Key result
Hypertrophy and hypoxia more than double myocardial intracellular resistivity in late-stage preclinical models.
Why the study?
Changes in intracellular resistivity during hypertrophic growth and cellular hypoxia in left ventricular myocardium were not quantified.
Does hypertrophic growth and cellular hypoxia alter intracellular resistivity and conduction velocity in guinea-pig left ventricular myocardium?
Population
Guinea-pigs with induced left ventricular hypertrophy and isolated myocytes
Comparison
Hypertrophied and hypoxic myocardium vs age-matched controls
Design
Experimental study measuring electrical properties of isolated myocardium and myocytes
Follow-up
50 and 150 days post-operation
Authors
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In vitro data link late LVH to higher junctional resistivity; leaves open arrhythmia risk and hypoxia interactions in vivo.
Does hypertrophic growth and cellular hypoxia alter intracellular resistivity and conduction velocity in guinea-pig left ventricular myocardium?
The increase in intracellular resistivity in hypertrophied, hypoxic myocardium creates conditions conducive to generating re-entrant arrhythmias.
Cooklin et al. (1998) studied Left ventricular hypertrophy and hypoxia. Thoracic aorta constriction (LVH) and hypoxia vs. Age-matched controls was evaluated on Intracellular resistivity (Ri) and conduction velocity. Thoracic aorta constriction-induced hypertrophy and hypoxia increased intracellular resistivity in guinea-pig myocardium (e.g., from 253±39 to 544±130 Ω cm in later stage hypertrophy).
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