N-acetylcysteine does not improve the endothelial and smooth muscle function in the human saphenous vein.

Oxidative stress can lead to vein graft dysfunction in the saphenous vein. This ex vivo study is aimed to compare the effects of increasing concentrations of the antioxidant N-acetylcysteine (NAC) with heparinized saline (HS) on endothelial and smooth muscle function in the human saphenous vein. Long saphenous vein segment obtained during infrainguinal bypass surgery was divided into 7 rings; 1 immersed in HS and the remaining 6 in increasing NAC concentrations (0.0025%, 0.005%, 0.01%, 0.02%, 0.03%, and 0.04%). Rings were mounted in an organ bath, and relaxant responses to acetylcholine and sodium nitroprusside were assessed through isometric tension studies. Endothelium-dependent relaxations were observed in 77 vein segments from 11 patients. No significant difference was seen in veins treated with either lower NAC concentrations (0.0025%, 0.005%, 0.01%, 0.02%, and 0.03%) or HS. However, HS-treated veins showed significantly better relaxation compared to those treated with maximum (0.04%) NAC (P < .05). Endothelium-independent relaxations were observed in 91 segments from 13 patients. No difference in relaxation was observed between veins treated with HS or any of the NAC concentrations. In conclusion, lower NAC concentrations do not offer better endothelial protection than HS, whereas the highest NAC concentration has a detrimental effect on endothelium-dependent relaxation. Moreover, NAC did not show beneficial effect on direct smooth muscle relaxation.

A rapid methodology for the isolation of intermediate-density lipoprotein: characterization of lipid composition and apoprotein content.

BACKGROUND: Intermediate-density lipoprotein (IDL) is a structurally related precursor of low-density lipoprotein (LDL). Although found in significantly lower levels, extensive evidence suggests that IDL shares LDL's capacity to promote atherosclerosis. To assist further investigation into IDL's composition and physiological relevance, we have established a rapid method to extract IDL from plasma. METHODS: IDL was isolated from plasma by sequential floatation ultracentrifugation in 3 h, a significantly shorter isolation time than previously published methods. Apoproteins (apo) B100, CIII, and E, together with the level of albumin contamination, were quantified using single radial immunodiffusion. The lipid composition of IDL was measured using automated enzyme assays. RESULTS: The percent recovery of lipid from all lipoprotein fractions (VLDL+IDL+LDL+HDL) was 97.0+/-4.9% when compared to total plasma lipid. IDL had a reduced concentration of apo CIII, apo E, triglyceride, and free cholesterol, and had a higher concentration of apo B100, cholesterol ester, and phospholipid when compared to VLDL. Pure IDL migrated in advance of LDL during agarose electrophoresis. CONCLUSIONS: This rapid technique minimizes damage to the integrity of IDL and yields sufficient quantities to allow accurate assessment of composition and susceptibility to in vitro oxidation, and thus facilitates further investigation of IDL in the development of atherosclerosis.