ABSTRACT
AIM: To study the electrophysiological effects of nitric oxide (NO) on the pacemaker cells in guinea-pig left ventricular outflow tract under the condition of ischemia/reperfusion ( I/R) .METHODS:The spontaneous slow action potentials of guinea-pig left ventricular outflow tract were recorded by conventional intracellular microelectrode technique.The effects of NO donor sodium nitroprusside ( SNP) on the spontaneous slow action potentials under normal or I/R condition were investigated.RESULTS:SNP at concentrations of 1, 10 and 100μmol/L but not 1000μmol/L signif-icantly increased velocity of diastolic depolarization ( VDD) and rate of pacemaker firing ( RPF) , SNP at concentrations of 1, 10, 100 and 1 000μmol/L notably increased maximal diastolic potential (MDP), amplitude of action potential (APA) and maximal rate of depolarization ( Vmax ) , shortened 50%and 90%of the duration ( APD50 and APD90 ) .In ischemia 10 min group, VDD and RPF were significantly decreased, APA and Vmax were notably increased, and APD50 and APD90 were markedly lengthened compared with control group.In reperfusion 10 min group, VDD and RPF were significantly in-creased, MDP and APA were notably decreased, and APD50 and APD90 were markedly shortened compared with I 10 min group.In reperfusin 10 min group, the pacemaker activity was always irregular.In reperfusion 10 min group, the parame-ters of spontaneous slow action potentials restored to the levels of control group except for VDD and Vmax .In 1, 10 and 100 μmol/L SNP+R groups, VDD and RPF were significantly increased than in ischemia 10 min group .In 1, 10, 100 and 1 000 μmol/L SNP+R groups, APA, APD50 and APD90 were restored to the levels of control group.CONCLUSION:SNP significantly increases the spontaneous activity of left ventricular outflow tract, and relieves the effects of I/R on the sponta-neous slow action potential markedly.