摘要
目的：研究肾缺血预处理（ＩＰＣ）对心脏电稳定性的影响和机理。方法：２４只大耳白兔随机分为对照组、肾缺血再灌流（Ｉ／Ｒ）组和肾ＩＰＣ＋Ｉ／Ｒ组。观察肾再灌流２４ｈ时及用垂体后叶素（Ｐｔ）和肾上腺素（Ａｄｒ）后的心电图动态变化以及血中一氧化氮（ＮＯ）和心肌中丙二醛（ＭＤＡ）的浓度改变。结果：用Ｐｔ和Ａｄｒ后，肾Ｉ／Ｒ组缺血性ＳＴ段抬高和心律失常发生率同肾ＩＰＣ＋Ｉ／Ｒ组差异显著；肾ＩＰＣ＋Ｉ／Ｒ组ＮＯ代谢物升高和ＭＤＡ降低同Ｉ／Ｒ组差异显著（Ｐ＜０．０５）；除ＭＤＡ外，上述指标在肾ＩＰＣ＋Ｉ／Ｒ组与对照组间差异无显著。结论：肾ＩＰＣ通过减轻心肌缺血性改变使心脏电稳定性增强；ＮＯ可能通过增加氧自由基的清除和扩血管效应而参与此作用。
AIM: The effect of kidney ischemic preconditioning on electrocardiac stability and it's mechanism were studied in the article. METHODS:24 adult Japanese white rabbits were randomly divided into three groups: control group ( n=6 ), left renal artery (LRA) received no clamping; ischemic reperfusion (I/R) group ( n=9 ),LRA received clamping for 1 hour followed by 24 hours of reperfusion; ischemic preconditioning (IPC) and I/R group ( n=9 ), LRA received clamping for 5 minutes followed by 10 minutes of reperfusion, which was done repeatedly 3 times, then, do the same process again as in I/R group. The dynamic changes of electrocardiogram were observed at 24th hour of reperfusion and after intravenous pituitrin (Pt) 2U·kg 1 for 10 minutes and adrenalin (Adr) 0.03 mg·kg -1 for 15 minutes. Concentration of nitric oxide (NO) in blood and molonyldehyde (MDA) content in cardiac tissue were chected in three groups. RESULTS:There was a considerable difference in the ischemic ST segment elevation and also in arrhythmogenic rate between I/R group (0.270±0.160 mV, 88.89%) and IPC+I/R group (0.090±0.300 mV, 22.22%) after Pt and Adr administration. In addition, there was a significant difference ( P <0.05) increase in NO and decline in MDA in IPC+I/R group (176.750±69.057, 12.540±3.100) of with I/R group (86.875±32.874, 20.730±0.700). However, there was no marked difference in the above parameters except MDA between IPC+I/R group and control group. CONCLUSIONS:The increase in electrocardiac stability through modifying cardiac ischemia by kidney IPC, in which NO could play an important role through increasing in scavenging of the oxygen free radical and also through vasodilation itself.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第5期444-446,共3页
Chinese Journal of Pathophysiology
