To study the effect of simulated ischemia-reperfusion (I/R) on If of sinoatrial node (SAN) cellsand the ntervention of KATP channel opener Pinacidil. Methods: The SAN cells of the neonatal rats were detached and pu-rified 2 d efore the experiment. The experimental animals were randomly divided into the control group, group of simulatedI/R, group intervened with KATP channel opener Pinacidil (P + I/R) and group intervened with KATP channel blockingagent 5-HD (5-HD + P + I/R & 5-HD + I/R). The If density of each group was measured by technique of routine whole elldifferent directive potentials, the If density of the SAN cells in I/R group increased significantly, compared with that in thecontrol group ( P ＜ 0.01 ); that in P + I/R group decreased significantly, compared with that in I/R group ( P ＜ 0.01 ); theIf density values in 5-HD + P + I/R group and 5-HD + I/R group increased significantly, compared with that in P + I/Red curve of the SAN cells moved rightwards under ultimate activating potential, half of which was from - 108.0 ± 12.4 to- 89.5 ± 7.2 mV ( P ＜ 0.01 ); compared with that in I/R group, If activated curve of the SAN cells moved leftwards underultimate activating potential, half of which was the range from - 99.5 ± 10.8 mV ( P ＜ 0.05 ); KATP channel blockingagent 5-HD could block the effect of Pinacdil on If activated curve. Conclusion: KATP channel opener Pinacidil can antago-nize the effect of simulated I/R on the If of SAN cells, which may be beneficial to the maintenance of the relative stability ofion steady state and electrophysiological activities under condition of simulated I/R.