Studies on the permeability to lipids and lipoproteins of inflamed skin capillaries (Cantharidine-blister-fluid) in hyperlipoproteinemias (Type II a/b,IV)

Abstract

One factor in the pathogenesis of atherosclerosis is an alteration in permeability to lipids and lipoproteins in the wall of the greater vessels, of the arterioles and of capillaries. A model to study the permeability of capillaries is the cantharidine blister fluid (CBF) and the filtrate which is passing through the membrane of the cantharidine-blister-base after applying negative pressure from 40 to 100 torr.

The concentration of lipids etc. is lower in the blister fluid than in the serum. There is no relation between the sieving quotient C2/C1 of proteins (0,65) and of lipids in type IIa (0,49), in type lIb (0,41), and in type IV (0,38). The concentration of lipids and lipoproteins in the CBF was not strictly correlated to those of the serum. In type IV the diffusion of the TG was more restricted (0,39) than in type IIb/a (0,40). The three fractions of lipoproteins (LDL, VLDL, HDL) had nearly the same relative distribution in the CBF as in the serum. The percentage of LDL and VLDL was in the CBF lower than in the serum. There is no difference of concentration for the HDL between both fluids. The sieving quotient C2/C1 for the lipoproteins etc. was different in the three HLP-types. TG, VLDL, CH and LDL were mostly restricted in type IV (C2/C1: TG = 0,39, VLDL = 0,38, CH = 0,36, LDL = 0,35). But the concentration of CH and LDL in the CBF was greater in type IIa/b than in type IV. The volume of capillary filtrate (ml/cm₂/min/mm Hg) was proportional to the negative pressure. With increasing filtrate volume the concentrations of lipids etc. decreased especially those of cholesterol and LDL. High blood pressure restricts the diffusion of cholesterol and LDL and promotes the deposition of these lipids in the vascular wall.