摘要
目的 :探讨脱氧肾上腺素 (PH)和血管紧张素 (AT)对离体大鼠心肌缺血后再灌注心律失常的影响及机制。方法 :用双冠脉分别灌流模型 ,经 15 m in正常灌注后 ,将左冠脉血流量减少到原灌流量的 5 % ,灌流 12 m in,此间将不同药物注入左冠。观察再灌注后 5 min室性心动过速 (VT)及室颤 (VF)的发生情况。结果 :PH可明显加重再灌注心律失常 ,而单纯应用 AT却无明显作用。用选择性 Na+ / H+ 交换 (NHE)阻滞剂 HOE 6 42可完全阻断PH的作用 ,而用蛋白激酶 C(PKC)阻滞剂 GF10 92 0 3X(GF)只能部分阻断 PH的作用 ,单纯应用 AT2 受体阻滞剂PD12 3319(PD)可增加再灌注心律失常的发生率 ,但与对照组比较未见统计学差异 ,而 PD与 AT合用可使再灌注心律失常发生率明显增加。结论 :α1 肾上腺素受体兴奋可加重缺血后再灌注心律失常 ,其机制可能与 NHE活性增加有关 ,PKC的中介不是 NHE激活的唯一途径。血管紧张素 可通过兴奋 AT1 受体加重再灌注心律失常。
Objective: Our aim was to investigate the effects of phenylephrine (PH) and angiotensin Ⅱ (AT) on reperfusion arrhythmias in the isolated rat heart and its mechanism. Methods: Isolated rat hearts were subjected to dual coronary perfusion. After 15 minutes of aerobic perfusion of both coronary beds, flow to the left coronary bed infused selectively into that bed. Ventricular tachycardia (VT) and fibrillation (VF) were analyzed 5 minutes after reperfusion. Results: The reperfusion arrhythmias was significantly exacerbated by PH; however, AT alone did not have the same effect. The selective Na +/H + exchanger (NHE) inhibitor, HOE642, which was infused along with PH, reversed the proarrhythmic effects of PH. The specific protein kinase C (PKC) inhibitor GF109203X (GF) infused along with PH can only partially reverse the proarrhythmic effect of PH. The AT 2 receptor inhibitor PD123319 (PD) alone increased the incidence of reperfusion induced arrhythmias. However, no statistical significance showed. Combination of PD and AT significantly increased the incidence of reperfusion induced arrhythmias. Conclusion: Activation of α 1 adrenoceptor can exacerbate reperfusion induced arrhythmias. The AT 1 receptor activated by AT can exacerbate reperfusion induced arrhythmias. The activation of AT 2 receptor may reduce reperfusion-induced arrhythmias.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2001年第1期12-14,共3页
Journal of China Medical University
