精氨加压素对失血性休克大鼠心肌收缩力的影响及与Rho激酶的关系

摘要

目的 探讨精氨酸加压素(AVP)对失血性休克大鼠心肌收缩力的影响及与Rho激酶的关系.方法 失血性休克大鼠的离体乳头肌分别用AVP 0.1 μmol·L-1 和 Y-27632 10 μmol·L-1预孵育,或Y-27632+AVP合用时,先用Y-27632 孵育10 min后,再加入AVP作用10 min.平衡30 min后依次用含异丙肾上腺素(Iso)1和10 μmol·L-1,0.1,1,10 mmol·L-1的H-K液灌流乳头肌,观察加入Iso前后收缩力变化.制备离体心脏,稳定后,进行相应再灌流30 min,检测左心室收缩压(LVSP)和左心室压力上升或下降的最大速率(±dp/dtmax).结果 失血性休克2 h,经Iso 0.1,1 及10 mmol·L-1灌流后,离体乳头肌收缩力显著低于假手术组(P<0.05),AVP 0.1 μmol·L-1预孵育可明显升高乳头肌对心肌的收缩力;与休克模型组相比,在Iso 1和10 mmol·L-1灌流后,乳头肌收缩力明显升高(P<0.05);Y-27632 10 μmol·L-1离体乳头肌收缩力无明显影响,但Y-27632+AVP可明显降低由AVP引起的乳头肌收缩力的增加.失血性休克2 h后,离体心脏血流动力学指标明显降低,AVP可明显改善休克模型大鼠离体心脏的血流动力学指标,同时Y-27632可明显拮抗由AVP引起休克大鼠离体心脏血流动力学指标的增加.结论 AVP可改善失血性休克所致的心肌收缩力的降低,其机制与其激活Rho 激酶有关.%OBJECTIVE To explore the effect of argipressin (arginine vasopressin, AVP) on myocardium contraction following hemorrhagic shock and its relationship to Rho kinase.METHODS Cardiac papillary muscles from shocked SD rats were incubated AVP 0.1 μmol· L-1 or Y-27632 10 μmol· L-1 for 10 min, respectively. Cardiac papillary muscles in Y-27632 + AVP group were given Y-27632 for 10 min and then AVP for 10 min. Contractile responses to isoprenaline(Iso) 1 and 10 μmol·L-1, and 0. 1, 1 and 10 mmol·L-1 with H-K solution were measured. Hemodynamic parameters of isolated hearts, including left intraventricular systolic pressure ( LVSP), the maximal change rate of left intraventricular pressure ( ± dp/dtmax ) was measured from isolated hearts. RESULTS Contractile response of cardiac papillary muscle to Iso was decreased after shock. AVP 0.1 μmol· L- 1 significantly improved contractile response. Compared with shock model group, cardiac papillary muscle contration significantly increased after Iso 1 and 10 mmol·L-1 treatment. Y-27632 10 μmol·L-1 pretreatment didn't affect the contractile respose of cardiac papillary muscle of shock group, but it abolished effect of AVP on contractile response. The hemodynamic parameter was decreased after shock, but was improved by AVP. The effect of AVP on the hemodynamic parameter was abolished by Y-27632. CONCLUSION AVP can improve cardiac contractility following hemorrhagic shock, and its mechanism is related to activation of Rho kinase.