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COI with an IAP of 10 mmHg may be deleterious in animals with hemorrhagic shock due to an intraabdominal lesion. These findings could be clinically significant in abdominal trauma patients.

The biodistribution and removal from plasma (measured as fractional clearance rate, FCR, per hour) of native and oxidatively modified 99m technetium-labeled ß-very low density lipoprotein ( 99m Tc-ß-VLDL) were investigated in hypercholesterolemic (HC) and control (C) threemonth old New Zealand rabbits. The intracellular accumulation of ß-VLDL labeled with 99m Tc was studied in vitro in THP-1 cells and monocyte-derived macrophages isolated from rabbits. After intravenous injection into C rabbits, copper-oxidized ß-VLDL ( 99m Tc-ox-ß-VLDL) was cleared from the circulation faster (0.362 ± 0.070/h) than native ß-VLDL ( 99m Tc-nat-ß-VLDL, 0.241 ± 0.070/h). In contrast, the FCR of 99m Tc-ox-ß-VLDL in HC rabbits was lower (0.100 ± 0.048/h) than that of 99m Tc-nat-ß-VLDL (0.163 ± 0.043/h). The hepatic uptake of radiolabeled lipoproteins was lower in HC rabbits (0.114 ± 0.071% injected dose/g tissue for 99m Tc-nat-ß-VLDL and 0.116 ± 0.057% injected dose/g tissue for 99m Tc-ox-ß-VLDL) than in C rabbits (0.301 ± 0.113% injected dose/g tissue for 99m Tc-nat-ß-VLDL and 0.305 ± 0.149% injected dose/g tissue for 99m Tc-ox-ß-VLDL). The uptake of 99m Tc-nat-ß-VLDL and 99m Tc-ox-ß-VLDL by atherosclerotic aorta lesions isolated from HC rabbits ( 99m Tc-nat-ß-VLDL: 0.033 ± 0.012% injected dose/g tissue and 99m Tc-ox-ß-VLDL: 0.039 ± 0.017% injected dose/g tissue) was higher in comparison to that of non-atherosclerotic aortas from C rabbits ( 99m Tc-nat-ß-VLDL: 0.023 ± 0.010% injected dose/g tissue and 99m Tc-ox-ß-VLDL: 0.019 ± 0.010% injected dose/g tissue). However, 99m Tc-nat-ß-VLDL and 99m Tc-ox-ß-VLDL were taken up by atherosclerotic lesions at similar rates. In vitro studies showed that both monocyte-derived macrophages isolated from rabbits and THP-1 macrophages significantly internalized more 99m Tc-ox-ß-VLDL than 99m Tc-nat-ß-VLDL. These results indicate that in cholesterol-fed rabbits 99m Tc-ox-ß-VLDL is slowly cleared from plasma and accumulates in atherosclerotic lesions. However, although the extent of in vitro uptake of 99m Tc-ox-ß-VLDL by macrophages was high, the in vivo accumulation of this radiolabeled lipoprotein by atherosclerotic lesions did not differ from that of 99m Tc-nat-ß-VLDL.

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