Cellular hypertrophy can alter the distribution of residual stress in the myocardium, hence can affect active and passive ventricular mechanics. It is hypothesized that an increase in stress-free cell cross-sectional area will tend to increase residual stresses. Therefore transmural distributions of myocyte cross-sectional areas and global ventricular dimensions in young rats 0-21 days following thoracic aortic handling with sham-operated and unoperated control groups were measured in tissue free of all external and residual stresses. Cell cross-sectional area increased in the stress-free state and was uniform across the wall except at 21 days when there was a transmural gradient with cells at the endocardium 46% larger in diameter than those in the outer wall. Cell area increased from a mean of 156 +/- 30 microM2 at 0 days to a mean of 627 +/- 164 microM2 at 21 days, although during this time there were no statistical changes in the opening angles of stress-free tissue sections. Because the time course of opening angle did not follow the changes in cell thickening, the cellular growth measured in this study is probably not the only factor responsible for the distribution of residual stress.