심실세동의 유발과 지속시 KATP 통로의 역할에 관한 연구 - 심실세동 유발의 억제 및 예방을 위한 심근 전기 생리적 특성의 규명

초록

Objectives To investigate the role of ATP-sensitive potassium channel (KATP) during sustained ventricular fibrillation (VF), the effects of gliburide, a specific blocker of KATP channel and PCO400, an KATP opener, were studied in isolated and perfused swine right ventricular free walls (n=). Methods Recording of single cell transmembrane potentials was performed and constructed action potential duration restitution (APDR) curve by plotting APD 90%(APD90) versus preceding diastolic interval (DI). Results All isolated tissues fibrillated spontaneously. In this preparation, stable VF could persist over a 4-hour period if it was allowed to continue undisturbed (n=). Gliburide (1-5 uM) increased DI without significant changes in APD90 during VF, resulting in more regularization of VF. Higher concentration (10-20 uM) increased both APD90 and DI, and converted to monomorphic ventricular tachycardia (MVT) through the transitional period characterized by APD alternans. PCO400 (1-2.5 uM) caused a significant shortening of APD during MVT and a period of APD alternans became more evident before conversion from MVT to VF. Gliburide eliminated profibrillatory effect of PCO400. This antifibrillatory action of gliburide was accompanied by gradual decrease in the maximum slope of APDR curve during VF. Conclusion KATP channel blockade causes a transition from VF to MVT via lengthening of DI and APD alternans, concomitantly with a reduction of the slope of APD restitution curve.

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