Abstract
Lipid and energy metabolism was investigated in the aorta and brain microvessels to clarify the mechanisms of the formation of atherosclerosis or angionecrosis.
The aorta had fairly high enzyme activities to hydrolyze or synthesize lipids in lysosomes and microsomes. These enzyme activities were affected by hypercholesterolemia but not by hypertension. In the hypercholesterolemic rabbits cholesterol esterase activity was not increased whereas acyl-CoA: cholesterol acyltransferase activity was 38 times higher than in the control. These results suggest aortic enzyme activities changed in the direction to accumulate cholesterol ester. The aorta had a low activity of fatty acid oxidation and was not affected by hypertension.
Brain microvessels had higher enzyme activities to hydrolyze or synthesize lipids than the aorta. However, these enzyme activities were not affected either by hypercholesterolemia or by hypertension. Brain microvessels had high activities of fatty acidand glucose oxidation. These oxidation activities were decreased as a function of the persistence of hypertension. At the same time mitochondria of smooth muscle cells in brain microvessels were damaged in hypertension. These phenomenon were considered to be an early change of angionecrosis.
Above results suggest that the aorta and brain microvessels had different metabolic properties, i. e., “esterifying” in the former and “oxidizing” in the latter, and that this difference explains in part the formation of different vascular injuries such as atherosclerosis and angionecrosis in response to hypercholesterolemia and hypertension.
