论文部分内容阅读
目的探讨吡那地尔超极化停搏对大鼠离体心脏p38丝裂原活化蛋白激酶(p38MAPK)的影响。方法成年雄性SD大鼠随机分为四组:自然停搏组(A组)、St.Thoma液停搏组(B组)、吡那地尔超极化液停搏组(C组)和SB203580液停搏组(D组),每组8只。采用Langen-dorff离体心脏灌注模型,检测冠脉流量(CF)、心率(HR)、左室发展压(LVDP)、左室收缩峰压(LVSP)和左室压力瞬时最大变化率(dp/dtmax)、心肌磷酸化p38MAPK和非磷酸化p38MAPK的表达。结果与K-H液平衡灌注15min时比较,再灌注20min时,A组、B组、D组CF、HR、LVSP、LVDP及dp/dtmax降低(P<0.05)。与C组比较,A组、B组、D组再灌注20min时CF、HR、LVSP、LVDP及dp/dtmax降低,再灌注30min时磷酸化p38MAPK表达下调(P<0.05),非磷酸化p38MAPK表达上调(P<0.05)。结论磷酸化p38MAPK介导了吡那地尔超极化停搏对大鼠离体心脏的保护,促进大鼠心肌缺血-再灌注时心功能恢复。
Objective To investigate the effect of pinacidil hyperpolarized arrest on p38 mitogen-activated protein kinase (p38 MAPK) in isolated rat hearts. Methods Adult male Sprague-Dawley rats were randomly divided into four groups: spontaneous arrest group (group A), St.Thoma fluid group (group B), pinacidil hyperpolarization suspension group (group C) and SB203580 Fluid stop group (group D), each group of eight. The left ventricular systolic pressure (LVSP) and left ventricular pressure (dp / dt) were measured by Langen-dorff perfusion model in vitro. dtmax), phosphorylated p38MAPK and non-phosphorylated p38MAPK in myocardium. Results Compared with the balanced infusion of K-H solution for 15 min, the CF, HR, LVSP, LVDP and dp / dtmax in group A, group B and group D decreased at 20 min after reperfusion (P <0.05). Compared with group C, the levels of CF, HR, LVSP, LVDP and dp / dtmax in group A, group B and group D were decreased after reperfusion for 20min, and the expression of p38MAPK phosphorylation was downregulated at 30min after reperfusion (P <0.05) (P <0.05). Conclusion Phosphorylation of p38MAPK mediates the protection of isolated rat heart by hyperpolarized arrest of pinacidil and the recovery of cardiac function during myocardial ischemia-reperfusion in rats.