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- W2404018681 abstract "UNLABELLED The main changes of the plasma lipid profile patients with endothelial dysfunction are the increased triglyceride content of the lipoprotein remnant particles, the presence of the small and dense LDL particles and the decreasing of the HDL-cholesterol level. MATERIAL AND METHOD Considering these observations, we performed in vitro experiments using human mammary artery rings, order to examine the effect of the lipoprotein on endothelium-dependent vasodilatation induced by cumulative doses (10(-9) M - 10(-4) M) of adenosine (ADP) and to study the effect on endothelial--independent vasodilatation induced by cumulative doses (10(-9) M-10(-4) M) of sodium-nitropruside (NSP), respectively. RESULTS Our results showed that 1 hour pre-incubation with triglyceride--rich lipoprotein remnants diminished the endothelial-dependent vasodilator response to ADP, but it has not modified the endothelial-independent vasodilator response to NSP. Vascular response was expressed as maximal vasodilatation from the 10(-4)M phenilephrine (PE) induced pre-contraction, considered as reference. In the case of ADP, the maximal vasodilatation was ranged 36.50% +/- 10.81% interval, comparing with the control group that presented a maximal vasodilatation of 66.15% +/- 19.41% (p < 0.005). In the case of NSP the maximal vasodilatation was ranged 99.78% +/- 10.53% interval, comparing with the control that presented a maximal vasodilatation of 98.99% +/- 12.45% (p = 0.44). One hour co-incubation of the rings with a solution containing lipoprotein remnants (1% oxidized IDL (ox-IDL) and antioxidant factor (150 U/mL 10(-4) M Superoxid dismutase (SOD) significantly reduced the impairment of the vasodilatation response to ADP. Maximal vasodilatation of ox-IDL and SOD coincubated human mammary artery rings was 58.50% +/- 10.63% compared to the control, were the maximal vasodilatation was 66.15% +/- 19.41% (p < 0.01), but has not modified the vasodilatation response to NSP (99% +/- 0.53% vs control 98.99% +/- 12.45%, p = 0.56). CONCLUSION The endothelial dysfunction induced by the triglyceride-rich lipoprotein remnants, could contribute to the pathogenesis of atherosclerosis and the treatment with high doses of antioxidants could protect the endothelium against the pro-atherogenic action of the lipoprotein remnants." @default.
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- W2404018681 date "2009-10-01" @default.
- W2404018681 modified "2023-10-04" @default.
- W2404018681 title "The protective effect of superoxide dismutase on isolated human mammary arteries preincubated with triglyceride-rich remnant lipoproteins." @default.
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