The passive and active electrical properties of left ventricular myocardium were measured, using conducted action potentials and current clamp of isolated myocytes. The objective was to quantify changes of intracellular resistivity, Ri, during hypertrophic growth and the simultaneous imposition of cellular hypoxia. Ri was estimated from the time course of the rising phase of a conducted action potential using a solution of the two-dimensional cable equation. The thoracic aorta of guinea-pigs was constricted to induce left ventricular hypertrophy (LVH) and myocardium used 50 and 150 days post-operation. Conduction velocity increased in the earlier stage of LVH and declined in the later stage, compared with age-matched controls. Hypoxia reduced conduction velocity in all experimental groups. Ri increased only in the later stage of hypertrophy (253 ± 39 [Omega] cm to 544 ± 130 [Omega] cm) and was additionally increased by hypoxia in all groups (e.g. control myocardium 252 ± 39 [Omega] cm to 506 ± 170 [Omega] cm). The magnitude of the increase of Ri in hypertrophied, hypoxic myocardium can create conditions required to generate re-entrant arrhythmias.