M. Cooklin et al., Conduction velocity and gap junction resistance in hypertrophied, hypoxic guinea-pig left ventricular myocardium, EXP PHYSIOL, 83(6), 1998, pp. 763-770
The passive and active electrical properties of left ventricular myocardium
were measured, using conducted action potentials and current clamp of isol
ated myocytes. The objective was to quantify changes of intracellular resis
tivity, R-1, during hypertrophic growth and the simultaneous imposition of
cellular hypoxia. R-1 was estimated from the time course of the rising phas
e of a conducted action potential using a solution of the two-dimensional c
able 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 d
eclined in the later stage, compared with age-matched controls. Hypoxia red
uced conduction velocity in all experimental groups. Ri increased only in t
he 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 myoc
ardium 252 +/- 39 Omega cm to 506 +/- 170 Omega cm). The magnitude of the i
ncrease of R-1 in hypertrophied, hypoxic myocardium can create conditions r
equired to generate re-entrant arrhythmias.