THE ANTIOXIDANT FACTORS REDUCED THE IMPAIRMENT OF ENDOTHELIAL-DEPENDENT VASODILATATION IN ISOLATED HUMAN MAMMARY ARTERIES PREINCUBATED WITH TRIGLYCERIDE-RICH REMNANT LIPOPROTEINS

GERMAINE SĂVOIU*, LAVINIA NOVEANU**, O. FIRA-MLADINESCU*, CORINA GORUN*, SIMONA DRĂGAN***, SILVIA MIRICA*, CORNELUŢA FIRA-MLADINESCU****, CĂLIN MUNTEAN*****, DANINA MUNTEAN*, GEORGETA MIHALA

*Department of Physiopathology, “Victor Babeş” University of Medicine and Pharmacy, Timişoara,
**Department of Physiology, “Victor Babeş” University of Medicine and Pharmacy, Timişoara,
*** Department of Preventive Cardiology and Rehabilitation, “Victor Babeş” University of Medicine and Pharmacy, Timişoara
****Research Centre of Preventive Medicine, “Victor Babeş” University of Medicine and Pharmacy, Timişoara,
*****Department of Medical Informatics, “Victor Babeş” University of Medicine and Pharmacy, Timişoara

Abstract. The main changes of the plasma lipid profile in 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. Considering these observations, we performed in vitro experiments using human mammary artery rings, in order to examine the effect of the lipoprotein „remnants” on endothelium-dependent vasodilatation induced by cumulative doses (10–9–10–4 M) of adenosine (ADP) and to study the effect on endothelial-independent vasodilatation induced by cumulative doses (10–9–10–4 M) of sodium-nitropruside (SNP), respectively. 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 SNP. Vascular response was expressed as maximal vasodilatation from the 10–5 M phenilephrine (PE) induced pre-contraction, considered as reference. In the case of ADP, the maximal vasodilatation was ranged in 14.39% ± 5.80% interval, comparing with the control group that presented a maximal vasodilatation of 64.3% ± 15.80% (p ≤ 0.001). In the case of SNP the maximal vasodilatation was ranged in 93.33% ± 7.36% interval (p ≤ 0.001), comparing with the control that presented a maximal vasodilatation of 95.86% ± 3.48% (p = 0.46). One hour co-incubation of the rings with lipoprotein „remnants” and antioxidant factors, such as 10–3 M reduced glutathione (GSH) or 10–3 M ascorbic acid significantly reduced the impairment of the vasodilatation response to ADP (p = 0.02 for GSH, and p = 0.008 for ascorbic acid) but has not modified the vasodilatation response to SNP. As a 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”.
Key words: endothelial dysfunction, lipoproteic remnants, antioxidant factors.

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