HYPOALBUMINEMIA CAUSES HIGH BLOOD-VISCOSITY BY INCREASING RED-CELL LYSOPHOSPHATIDYLCHOLINE

Albumin deficiency is accompanied by a reduction in red cell deformabi lity and blood hyperviscosity. Albumin deficiency increases plasma fib rinogen and triglyceride levels and may alter red cell membrane lipid composition. These options, which could all contribute to reduced red cell deformability (RCD) and hyperviscosity, were studied in the Nagas e analbuminemic rat (NAR), a mutant Sprague Dawley rat (CON), characte rized by normal total protein levels, with an absolute deficiency of a lbumin, but elevated levels of non-albumin proteins and hyperlipidemia . Plasma protein-binding of the polar phopholipid lysophosphatidylchol ine (LPC) was markedly decreased. LPC comprised only 26 +/- 1% of tota l plasma phospholipids as compared to 42 +/- 2% in CON. NAR red cells in CON plasma had a viscosity that was similar to CON red cells in CON plasma. Conversely, CON red cells in NAR plasma show an increased vis cosity as compared to CON red cells in CON plasma. The maximum deforma tion index of bath NAR and CON red cells was markedly decreased in NAR plasma as compared to either NAR or CON cells in CON plasma (0.04 +/- 0.03 and 0.02 +/- 0.02 vs. 0.22 +/- 0.06 and 0.15 +/- 0.04, respectiv ely; P < 0.05). Thus, plasma composition causes hyperviscosity and red uced RCD in NAR. Fibrinogen is not responsible since red cells in seru m and red cells in plasma had a similar viscosity and differences in v iscosity and RCD between NAR and CON were maintained. Plasma triglycer ides are also not responsible since the viscosity of red cells in seru m with a 50% reduction in triglycerides was not reduced. LPC levels in red cells were increased in NAR (8.7 +/- 0.2 vs. 5.5 +/- 0.3% of tota l phospholipids; P < 0.01). Adding albumin to NAR blood dose-dependent ly decreased whole blood viscosity, despite marked increases in plasma viscosity, and increased RCD of NAR cells (from 0.04 +/- 0.03 to 0.21 +/- 0.01; P < 0.05). There was also some effect on CON RCD of similar albumin addition to CON blood (from 0.15 +/- 0.04 to 0.29 +/- 0.03; P < 0.05). Adding albumin to NAR blood reduced red cell LPC content and increased plasma LPC content in a dose-dependent fashion, whereas the re were only slight effects of adding albumin to CON blood. There was a reciprocal relation between red cell LPC and the other polar phospho lipids in the red cell membrane, probably indicating exchange. The max imum deformability index of either NAR or CON cells was not affected m uch by adding LPC to CON plasma (NAR, from 0.22 +/- 0.06 to 0.18 +/- 0 .10; CON, from 0.15 +/- 0.04 to 0.12 +/- 0.05; NS), whereas adding LPC to NAR plasma caused the red cells to become rigid. Adding LPC to CON red cells in NAR plasma caused a much stronger increase in relative L PC content (from 6.6 +/- 0.7 to 10.9 +/- 0.9%; P < 0.05) than adding L PC to CON red cells in CON plasma (from 5.6 +/- 0.4 to 6.4 +/- 0.8%; N S). Thus, in the absence of albumin, LPC in red blood cells is increas ed. As a consequence of the latter, RCD is decreased and whole blood v iscosity increased. Alterations in red cell phospholipids are far more important than increases in plasma fibrinogen or triglycerides in det ermining hyperviscosity of blood and reduced RCD in NAR.