The biosynthesis of polyamines has been well established in the embryonic, neonatal, and adult heart, and it displays significant changes that might be correlated to the physiological, biochemical, and ultrastructural changes occurring at the various stages of developing heart. In vitro experiments with cell-free systems have shown that polyamines might positively affect various steps involved in nucleic acid and protein biosynthesis. In accordance with this, the perfusion of isolated hearts with polyamines has been reported to increase the rate of incorporation of ribose, phenylalanine, and acetate into myocardial RNA, protein, and histone, respectively. The possible involvement of cellular polyamines in determining heart cell sensitivity is clearly supported by the fact that inhibition of polyamine accumulation leads to an improved or an impaired responsiveness to cAMP or cGMP-mediated effectors, respectively. Conversely, serum-mediated induction of TAT is completely prevented by blocking polyamine sythesis, thus suggesting that polyamine accumulation is a requirement for the cAMP-independent mechanism of TAT induction.

Biochemical and structural changes occurring in the myocardium with aging are mainly resulting from the association of a general tissue atrophy with the hypertrophy of the remaining myocytes. Whilst hypertrophy seems to be a compensatory process to the loss of cardiomyocytes and to a mild systolic hypertensive condition that accompanies elderly people, atrophy should be the modification more closely related to aging 'per se.' In support to the free radical theory of aging, several signs of oxidative damage have been shown in the aged heart, such as lipofuscin accumulation, decreased phospholipid unsaturation index, greater formation of both hydrogen peroxide and 8-hydroxy-2'deoxyguanosine. As a compensatory reaction, the activities of the main oxygen-radical scavenger enzymes are stimulated in the mitochondria of aged rat heart. Endothelium-mediated vasoregulation is more susceptible to oxidative stress in aged with respect to young rats, suggesting that also the vasculature can be negatively influenced by the oxygen free radicals generated during aging. The possible primary role of oxygen free radicals in the development of myocardial atrophy is also discussed.