ABSTRACT
Aging is considered a risk factor in the pathogenesis of atherosclerosis. It is not clear, however, whether the relationship between aging and atherosclerosis is the result of increased susceptibility of the arterial wall related to intrinsic alterations or the expression of the increase in intensity or duration of exposure to risk factors. In this study, we used aged (median age 46 months) and young (4 months old) New Zealand white rabbits. Nine aged and 11 young rabbits received a hyperlipemic diet enriched with a low dose of cholesterol for 18 months. Eleven aged and 8 young rabbits, fed standard chow for the same period, were used as controls. Using morphologic and morphometric methods, we detected in aged hyperlipemic rabbits (a) a marked prevalence of fibroatheromatous plaques (as opposed to fatty streaks in young hyperlipemic rabbits); (b) aortic lesions more extensive and of greater dimensions than in young hyperlipemic rabbits; (c) fibroatheromatous plaques in carotids and raised fatty streaks in the large subepicardial coronary branches. Our results show an increased susceptibility of the aged arterial wall to hypercholesterolemia.
Subject(s)
Aging/pathology , Arteriosclerosis/pathology , Animals , Aorta/pathology , Arteriosclerosis/metabolism , Carotid Arteries/pathology , Cholesterol/metabolism , Coronary Vessels/pathology , Dietary Fats/administration & dosage , Female , Hyperlipidemias/complications , Hyperlipidemias/metabolism , Hyperlipidemias/pathology , Lipid Metabolism , Male , Myocardium/pathology , RabbitsABSTRACT
By using fluorescence microscopy and microfluorimetric techniques, the effects of ageing and of 11 months acetyl-L-carnitine (ALCAR) treatment on lipofuscin deposition within the cytoplasm of pyramidal neurons of rat prefrontal cortex and hippocampus (CA3 field) were assessed. No lipofuscin autofluorescence was observed in the nerve cell bodies of neurons under study in young rats (3 months of age), but lipopigment had accumulated in the same nerve cells of senescent rats (22 months of age). ALCAR administration significantly reduced the accumulation of lipofuscin within pyramidal neurons of the brain areas examined.
Subject(s)
Acetylcarnitine/pharmacology , Aging/metabolism , Brain/drug effects , Carnitine/analogs & derivatives , Lipofuscin/metabolism , Pigments, Biological/metabolism , Acetylcarnitine/administration & dosage , Animals , Brain/metabolism , Female , Rats , Rats, Inbred StrainsABSTRACT
The effect of senescence on the metabolic profile of rat coronary arteries and arterioles was studied using enzyme histochemical techniques. In coronary arteries anaerobic metabolism predominates. In senescence an increase of adenosine triphosphatase (ATPase) occurred. The succinate dehydrogenase (SDH) and the respiratory chain metabolism marker NADH2-tetrazolium reductase (NADHD) showed an age-related decrease. Lactate dehydrogenase was unchanged. In the coronary arterioles, on the contrary, aerobic metabolism dominates. In senescence a significant decrease of NADHD and a moderate reduction of SDH and ATPase was observed. L-Carnitine administration significantly stimulated some enzymatic activities related to aerobic metabolism primarily at the arteriolar level.
