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PubMed2004

Overweight in children is associated with arterial endothelial dysfunction and intima-media thickening.

OBJECTIVE: We sought to study arterial endothelial function and carotid intima-media thickness (IMT), both early markers of atherosclerosis, in overweight compared to normal children. DESIGN: Case-control comparison. SUBJECTS: A total of 36 asymptomatic overweight children (body mass index (BMI)>23; mean 25+/-3) aged 9-12 y and 36 age- and gender-matched nonobese healthy children (BMI<21) from a school community. MEASUREMENTS: The key parameters were: BMI, arterial endothelial function (ultrasound-derived endothelium-dependent dilation) and carotid artery IMT. The secondary parameters measured included body fat content, waist-hip ratio (WHR), blood pressures, blood lipids, insulin and glucose. RESULTS: The two groups were well matched for blood pressures, cholesterol and glucose levels, but BMI (P<0.0001), body fat (P=0.001), WHR (P<0.05), fasting blood insulin (P=0.001) and triglyceride levels (P<0.05) were higher in obese children. Overweight was associated with impaired arterial endothelial function (6.6+/-2.3 vs 9.7+/-3.0%, P<0.0001) and increased carotid IMT (0.49+/-0.04 mm vs 0.45+/-0.04 mm, P=0.006). The degree of endothelial dysfunction correlated with BMI (P<0.003) on multivariate analysis. CONCLUSION: Obesity, even of mild-to-moderate degree, is independently associated with abnormal arterial function and structure in otherwise healthy young children.

Anthropometry↗

PubMed2002

Peroxisome proliferator ameliorates endothelial dysfunction in a murine model of hyperhomocysteinemia.

To test the hypothesis that endothelial dysfunction in hyperhomocysteinemia was due to increased levels of nitrotyrosine and matrix metalloproteinase (MMP) activity in response to antagonism of peroxisome proliferator-activated receptor-alpha (PPAR-alpha), cystathionine beta-synthase (CBS) -/+ mice were bred, tail tissue was analyzed for genotype by PCR, and tail vein blood was analyzed for homocysteine (Hcy) by spectrofluorometry. To induce PPAR-alpha, mice were administered 8 microg/ml of ciprofibrate (CF) and grouped: 1) wild type (WT), 2) WT + CF, 3) CBS, 4) CBS + CF (n = 6 in each group). In these four groups of mice, plasma Hcy was 3.0 +/- 0.2, 2.5 +/- 1.2, 15.2 +/- 2.6 (P < 0.05 compared with WT), 11.0 +/- 2.9 micromol/l. Mouse urinary protein was 110 +/- 11, 86 +/- 6, 179 +/- 13, 127 +/- 9 microg.day(-1). kg(-1) by Bio-Rad dye binding assay. Aortic nitrotyrosine was 0.099 +/- 0.012, 0.024 +/- 0.004, 0.132 +/- 0.024 (P < 0.01 compared with WT), 0.05 +/- 0.01 (scan unit) by Western analysis. MMP-2 activity was 0.053 +/- 0.010, 0.024 +/- 0.002, 0.039 +/- 0.009, 0.017 +/- 0.006 (scan unit) by zymography. MMP-9 was specifically induced in CBS -/+ mice and inhibited by CF treatment. Systolic blood pressure (SPB) was 90 +/- 2, 88 +/- 16, 104 +/- 8 (P < 0.05 compared with WT), 96 +/- 3 mmHg. Aortic wall stress [(SPB. radius(2)/wall thickness)/2(radius + wall thickness)] was 10.2 +/- 1.9, 9.7 +/- 0.2, 16.6 +/- 0.8 (P < 0.05 compared with WT), 13.1 +/- 2.1 dyn/cm(2). The results suggest that Hcy increased aortic wall stress by increasing nitrotyrosine and MMP-9 activity.

Animals↗

PubMed2006

Endothelial dysfunction in MELAS improved by l-arginine supplementation.

The authors evaluated endothelial function in patients with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke) by flow-mediated vasodilation (FMD) and found a significant decrease vs controls. Two years of supplementation with oral l-arginine, a nitric oxide precursor, significantly improved endothelial function to control levels and was harmonized with the normalized plasma levels of l-arginine in patients. l-Arginine therapy improved endothelial dysfunction and showed promise in treating strokelike episodes in MELAS.

Administration, Oral↗

PubMed2003

Weight loss in combination with physical activity improves endothelial dysfunction in human obesity.

OBJECTIVE: To test whether weight loss may improve endothelial dysfunction in human obesity, we recruited 28 healthy obese subjects, aged 30-46 years, with BMI 30-43 kg/m(2). RESEARCH DESIGN AND METHODS: Endothelium-dependent and -independent vasodilation were investigated by intra-arterial infusion of increasing doses of acetylcholine (ACh; 7.5, 15, and 30 microg x ml(-1) x min(-1)) and sodium nitroprusside (0.8, 1.6, and 3.2 microg x ml(-1) x min(-1)). Insulin resistance was estimated by homeostasis model assessment (HOMA). Weight loss was obtained by caloric restriction and physical activity. RESULTS: We observed a significant reduction in BMI (from 33.1 +/- 4.2 to 27.5 +/- 4.5 kg/m(2), -16.9%, P < 0.0001) and in waist circumference (from 108.2 +/- 12.1 to 96.8 +/- 12.9 cm, -10.5%, P < 0.0001). Weight loss was also associated with a significant increase in ACh-stimulated forearm blood flow (FBF), from 7.4 +/- 2.8 to 12.9 +/- 3.4 ml. 100 ml(-1) of tissue x min(-1) kg/m(2) (P < 0.0001). Multivariate regression analysis demonstrated that the only independent predictor of FBF was HOMA, accounting for 44.5% of the variation, whereas the addition of BMI explained another 2.3% of the variation. CONCLUSIONS: Our data demonstrate that energy-restricted diet associated with physical activity induce a significant and clinically relevant improvement in ACh-stimulated vasodilation in obese healthy subjects.

Acetylcholine↗

PubMed1995

[In vitro endothelial dysfunction after cold storage: comparison with various preservative solutions].

Optimal solution for endothelial function preservation during cold storage for organ transplant has not yet been defined. To assess this issue, rat aortic rings (n = 28) were stored for 4 hours at 4 degrees C in different preservation solutions: Krebs Ringer (KR), normal saline (NS), rat blood (RB), and the University of Wisconsin solution (UW). Subsequently, rings were suspended in organ chambers for endothelial and smooth muscle assessment. Endothelial-dependent relaxation responses were tested by exposure to cumulative doses of acetylcholine (ACH), adenosine diphosphate (ADP), and histamine (HIS). Smooth muscle function was evaluated by exposure to norepinephrine (NE) and sodium nitroprusside (SNP). A fifth group not submitted to a storage period was used as control (CTL, n = 7). Results are expressed as maximal relaxation (%) from initial precontraction level. Compared to the CTL group, all storage groups showed a significant decrease in endothelial-dependent relaxations to ACH, ADP and HIS (p < 0.05). Among the stored groups, endothelial-dependent relaxation to ACH was significantly decreased in the NS group when compared to the UW group (p < 0.05). Endothelial-independent relaxation to SNP was comparable for all groups. However significant hypercontractility to NE was observed for all stored groups compared to the control group (p < 0.01). A significant decrease in ADP response was observed with NS and RB storage when compared to KR (p < 0.01). In conclusion, cold storage affects both endothelial and smooth muscle function by decreasing endothelial-dependent responses to ACH, ADP and HIS and increasing smooth muscle reactivity to NE. However, endothelial dysfunction was lessened with UW or KR storage compared to NS or RB.

Adenosine↗

PubMed2000

[Endothelial dysfunction and injury of placental and umbilical vessels in pregnancy-induced hypertension is associated with tumor necrosis factor].

OBJECTIVE: To investigate the relation between endothelial dysfunction and injury of placental and umbilical vessels in pregnancy-induced hypertension (PIH) and tumor necrosis factor (TNF). METHODS: The concentration of plasma TNF, endothelin (ET) and nitric oxide (NO) in PIH women and normal pregnant women (control group) were measured. The ultrastructure of placenta and umbilical vein endothelial cells in PIH and normal pregnant women was observed. The ultrastructure of endothelial cells in culture with TNF (400 u/ml) was also observed. RESULTS: Maternal plasma TNF and ET levels in PIH patients were (2.27 +/- 0.42) micrograms/L and (73.31 +/- 9.98) ng/L, respectively, higher than that in the control [TNF and ET lever were (1.72 +/- 0.25) micrograms/L and (2.32 +/- 10.44) ng/L, respectively]. NO level in PIH patients was (104.93 +/- 20.54) mumol/L, lower than that in the control [NO lever was (138.25 +/- 22.16) mumol/L] (P < 0.05). The ultrastructure of placental and umbilical vascular endothelial cells in moderate and severe PIH patients revealed injured. Similar injury was observed in endothelial cells in culture with TNF. CONCLUSIONS: TNF can induce the endothelial cells dysfunction and injury. It may be involved the pathogenesis of PIH.

Adult↗

PubMed1997

Endothelial dysfunction and hypertension.

Vascular endothelial cells play a key role in cardiovascular regulation by producing a number of potent vasoactive agents, including the vasodilator molecule nitric oxide (NO) and the vasoconstrictor peptide endothelin (ET)-1. A dysfunction of the vascular endothelium has been implicated in the pathophysiology of a number of cardiovascular diseases, important among which is essential hypertension. Impairment of NO synthesis, or increased inactivation of NO by superoxide radicals, may account for the increased peripheral vascular tone associated with hypertension, as well as contribute to the clinical consequences of this condition, which include vascular hypertrophy, increased platelet and monocyte adhesion to the endothelium, atherosclerosis, myocardial infarction and stroke. Similarly, increased ET-1 synthesis, or increased smooth muscle sensitivity to ET-1, could account for many of the features of hypertension, including increased peripheral vascular tone and vascular hypertrophy. Modulation of endothelial function is, therefore, an attractive therapeutic option in the treatment of hypertension. Calcium antagonists have been shown to enhance the effects of NO, and inhibit those of ET-1, on vascular smooth muscle cells. In addition, calcium antagonists have antiatherogenic and antioxidant properties and could, therefore, prove to be useful therapeutic agents in preventing some of the important complications of hypertension. The long term effects on cardiovascular morbidity and mortality of the long-acting nifedipine gastrointestinal therapeutic system (nifedipine GITS) used in the treatment of essential hypertension are currently being investigated in the first multinational outcome study (INSIGHT) of an antihypertensive agent since the major studies of beta-adrenoceptor blockers or thiazide diuretics. The results of this study are awaited with considerable interest.

Calcium Channel Blockers↗

PubMedDate not supplied

Vascular endothelial dysfunction.

Injury or activation of the endothelium changes its regulatory functions and results in abnormal endothelial cell function. Dysfunction of the endothelium has been defined as an imbalance between relaxing and contracting factors, between procoagulant and anticoagulant mediators or between growth-inhibiting and growth-promoting substances. The first part of this review describes endothelial dysfunction in hypercholesterolemia, and atherosclerosis in intimal thickening induced by perivascular and intravascular techniques. We focus on the implications of endothelial dysfunction in these conditions and the role of nitric oxide, endothelium-dependent hyperpolarization, endothelin, cytokines, adhesion molecules, growth factors, and thrombosis. In the second part, the endothial dysfunction in other diseases including hypertension, syndrome X, and diabetes is discussed. Finally, a short overview of therapeutic approaches of the dysfunctional endothelium is given.

Angioplasty, Balloon↗

PubMed2006

Endothelial dysfunction and impaired L-arginine transport in hypertension and genetically predisposed normotensive subjects.

The term endothelial dysfunction (ED) generally refers to a pathological circumstance in which normal endothelial regulation of vasomotor tone is disturbed. ED has been described in a broad range of cardiovascular and related disease states. In association, deranged endothelial function also has the potential to result in abnormal platelet aggregation and monocyte adhesion. Over the past decade, it has become apparent that reduced availability of nitric oxide is a key mechanism for ED. A range of biochemical disturbances, including depressed L-arginine, have been shown to be associated with ED, and recent evidence indicates this may be genetically determined.

Arginine↗

PubMed2002

Aldosterone induces acute endothelial dysfunction in vivo in humans: evidence for an aldosterone-induced vasculopathy.

Experimental studies have suggested a role for aldosterone and glucocorticoids in the pathogenesis of endothelial dysfunction. We therefore set out to characterize the acute effects of these hormones on vascular function in vivo in normal humans. A randomized, placebo-controlled, double-blind crossover study was performed on 16 healthy male volunteers (aged 19-29 years), examining the vascular effects of acute intravenous aldosterone infusion (12 pmol.min(-1).kg(-1) for 4 h) and of oral prednisolone (single 50 mg dose). Peripheral arterial vascular function was assessed by bilateral forearm venous occlusion plethysmography using two parallel study protocols. In the first protocol, eight subjects received, successively, acetylcholine, sodium nitroprusside, noradrenaline, angiotensin I and angiotensin II. The remaining eight subjects received, successively, acetylcholine, sodium nitroprusside, verapamil and noradrenaline. Aldosterone attenuated endothelium-dependent vasodilatation to acetylcholine as compared with either prednisolone or placebo (maximum vasodilatation: placebo, 357+/-38%; aldosterone, 257+/-21%; P <0.05). However, background endothelium-independent vasodilatation was not affected by either aldosterone or prednisolone. There were also no significant changes in vasoconstriction induced by angiotensin or noradrenaline following aldosterone or prednisolone treatment compared with placebo. Blood pressure and baseline blood flow did not differ between any of the study phases. Thus acute short-term systemic administration of aldosterone results in endothelial vasodilator dysfunction in normal men, providing evidence for an aldosterone-induced vasculopathy, which may be particularly relevant not only in heart failure but also in hypertensive patients with high aldosterone/renin ratios.

Adult↗

PubMed2003

Vascular endothelial dysfunction in aging: loss of Akt-dependent endothelial nitric oxide synthase phosphorylation and partial restoration by (R)-alpha-lipoic acid.

Aging is the single largest risk factor for cardiovascular diseases, which in turn are the leading cause of death of individuals over the age of 65 years. In part, this risk is due to a profound loss of vasomotor function of the major conduit arteries, primarily because of lower levels of endothelial-derived nitric oxide. The mechanisms involved in vascular dysfunction are not entirely understood, but age-related alterations in eNOS (endothelial nitric oxide synthase) activity appear to be a likely source of the aging lesion. However, age-related changes in cell signalling that ultimately affect eNOS phosphorylation and its activity have not been explored. Results in our laboratory indicate that levels of eNOS phosphorylation in aortas from aged F344xBN rats (28-30 months old) are almost 50% lower than in aortas from young animals (3 months old). Lower eNOS phosphorylation is directly attributable to loss of constitutive Akt/protein kinase B activity. The decline in eNOS phosphorylation can be partially restored by treating old rats with (R)-alpha-lipoic acid. These results thus suggest that age-related changes in eNOS phosphorylation may be a significant factor in the overall loss of vasomotor function in the elderly.

Aging↗

PubMedDate not supplied

Correction of endothelial dysfunction in coronary microcirculation of hypercholesterolaemic patients by L-arginine.

Hypercholesterolaemia impairs endothelial function, possibly by interference with the intracellular formation of endothelium-derived relaxing factor from its precursor L-arginine. Whether L-arginine reverses hypercholesterolaemia-induced endothelial dysfunction in the coronary circulation was thus investigated. Epicardial artery cross-sectional area and coronary blood flow velocity were measured in 8 hypercholesterolaemic patients (mean serum cholesterol 7.8 [SE 0.3] mmol/l) and 7 age-matched controls before and after graded intracoronary infusions of the endothelium-dependent agent acetylcholine (0.036, 0.36, 3.6 micrograms/min). The effect of intracoronary infusion of L-arginine (160 mumol/min via the guiding catheter) on these measurements was then examined. In controls, acetylcholine induced a moderate dose-dependent constriction of the epicardial artery segment of the left anterior descending artery and increased coronary blood flow (by 239% [SE 57] at the highest dose). In patients with hypercholesterolaemia, the vasoconstrictive effect of acetylcholine on epicardial segments was similar to that in controls, but the increase in coronary blood flow with acetylcholine was significantly attenuated (highest dose: 61%, p less than 0.02 vs controls). L-arginine restored the acetylcholine-induced increase in blood flow in patients with hypercholesterolaemia (198% [61] vs baseline) but did not affect coronary blood flow in controls. The findings suggest that hypercholesterolaemia impairs endothelium-dependent dilatation of the coronary microcirculation and that this impairment can be restored by short-term administration of L-arginine. The possibility that L-arginine might form the basis of treatment for coronary endothelial abnormalities induced by hypercholesterolaemia could be worth investigating.

Acetylcholine↗

PubMed2004

Doxycycline ameliorates ischemic and border-zone remodeling and endothelial dysfunction after myocardial infarction in rats.

BACKGROUND: Although matrix metalloproteinase (MMP) activity increases, endothelial function decreases after myocardial infarction (MI). The antibiotic doxycycline inhibits MMP activity in vitro. The role of doxycycline-mediated MMP inhibition in endothelial function is unclear. HYPOTHESIS: Doxycycline ameliorates endothelial dysfunction, in part, by inhibiting MMP activity. METHODS: We subjected Sprague-Dawley male rats to MI by ligating the left anterior descending arteries. We subjected another group of rats to sham surgery. We administered doxycycline in drinking water (0.67 mg/ml) to both groups 2 days before surgery: the sham group underwent sham surgery and received doxycycline therapy, and the MI group underwent MI and received doxycycline therapy (n = 6 in each group). After 4 weeks, we anesthetized rats and prepared left ventricular rings from infarcted-ischemic (I), non-infarcted near-infarcted (NI), and sham surgery hearts with and without doxycycline treatment. RESULTS: The MMP-2 activity increased significantly in I and NI hearts, and we observed a selective increase in MMP-9 activity only in I hearts, when compared with other groups (p < 0.05), measured by zymography. Cardiac inhibitor of metalloproteinase decreased only in I hearts (p < 0.05 vs other groups), measured by Western analysis, and doxycycline treatment reversed this decrease. Contractile response of rings to acetylcholine was attenuated in the I group, suggesting nitric oxide-mediated dysfunction, and was reversed by doxycycline. The response to nitroprusside was attenuated in I hearts and ameliorated by doxycycline, suggesting cardiomyocyte dysfunction. Bradykinin induced relaxation in rings from sham surgery hearts and from NI hearts, but induced paradoxic contraction in rings from I hearts. Treatment with doxycycline reversed the paradoxic contraction. CONCLUSION: Results suggest a protective action of doxycycline in the ischemic heart, possibly because of additional pharmacologic actions such as metalloproteinase inhibition.

Animals↗

PubMed2003

Tetrahydrobiopterin attenuates homocysteine induced endothelial dysfunction.

Homocysteine is an independent risk factor for atherosclerotic vascular disease. It impairs endothelial function via increasing superoxide production and quenching nitric oxide (NO) release. Tetrahydrobiopterin (BH4) is a critical cofactor that couples nitric oxide synthase and facilitates the production of nitric oxide (vs. superoxide anions). In the first study, the effects of hyperhomocysteinemia (0.1 mM, 3 h) on endothelium-dependent vasorelaxation to ACh and A23187 were examined in isolated segments of rat aortae in the presence or absence of BH4 (0.1 mM). In the second study, the effects of hyperhomocysteinemia (24 h) on nitric oxide production and superoxide release (using lucigenin chemiluminescence) were studied in human umbilical vein endothelial cells in the absence or presence of BH4 (10 microM). Homocysteine incubation impaired receptor-dependent and -independent endothelial function to ACh and A23187. This effect was attenuated by BH4. Furthermore, homocysteine exposure increased superoxide production and impaired agonist-stimulated nitric oxide release. These effects were attenuated by BH4 (p < 0.05). Hyperhomocysteinemia impairs endothelial function, in part due to a diminished bioavailability of BH4 with resultant uncoupling of nitric oxide synthase. BH4 may represent an important target for strategies aimed at improving endothelial dysfunction secondary to hyperhomocysteinemia.

Acetylcholine↗

PubMed2005

Radiation induces endothelial dysfunction in murine intestinal arterioles via enhanced production of reactive oxygen species.

OBJECTIVE: Endothelial dysfunction and vascular dysregulation contribute to the pathological effects of radiation on tissues. The objectives of this study were to assess the acute effect of irradiation on acetylcholine (Ach)-induced dilation of gut submucosal microvessels. METHODS AND RESULTS: Rats were exposed in vivo to 1 to 9 cGy in 3 fractions per week on alternate days for 3 successive weeks for a total dose of up to 2250 cGy. Submucosal microvessels were isolated after varying levels of irradiation. Diameters of isolated vessels were measured using videomicroscopy, and the dose-response relationship to Ach was determined. Dihydroethidine and 2', 7'-dichlorodihydrofluorescein diacetate fluorescent probes were used to assess reactive oxygen species (ROS) production. After constriction (30% to 50%) with endothelin, dilation to graded doses of Ach (10(-9)-10(-4) M) was observed in control vessels (maximal dilation [MD] 87+/-3%; n=7). However, Ach-induced dilation was reduced in vessels from irradiated rats (MD=3+/-9%; n=7; P= or <0.05 versus controls). Significant increases in superoxide and peroxides were observed in irradiated microvessels. Irradiated microvessels pretreated with superoxide dismutase-mimetic demonstrated significant improvement in Ach-induced vasodilation compared with irradiation alone, suggesting that superoxide contributes to impaired dilation to Ach after irradiation. CONCLUSIONS: Radiation induces acute microvascular dysfunction in the resistance arterioles of the intestine. Enhanced ROS contribute to this dysfunction and therefore may represent a novel therapeutic target to minimize radiation toxicity in the gut.

Acetylcholine↗

PubMed2002

Withdrawal of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors elicits oxidative stress and induces endothelial dysfunction in mice.

3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) improve endothelial function. We determined whether withdrawal of statin therapy affects endothelium-dependent relaxation in mice and studied the underlying mechanism. Mice were treated with daily injections of cerivastatin (2 mg/kg per day SC), atorvastatin (1 and 10 mg/kg per day SC), or placebo. Vascular reactivity was studied in aortic rings from these mice after 10 days of treatment and after cessation of therapy for several days. Both statins improved endothelium-dependent relaxation to acetylcholine. Compared with control, withdrawal of statin treatment transiently (from day 4 to 7) attenuated endothelium-dependent relaxation. In vessels from animals subjected to atorvastatin withdrawal, the antioxidant tiron restored relaxations. Vascular superoxide anion generation was unaffected by statin therapy but was increased during withdrawal. In mice lacking the gp91phox subunit of the NADPH oxidase, no attenuation of acetylcholine-induced relaxation and no increase in superoxide generation were observed after withdrawal of atorvastatin. In human umbilical vein endothelial cells, statins, which decrease the membrane association of NADPH oxidase-activating Rac-1, increased the activity of this GTPase in whole-cell lysates. Withdrawal of statins induced a translocation of Rac-1 from the cytosol to the membrane and transiently increased NADPH-induced lucigenin chemiluminescence in membrane preparations. Rac-1 inactivation by Clostridium difficile toxin B inhibited the cerivastatin-induced oxygen radical production in human umbilical vein endothelial cells. These observations indicate that the withdrawal of statins induces endothelial dysfunction. The underlying mechanism involves activation of a gp91phox-containing NADPH oxidase by Rac-1 and the subsequent scavenging of endothelium-derived NO by superoxide anions generated from this enzyme.

Acridines↗

PubMed2004

Amenorrhea in female athletes is associated with endothelial dysfunction and unfavorable lipid profile.

The aim of this study was to evaluate endothelial function measured as flow-mediated dilatation (FMD) of the brachial artery and blood markers of cardiovascular disease in young female endurance athletes with menstrual disturbance. Age- and body mass index-matched groups of young endurance athletes with amenorrhea (n = 14), oligomenorrhea (n = 9), and regular cycles (n = 12) and sedentary controls (n = 12) were compared with respect to endothelial function, lipid profile, markers of inflammation, and endocrine status. We found a significantly decreased FMD in the amenorrheic athletes, compared with all other groups. Amenorrheic athletes also had the most unfavorable lipid profile with significantly higher total cholesterol and low-density lipoprotein, compared with the other athlete groups. The oligomenorrheic athletes had the lowest levels of total cholesterol, low-density lipoprotein, and apolipoprotein B of all groups and significantly lower in comparison with the amenorrheic group. However, with respect to FMD, the oligomenorrheic group represented an intermediate between amenorrheic and regularly cycling subjects. There was a gradual impairment of FMD and the lipid profile to the degree of menstrual disturbance supporting an association with estrogen status. We conclude that amenorrhea in young endurance athletes is associated with endothelial dysfunction and unfavorable lipid profile. Additional studies are needed to elucidate the clinical implications of these results with regard to long-term risk for cardiovascular disease.

Adolescent↗

PubMed2006

[Venous endothelial dysfunction in Chagas' disease patients without heart failure].

OBJECTIVE: To analyze the venous endothelial function in Chagas' disease patients without heart failure. METHODS: The Chagas' disease Group (G1) was composed by 14 women and 2 men aged 46 +/- 2.7 and the Control Group (G0) by 7 women and 1 man matched by age, weight and height. Dorsal Hand Vein Compliance Technique was used to evaluate the venous endothelial function. Crescent doses of phenylephrine were infused to get a 70% pre-constriction of the vein; after that, acetylcholine and sodium nitroprusside were respectively administrated to analyze the endothelium-dependent and -independent venodilation. RESULTS: No significant systemic hemodynamic changes were observed in both groups during the experiment. The necessary phenylephrine dose to reach 70% pre-constriction of the vein was significantly higher in the G1 (1116 +/- 668.2 ng/ml) compared to G0 (103 +/- 28 ng/ml) p = 0.05. The endothelium-dependent venous dilation was significantly lower in G1 (65.5 +/- 8%) compared to G0 (137 +/- 20%) p = 0.009. No difference was observed in the endothelium-independent venous dilatation between groups. CONCLUSION: Patients with Chagas' disease without heart failure presented venous endothelial dysfunction.

Acetylcholine↗