Conduction velocity and gap junction resistance in hypertrophied, hypoxic guinea-pig left ventricular myocardium.
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.
Academic Cardiology Unit, Division of the National Heart and Lung Institute, Imperial College School of Medicine, St Mary's Hospital, South Wharf Road, London W2 1NY, UK.
M
M
Cooklin
W R
WR
Wallis
D J
DJ
Sheridan
C H
CH
Fry
D000200:Action Potentials / Q000502:physiology; D000465:Algorithms; D000818:Animals; D001013:Aorta, Thoracic / Q000503:physiopathology; D017629:Gap Junctions / Q000502:physiology*; D006168:Guinea Pigs; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology; D066298:In Vitro Techniques; D008839:Microelectrodes; D009119:Muscle Contraction / Q000502:physiology; D009431:Neural Conduction / Q000502:physiology*