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.