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At least 1,693 records · Page 94Linked to original sources
PubMed2004

Arterial stiffness and endothelial dysfunction in HIV-infected children.

BACKGROUND: The role of antiretroviral therapy in acceleration of atherosclerosis in HIV-infected adults is controversial, partly because of the confounding effects of the involvement of classic cardiovascular risk factors. OBJECTIVE: To study vascular function in HIV-infected children. DESIGN: Cross-sectional study of 49 HIV-infected children (34 receiving antiretroviral therapy and 15 never treated) and if 24 age- and sex-matched controls. METHODS: Automatic, computerized, ultrasonic procedure evaluation of geometric and mechanical properties of the common carotid artery, and of the endothelium-dependent dilation and endothelium-independent dilation. RESULTS: Relative systolodiastolic variations in diameter of the carotid artery in HIV-infected children were significantly lower than those in controls, but there was no significant difference in intima-media thickness. Cross-sectional compliance and distensibility were also significantly lower. Wall stiffness, assessed as the incremental elastic modulus, was larger in HIV-infected children. Endothelium-dependent dilation was lower in HIV-infected children but non-endothelium-dependent dilation was similar to that in controls. We did not find differences for any of the vascular variables between HIV-infected children receiving antiretroviral therapy and those never treated. All arterial variables were similar in children with and without dyslipidemia. CONCLUSIONS: HIV-infected children had a vascular dysfunction in the absence of cardiovascular risk factors. In this short series, no additional detrimental effects were observed after a mean of 5 years of antiretroviral therapy.

Adolescent↗
PubMed2004

Uric acid, endothelial dysfunction and pre-eclampsia: searching for a pathogenetic link.

BACKGROUND: Pre-eclampsia is strongly associated with hyperuricemia, and in some studies the increase in serum uric acid has been found to correlate with both maternal and fetal morbidity. The hyperuricemia is believed to result primarily from the decreased renal excretion that occurs as a consequence of the pre-eclampsia, and as such is widely viewed as a marker for pre-eclampsia as opposed to having a role in the pathogenesis. HYPOTHESIS: We present the hypothesis that hyperuricemia may also have a contributory role in the development of hypertension and renal disease in these patients, and we review recent experimental data that would support this hypothesis. RECOMMENDATION: We suggest that studies addressing the role of uric acid in pre-eclampsia may provide new insights into both the pathogenesis and treatment of this condition.

Endothelium, Vascular↗
PubMed2002

Factors critical to iontophoretic assessment of vascular reactivity: implications for clinical studies of endothelial dysfunction.

Skin microvascular responses to iontophoresis of acetylcholine, an endothelium-dependent vasodilator, and sodium nitroprusside, an endothelium-independent vasodilator, were measured using a laser Doppler imager whose software controlled iontophoretic current delivery in an integrated fashion. A novel feature involved monitoring voltage across the iontophoresis chambers during current application (total charge: 8 mC). Both drugs elicited vasodilatation but with differing magnitudes and time courses, whereas current delivery with only vehicle (0.5% NaCl) present was ineffective. During drug delivery a three-to fourfold difference in calculated skin resistance was observed between subjects, with higher resistance being associated with lower dilator responses to both drugs. There was a significant (p < 0.0001) linear inverse correlation between perfusion.time and resistance.time integrals for both acetylcholine ( r = -0.86) and sodium nitroprusside ( r = -0.96). This was corrected in individual subjects by multiplying individual perfusion values by the resistance.time integral, which reduced response variability. Cyclooxygenase inhibition by aspirin apparently attenuated acetylcholine and sodium nitroprusside vasodilator responses but after correcting for skin resistance there was no longer any difference. Monitoring voltage across the iontophoretic circuit is critical, as effective drug delivery in individual subjects is influenced by the circuit resistance that can be corrected for. These findings have implications for clinical studies that use the iontophoresis technique for assessing vascular function.

Acetylcholine↗
PubMed2003

Vitamins C and E improve endothelial dysfunction in intrauterine-undernourished rats by decreasing vascular superoxide anion concentration.

Epidemiological studies suggest that intrauterine undernutrition plays an important role in the development of arterial hypertension in adulthood. Ascorbic acid (vitamin C) and alpha-tocopherol (vitamin E) have antioxidant properties that could improve redox-sensitive vascular changes associated with hypertension. The authors determined whether vitamins C and E treatments ameliorate the hypertension and vascular function in male rats submitted to intrauterine undernutrition. Pregnant Wistar rats were fed either normal or 50% of the normal intake diets during the whole gestational period. At 14 weeks of age, male offspring of nutritionally restricted dams were divided into 3 subgroups: vehicle-treated (vehicle for 15 days, by gastric gavage, n = 9), vitamin C-treated (ascorbic acid, 150 mg/Kg/d for 15 days, by gastric gavage, n = 15) and vitamin E-treated (alpha-tocopherol, 350 mg/kg per day for 15 days, by gastric gavage, n = 15). Systolic blood pressure was determined before and after antioxidant treatments by the tail-cuff method. At 16 weeks of age, the rats were used for the study of microvascular reactivity and intravital fluorescence microscopy. Intrauterine undernutrition induced hypertension, and vitamins C or E treatments reduced the blood pressure levels. The decreased acetylcholine and bradykinin-induced vasodilation was restored in the vitamin-treated rats. These effects were associated with decreased vascular superoxide anion concentration. The results show that vitamins C and E reduce oxidative stress and high blood pressure levels, and improve vascular function in intrauterine-undernourished rats.

Animals↗
PubMed1994

Coronary vasoconstriction in response to acetylcholine after balloon angioplasty: possible role of endothelial dysfunction.

BACKGROUND: Abnormal endothelium-dependent vasomotion has frequently been observed early after coronary angioplasty. The aim of this study was to investigate endothelium-mediated coronary vasomotion caused by increasing intracoronary infusions of acetylcholine into epicardial coronary arteries 3-6 months after coronary angioplasty in patients without restenosis (50% luminal diameter reduction). METHODS: Intracoronary acetylcholine was infused during follow-up coronary angiography followed by an intracoronary bolus of 250 g nitroglycerin in 18 patients who had undergone successful angioplasty of 21 isolated coronary artery lesions. Using an automated edge-detection program, coronary artery measurements were performed in the proximal reference segment, in the proximal part of the angioplasty site, at the site of previous maximal stenosis, in the distal part of the angioplasty site, and in the distal reference segment. RESULTS: In the segments of the coronary artery not manipulated by balloon catheter, acetylcholine did not produce significant luminal diameter changes (+2 +/- 23% in the proximal segment and -3 +/- 27% in the distal segment at 10(-4) mol/l). All the angioplasty vessel segments, excluding the proximal reference segments, showed an abnormal dose-related reactivity to the acetylcholine. Maximal vasoconstriction was observed at 10(-4) mol/l and was 4.9 +/- 11.1% in the proximal reference segment, 9.3 +/- 19.1% in the proximal angioplasty site (P = 0.0314), 20.3 +/- 24.1% at the site of previous maximal stenosis (P = 0.0005), 10.7 +/- 16.8% at the distal angioplasty site (P = 0.0098), and 9.3 +/- 14.1% in the distal reference segment (P = 0.0032). The maximal response of the angioplasty site to acetylcholine and to nitroglycerin did not correlate either with the time to follow-up or with the follow-up stenosis. Nitroglycerin-induced vasodilation was significant in all segments, but was lower in the lesion-related segments. Acetylcholine evoked the same effect on both the vessels that were manipulated and those that were not. CONCLUSIONS: Three to 6 months after coronary angioplasty, endothelium-dependent vasodilation was impaired not only at the site of previous maximal stenosis, but also in segments directly injured by balloon inflation. In contrast, endothelium-independent vasodilation by nitroglycerin is maintained in all segments. These observations suggest that the endothelium is still functionally impaired in the area of balloon dilation.

Acetylcholine↗
PubMed1995

Lipid-lowering treatment: effects on endothelial dysfunction.

An association has been demonstrated between the extent of atherosclerotic involvement and vasodilatory capacity in coronary and cerebral circulation. Impairment of endothelium-dependent relaxation is inversely related to HDL concentrations in plasma. Angiographic studies in humans have shown improved vasodilation capacity of the coronary arteries after lipid-lowering treatment.

Animals↗