speculated that P6A as coronary recanalization adjuvant, has clinical application prospects.