Arachidonic acid-induced platelet aggregation and malondialdehyde production in dogs of various ages and in dogs affected with canine ceroid lipofuscinosis

Abstract

The arachidonate pathway of canine platelets was assessed in dogs of varying ages by examination of platelet aggregation to arachidonic acid and by measurement of arachidonic acid-induced platelet malondialdehyde production. As age increased, arachidonic acid-induced platelet aggregation showed a progressive prolongation in the lag phase before aggregation. The production of malondialdehyde by canine platelets significantly decreased with increasing age. Dogs affected with ceroid lipofuscinosis showed similar declines in platelet aggregation and malondialdehyde production, but at an earlier age. This suggests that changes occur in canine platelet reactivity during natural aging and in a disease of “premature” aging. The lack of change in platelet numbers and volume suggests that the alterations reported were related to the aging process rather than to advancing vascular disease. The findings support the free radical theory of aging.