Aortic wall metabolism in relation to susceptibility and resistance to experimental atherosclerosis.

Different segments of the aorta and its branches show differing susceptibilities to atherosclerosis. To identify metabolic features that may account for plaque formation and sparing, we studied aortic wall respiration and glycolysis proximal and distal to an aortic coarctation in 30 rabbits fed a standard or atherogenic diet. Three months after coarctation, blood pressure in the proximal aorta was elevated, and plaque occupied 98% +/- 28% of the intimal surface compared with 57% +/- 26% for control animals (p less than 0.05). Aortic pressure distal to the stenosis remained normal, but plaque formation was markedly decreased (5% +/- 4%) compared with controls (30% +/- 27%, p less than 0.05). Metabolic studies included measurement of oxygen consumption of proximal and distal aortic walls, lactic acid production, and 2-deoxyglucose uptake. Elevated pressure or hyperlipidemia increased respiration (22.6 +/- 4.0 or 16.3 +/- 6.0 pmol oxygen consumed/min/microgram deoxyribonucleic acid [DNA] vs 5.8 +/- 5.2 for controls; p values less than 0.05) without increasing glycolytic metabolism. The coexistence of hypertension and hyperlipidemia resulted in maximal plaque formation and a sevenfold increase in both oxidative metabolism (46.6 +/- 27.2 pmol oxygen consumed/min/microgram DNA vs 5.8 +/- 5.2 for controls, p less than 0.004) and glycolytic metabolism (44 +/- 10 ng lactic acid produced/90 min/microgram DNA vs 6 +/- 3 for controls, p less than 0.004). In the spared aortic segment distal to coarctation, glycolytic metabolism was increased (10 +/- 8 ng lactic acid produced/90 min/microgram DNA vs 2 +/- 1 for controls, p less than 0.05) but oxidative metabolism remained normal.(ABSTRACT TRUNCATED AT 250 WORDS)