Monophasic action potential recordings from intact mouse heart: Validation, regional heterogeneity, and relation to refractoriness

MAP Recordings from Mouse Heart. Introduction: The monophasic action potent ial (MAP) technique has been validated in humans and larger animals, but, i n mice, MAP recordings available to date show little resemblance to the mur ine ventricular transmembrane action potential (TAP) measured by convention al microelectrodes. We developed a miniaturized MAP contact electrode techn ique to establish in isolated mouse hearts: (1) optimal electrode size; (2) validation against TAP; (3) relationship between repolarization and refrac toriness; and (4) regional repolarization differences. Methods and Results: In 30 Langendorff-perfused mouse hearts, MAP electrode s of tip diameter 1.5, 1.0, and 0.25 mm were tested by comparing MAPS and T APs from epicardial and endocardial surfaces of both ventricles. Only the M AP contact electrode of 0.25-mm tip diameter consistently produced MAP reco rdings that had wave shapes nearly identical to TAP recordings. MAP duratio ns measured at 30%, 50%, 70%, and 90% repolarization (APD(30), AP(50), APD( 70), APD(90)) highly correlated with TAP measurements (r=0.97, P<0.00001). APD(50) was significantly longer in endocardial than in epicardial recordin gs (right ventricle: 9.3<plus/minus>1.1 msec vs 3.9 +/-1.1 msec; left ventr icle: 9.9 +/-2.1 msec vs 6.2 +/-1.9 msec; both P<0.001). demonstrating tran smural repolarization differences. Effective refractory period (ERP) determ ined at basic cycle lengths from 70 to 200 msec correlated with 80%<plus/mi nus>6% of total repolarization, with an ERP/APD(90) ratio of 0.85 +/-0.14. Conclusion: Murine myocardial repolarization, regional repolarization heter ogeneity, and relation to refractoriness can be assessed reliably by this m iniaturized MAP contact electrode technique, which renders action potential wave shapes similar to that of intracellular microelectrodes. This techniq ue may be useful for exploring repolarization abnormalities in genetically altered mice.