肾神经在肾缺血预处理对麻醉家兔心脏保护中的作用

在氨基甲酸乙酯麻醉家兔上,观察肾脏缺血预处理(RIP)对缺血-再灌注心肌的影响,旨在证实RIP对心肌有无保护效应,并明确肾神经在其中的作用。所得结果如下(1)在心脏45min缺血和180min再灌注过程中,血压、心率和心肌耗氧量呈进行性下降;心外膜电图ST段在缺血期明显抬高,再灌注过程中逐渐恢复到基础对照值。心肌梗塞范围占缺血心肌的55.80±1.25%。(2)RIP时心肌梗塞范围为36.51±2.8%,较单纯心肌缺血-再灌注显著减少(P<0.01),表明RIP对心肌有保护作用。(3)肾神经切断可取消RIP对心肌的保护效应,但肾神经切断本身对单纯缺血-再灌注所致的心肌梗死范围无明显影响。(4)肾缺血(10min)时,肾传入神经放电活动由0.14±0.08增至0.65±0.12imp/s(P<0.01)。(5)预先应用腺苷受体拮抗剂8-苯茶碱可明显减弱肾缺血所激活的肾传入神经活动,提示肾传入活动的增强是由肾缺血产生的腺苷所介导。以上结果表明,肾短暂缺血-再灌注所诱发的肾神经传入活动在RIP心肌保护效应中起重要作用。

Role of renal nerve in cardioprotection provided by renal ischemic preconditioning in anesthetized rabbits

The effects of renal ischemic preconditioning (RIP) on ischemia-reperfused myocardium were examined in the urethane-anesthetized rabbit to determine whether RIP may provide cardioprotection and to observe the role of the renal nerve in such condition. The results obtained are as follows: (1) During 45 min myocardial ischemia and subsequent 180 min reperfusion, blood pressure, heart rate and myocardial oxygen consumption decreased progressively. Epicardial electrographic ST-segment was elevated significantly in the period of ischemia and returned to the baseline gradually in the course of reperfusion. The myocardial infarct size occupied 55.80 +/- 1.25% of the area at risk. (2) RIP significantly reduced the myocardial infarct size to 36.51 +/- 2.80% (P < 0.01), indicating the cardioprotective effect of such an intervention. (3) Renal nerve section (RNS) completely abolished the cardioprotection afforded by RIP, though RNS per se did not affect the myocardial infarct size produced by ischemia-reperfusion. (4) During 10 min renal ischemia, the averaged multi-unit discharge rate of the renal afferent was increased from 0.14 +/- 0.08 to 0.65 +/- 0.12 imp/s (P < 0.01). (5) Pretreatment with an adenosine receptor antagonist 8-phenyltheophylline (10 mg/kg) markedly attenuated the discharge rate of the renal afferent induced by transient renal ischemia, implying that adenosine released in ischemic kidney activated the renal afferent. It is suggested that activation of renal afferents by transient renal ischemia-reperfusion plays an important role in the cardioprotection afforded by RIP.