It has been reported that systemic hypoxia aggravates the development of atherosclerotic lesions and systemic hyperoxia regresses it, but the mechanisms are not known. The aim of this report is to investigate, in in-vivo, the effects of hypoxic inhalation or hyperoxic inhalation on the rabbits with dietary hypexcholesterolemia or with spontaneous hyperlipidemia from birth for 8 weeks, and to.investigate, in in-vitro, the effects of 2% O2 on the cells which are cultured in the EME medium supplemented with 20% hyperlipidemic rabbits serum or 20% normolipidemic rabbits serum. The following results were obtained.
1) From in-vivo experiments, atherosclerotic lesions were accelerated by the inhalation of 10% oxygen (hypoxic) and regressed by the inhalation of 40% oxygen (hyperoxic).
2) Lipoperoxide levels in plasma were increased by the oxygen inhalation, but the increments were much higher in hypoxic condition than in hyperoxic condition.
3) There were significant correlation between the %-aortic lesions and the lipoperoxide contents ln aorta.
4) The contents of hydroxyprolin in aorta, precursor of collagen, were much higher in hypoxicgroup than hyperoxic group.
5) From in-vitro experiments, esterified cholesterol contents in the cells under the hypoxic condition were raised 2-3 fold as much as those in control, when the cells were incubated in the medium supplemented with hyperlipidemic glasma.
6) Lipoperoxide contents in the cell were increased under the hypoxic condition and reversed by the addition of antioxidant, a-tocopherol, under the identical condition.
From these results, we conclude that the development of atherosclerotic lesions is aggravated by the accumulation of esterified cholesterol and lipoperoxide in the cells surrounded by the hyperlipidemia under the hypoxic condition.
