Literature DB >> 11761418

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

B C Knollmann1, A N Katchman, M R Franz.   

Abstract

INTRODUCTION: The monophasic action potential (MAP) technique has been validated in humans and larger animals, but, in mice, MAP recordings available to date show little resemblance to the murine ventricular transmembrane action potential (TAP) measured by conventional microelectrodes. We developed a miniaturized MAP contact electrode technique to establish in isolated mouse hearts: (1) optimal electrode size; (2) validation against TAP; (3) relationship between repolarization and refractoriness; and (4) regional repolarization differences. METHODS AND
RESULTS: In 30 Langendorff-perfused mouse hearts, MAP electrodes of tip diameter 1.5, 1.0, and 0.25 mm were tested by comparing MAPs and TAPs from epicardial and endocardial surfaces of both ventricles. Only the MAP contact electrode of 0.25-mm tip diameter consistently produced MAP recordings that had wave shapes nearly identical to TAP recordings. MAP durations measured at 30%, 50%, 70%, and 90% repolarization (APD30, APD50, APD70, APD90) highly correlated with TAP measurements (r = 0.97, P < 0.00001). APD50 was significantly longer in endocardial than in epicardial recordings (right ventricle: 9.3+/-1.1 msec vs 3.9+/-1.1 msec; left ventricle: 9.9+/-2.1 msec vs 6.2+/-1.9 msec; both P < 0.001), demonstrating transmural repolarization differences. Effective refractory period (ERP) determined at basic cycle lengths from 70 to 200 msec correlated with 80%+/-6% of total repolarization, with an ERP/APD90 ratio of 0.85+/-0.14.
CONCLUSION: Murine myocardial repolarization, regional repolarization heterogeneity, and relation to refractoriness can be assessed reliably by this miniaturized MAP contact electrode technique, which renders action potential wave shapes similar to that of intracellular microelectrodes. This technique may be useful for exploring repolarization abnormalities in genetically altered mice.

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Mesh:

Year:  2001        PMID: 11761418     DOI: 10.1046/j.1540-8167.2001.01286.x

Source DB:  PubMed          Journal:  J Cardiovasc Electrophysiol        ISSN: 1045-3873


  64 in total

1.  In vivo temporal and spatial distribution of depolarization and repolarization and the illusive murine T wave.

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2.  Ventricular arrhythmogenesis following slowed conduction in heptanol-treated, Langendorff-perfused mouse hearts.

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4.  Calcium-calmodulin dependent protein kinase II (CaMKII): a main signal responsible for early reperfusion arrhythmias.

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5.  Left-to-right ventricular differences in I(KATP) underlie epicardial repolarization gradient during global ischemia.

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6.  Effect of stimulation rate, sarcomere length and Ca(2+) on force generation by mouse cardiac muscle.

Authors:  Bruno D Stuyvers; Andrew D McCulloch; Jiqing Guo; Henry J Duff; Henk E D J ter Keurs
Journal:  J Physiol       Date:  2002-11-01       Impact factor: 5.182

7.  Transmural heterogeneity of repolarization and Ca2+ handling in a model of mouse ventricular tissue.

Authors:  Vladimir E Bondarenko; Randall L Rasmusson
Journal:  Am J Physiol Heart Circ Physiol       Date:  2010-06-04       Impact factor: 4.733

8.  Mechano-electric feedback in the fish heart.

Authors:  Simon M Patrick; Ed White; Holly A Shiels
Journal:  PLoS One       Date:  2010-05-07       Impact factor: 3.240

9.  The inhibition of pyruvate dehydrogenase kinase improves impaired cardiac function and electrical remodeling in two models of right ventricular hypertrophy: resuscitating the hibernating right ventricle.

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Journal:  J Mol Med (Berl)       Date:  2009-12-01       Impact factor: 4.599

10.  Cardiac IK1 underlies early action potential shortening during hypoxia in the mouse heart.

Authors:  Lin Piao; Jingdong Li; Meredith McLerie; Anatoli N Lopatin
Journal:  J Mol Cell Cardiol       Date:  2007-04-10       Impact factor: 5.000

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