摘要
目的观察尼克酰胺腺嘌呤二核苷酸(NADH)对急性离体心房颤动模型心房肌有效不应期(AERP)的影响及部分通道mRNA的改变。方法选择新西兰大耳白兔24只,随机等分为正常对照组、起搏对照组、起搏/NADH组、起搏/NADH+Rotenone(NADH氧化还原酶拮抗剂)组。正常对照组和起搏对照组用普通台氏液灌流,起搏/NADH组用含NADH的台氏液灌流,起搏/NADH+Rotenone组用含NADH及Rotenone的台氏液灌流。监测起搏前后(正常对照组为灌流前后)AERP的变化。AERP检测完毕后,取右房心肌组织,行半定量逆转录-聚合酶链式反应RT-PCR测定肌浆网钙泵、L型Ca2+通道、Ryanod ine2型受体(RyR2)的相对表达。结果快速心房起搏1 h后,起搏对照组和起搏/NADH+Rotenone组AERP缩短,以起搏对照组变化最大;正常对照组和起搏/NADH组起搏前后无明显变化。同时,快速心房起搏使肌浆网钙泵和L型Ca2+通道表达下调,RyR2受体表达上调;起搏/NADH+Rotenone组L型Ca2+通道表达下调,RyR2表达上调而肌浆网钙泵的表达无明显改变;而起搏/NADH组各相关基因表达无明显改变。结论NADH能够抑制快速心房起搏时心肌的电重构,其作用可能是通过促进肌浆网钙泵基因的表达和抑RyR2介导的Ca2+释放来实现的。
Objective In order to examine the effect of nicotinamide adenine dinucleotide （NADH） on electrophysiological remodeling（ER）. Methods Twenty-four rabbits were randomly divided into four groups （control group, pacing/ control group, pacing/NADH group, pacing/NADH ＋ rotenone group）. The hearts were removed and perfused by the Iangendorff technique with continuous corresponding buffer, respectively. At the same time, pacing the right atrium was performed for 1 hour in all groups but not in control group. Before and after pacing/perfusing, atrial effective refractory period （AERP） was determined in all hearts. Then, fight atrium tissue was obtained for measurement of calcium-handling proteins mRNA using semiquantitative reverse transcription-polymerase chain reaction （RT-PCR）. Results After pacing 1 hour, AERP shortened significantly in pacing/control group and pacing/NADH ＋ rotenone group, but in pacing/NADH group, AERP did not obviously change. The mRNA level of L-type Ca^2＋ channel decreased and the mRNA level of ryanodine receptor type 2 increased in pacing/control group and pacing/NADH ＋ rotenone group, the mRNA level of sarcoplasmic retieulum calcium ATPase decreased in pacing/control group and held the line in pacing/NADH＋rotenone group , but these changes were not found in pacing/NADH group. Conclusions The activation of NADH maybe one mechanism underlying short-term ER.
出处
《中国心脏起搏与心电生理杂志》
2006年第1期66-68,共3页
Chinese Journal of Cardiac Pacing and Electrophysiology
