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PubMed1985

The relationship between endothelial dysfunction and collagen accumulation in irradiated rat lung.

Male rats were killed 2 months (early fibrosis) or 6 months (peak fibrosis) after a range of single doses of 60Co gamma rays to the right hemithorax. Pulmonary arterial perfusion scans were performed at 2 months on animals scheduled for autopsy at 6 months. Lung angiotensin converting enzyme (ACE) activity was used to monitor endothelial function, and hydroxyproline (HP) concentration served as an index of interstitial collagen accumulation (fibrosis). ACE activity also was measured in right lung bronchoalveolar lavage (BAL) fluid and blood serum, to determine whether information obtained from a minimally invasive procedure might serve as an index or predictor of the severity of lung damage. Linear dose-response curves (r = 0.92-0.99) were obtained for right lung arterial perfusion, ACE activity and HP concentration. At 2 months, perfusion decreased 2.7% per Gy, ACE activity (per lung, per mg wet weight, or per mg protein) decreased 3.0-4.2% per Gy, and HP concentration (per g dry weight) increased 1.7% per Gy. At 6 months, the slopes of the response curves were virtually identical to those at 2 months; the Y intercept of the response curve for ACE activity was unchanged, whereas that for HP concentration was 50% higher at 6 than at 2 months. ACE activity and protein concentration in the BAL increased with increasing dose, but the variation within groups was too large, and the sensitivity was too low to serve as a reliable index of lung status. Serum ACE activity was independent of radiation dose at both autopsy times. Thus in rat lung, arterial perfusion, endothelial dysfunction and interstitial fibrosis exhibit similar but not identical radiosensitivities. The dose-effect curves for these three responses of the lung in situ change less than 5% per Gy over the dose range of 10-30 Gy, a smaller variation than would be predicted from endothelial cell survival data based on clonogenic assays in vitro or in vivo.

Animals↗

PubMed2004

Endothelial dysfunction, inflammation, and insulin resistance: a focus on subjects at risk for type 2 diabetes.

Subjects with obesity, family history of type 2 diabetes, polycystic ovary syndrome, previous gestational diabetes, dyslipidemia, hypertension, impaired glucose tolerance or impaired fasting glucose, and those with metabolic syndrome are at risk for the development of type 2 diabetes. Some of them are also at risk for cardiovascular disease. Some underlying abnormalities such as insulin resistance, endothelial dysfunction, and low-grade chronic inflammation are frequently present and closely associated in all these groups. The flow of substrates, hormones, and cytokines from visceral fat to skeletal muscle and to the endothelial cells, along with some genetic abnormalities that lead to impaired insulin action in the peripheral tissues and to impaired insulin-stimulated nitric oxide production in endothelial cells, may play a role in establishing these shared metabolic and vascular derangements. Weight loss, thiazolidinediones, and metformin improve vascular function in subjects at risk for type 2 diabetes and may prove to reduce cardiovascular events in these individuals.

Animals↗

PubMed2000

Peripheral vascular endothelial dysfunction and apoptosis in old monkeys.

To determine the effects of aging on vasoactivity in a primate model (Macaca fascicularis), 13 young male monkeys (aged 7.1+/-0.4 years) and 9 old male monkeys (aged 19.8+/-0.6 years) were chronically instrumented for measurement of left ventricular and aortic pressures and cardiac output. Total cholesterol, triglyceride, and fasting blood sugar levels were not different between the 2 groups. There were no significant differences in baseline mean aortic pressure and total peripheral resistance (TPR) in the young monkeys versus the old monkeys. TPR fell less (P<0.05) with acetylcholine (1 microg/kg) in old monkeys (-25+/-1%) than in young monkeys (-34+/-2%), whereas decreases in TPR with sodium nitroprusside were similar in old and young monkeys. There was no evidence of atherosclerosis, but apoptosis of endothelial cells was enhanced (P<0.05) in the aortas and femoral arteries, but not in the media, of the old monkeys. There was a relationship (r=0.62, P=0.013) between the incidence of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive endothelial cells and endothelial cell density in the femoral artery. The reduced endothelial cell density was also correlated (r=0.82, P<0.01) with depressed TPR responses to acetylcholine. Thus, vascular endothelial dysfunction was present in old monkeys without evidence of atherosclerosis, which may be due to endothelial apoptosis and reduced endothelial cell density.

Acetylcholine↗

PubMed2006

Early experimental obesity is associated with coronary endothelial dysfunction and oxidative stress.

Obesity is independently associated with increased cardiovascular risk. However, since established obesity clusters with various cardiovascular risk factors, configuring the metabolic syndrome, the early effects of obesity on vascular function are still poorly understood. The current study was designed to evaluate the effect of early obesity on coronary endothelial function in a new animal model of swine obesity. As to method, juvenile domestic crossbred pigs were randomized to either high-fat/high-calorie diet (HF) or normal chow diet for 12 wk. Coronary microvascular permeability and abdominal wall fat were determined by using electron beam computerized tomography. Epicardial endothelial function and oxidative stress were measured in vitro. Systemic oxidative stress, renin-angiotensin activity, leptin levels, and parameters of insulin sensitivity were evaluated. As a result, HF pigs were characterized by abdominal obesity, hypertension, and elevated plasma lysophosphatidylcholine and leptin in the presence of increased insulin sensitivity. Coronary endothelium-dependent vasorelaxation was reduced in HF pigs and myocardial microvascular permeability increased compared with those values in normal pigs. Systemic redox status in HF pigs was similar to that in normal pigs, whereas the coronary endothelium demonstrated higher content of superoxide anions, nitrotyrosine, and NADPH-oxidase subunits, indicating increased tissue oxidative stress. In conclusion, the current study shows that early obesity is characterized by increased vascular oxidative stress and endothelial dysfunction in association with increased levels of leptin and before the development of insulin resistance and systemic oxidative stress. Vascular dysfunction is therefore an early manifestation of obesity and might contribute to the increased cardiovascular risk, independently of insulin resistance.

Animals↗

PubMed2000

Correction of endothelial dysfunction in chronic heart failure: additional effects of exercise training and oral L-arginine supplementation.

OBJECTIVES: The aim of this study was to analyze whether L-arginine (L-arg.) has comparable or additive effects to physical exercise regarding endothelium-dependent vasodilation in patients with chronic heart failure (CHF). BACKGROUND: Endothelial dysfunction in patients with CHF can be corrected by both dietary supplementation with L-arg. and regular physical exercise. METHODS: Forty patients with severe CHF (left ventricular ejection fraction 19 +/- 9%) were randomized to an L-arg. group (8 g/day), a training group (T) with daily handgrip training, L-arg. and T (L-arg. + T) or an inactive control group (C). The mean internal radial artery diameter was determined at the beginning and after four weeks in response to brachial arterial administration of acetylcholine (ACh) (7.5, 15, 30 microg/min) and nitroglycerin (0.2 mg/min) with a transcutaneous high-resolution 10 MHz A-mode echo tracking system coupled with a Doppler device. The power of the study to detect clinically significant differences in endothelium-dependent vasodilation was 96.6%. RESULTS: At the beginning, the mean endothelium-dependent vasodilation in response to ACh, 30 microg/min was 2.54 +/- 0.09% (p = NS between groups). After four weeks, internal radial artery diameter increased by 8.8 +/- 0.9% after ACh 30 microg/min in L-arg. (p < 0.001 vs. C), by 8.6 +/- 0.9% in T (p < 0.001 vs. C) and by 12.0 +/- 0.3% in L-arg. +/- T (p < 0.005 vs. C, L-arg. and T). Endothelium-independent vasodilation as assessed by infusion of nitroglycerin was similar in all groups at the beginning and at the end of the study. CONCLUSIONS: Dietary supplementation of L-arg. as well as regular physical exercise improved agonist-mediated, endothelium-dependent vasodilation to a similar extent. Both interventions together seem to produce additive effects with respect to endothelium-dependent vasodilation.

Acetylcholine↗

PubMed2002

Effect of vitamin C on endothelial dysfunction during N-alpha-tosyl L-arginine methyl ester [TAME]-esterase induced contractions in rat aorta in vitro.

Contractions induced by TAME-esterase on rat aorta strips mounted in vitro were significantly inhibited in presence of Vitamin C. The work lends support to the role of ascorbic acid in preventing endothelial dysfunction through release of nitric oxide. It is suggested that conclusions TAME-esterase could be an important biological marker associated with onset of vascular discases such as hypertension.

Animals↗

PubMed2001

Endothelial dysfunction marker von Willebrand factor antigen in haemodialysis patients: associations with pre-dialysis blood pressure and the acute phase response.

BACKGROUND: Increased plasma soluble von Willebrand factor antigen (vWF : Ag) level, a marker of vascular endothelial cell dysfunction, is a strong predictor of atherosclerotic cardiovascular disease (CVD) in the general population. We studied cross-sectional associations between vWF : Ag level, prevalence of CVD, and related factors including pre-dialysis arterial blood pressure (BP) and some markers of inflammation in maintenance haemodialysis (HD) patients. Methods and results. Plasma vWF : Ag level measured by an enzyme-linked immunosorbent assay (ELISA) was higher in 110 HD patients than in 20 controls. On bivariate regression analysis, vWF : Ag level was directly associated with the presence of CVD, age, fibrinogen and the use of enoxaparin (vs unfractionated heparin) during HD procedures, and inversely with albumin and pre-dialysis BP. The patients with prevalent CVD were older, had higher vWF : Ag, white blood cell and platelet counts, fibrinogen and triglycerides, lower albumin levels, and were less frequently on combination antihypertensive therapy. Multivariable analyses identified low pre-dialysis BP, hypoalbuminaemia and hyperfibrinogenaemia (in descending order of significance) as independent predictors of high vWF : Ag level. There were no associations between vWF : Ag levels and gender, ABO blood type, smoking, body mass index, renal failure cause, duration of HD therapy, K(t)/V, normalized protein catabolic rate, dialysate buffers, dialysers, viral hepatitis, erythropoietin treatment, specific antihypertensive drugs, haemoglobin, white blood cell and platelet counts, liver enzymes, phosphorous, total cholesterol, and triglycerides. CONCLUSION: Elevated plasma levels of endothelial dysfunction marker vWF : Ag in maintenance HD patients are associated with established cardiovascular mortality risk factors such as low pre-dialysis blood pressure and the activated acute phase response.

Adult↗

PubMed2005

Pharmacological neutropenia prevents endothelial dysfunction but not smooth muscle functions impairment induced by middle cerebral artery occlusion.

1. The polymorphonuclear neutrophils (PMN) activation and mobilization observed in acute cerebral infarction contribute to the brain tissue damage, but PMN could also be involved in postischemic functional injury of ischemied blood vessel. 2. This study was undertaken to investigate whether pharmacological neutropenia could modify the postischemic endothelial dysfunction in comparison to smooth muscle whose impairment is likely more related to reperfusion and oxidative stress. 3. A cerebral ischemia-reperfusion by endoluminal occlusion of right middle cerebral artery (MCA) was performed 4 days after intravenous administration of vinblastine or 12 h after RP-3 anti-rat neutrophils monoclonal antibody (mAb RP-3) injection into the peritoneal cavity, on male Wistar rats with 1-h ischemia then followed by 24-h reperfusion period. Brain infarct volume was measured by histomorphometric analysis and vascular endothelial and smooth muscle reactivity of MCA was analysed using Halpern myograph. 4. Neutropenia induced a neuroprotective effect as demonstrated by a significant decrease of brain infarct size. In parallel to neuroprotection, neutropenia prevented postischemic impairment of endothelium-dependent relaxing response to acetylcholine. In contrast, smooth muscle functional alterations were not prevented by neutropenia. Ischemia-reperfusion-induced myogenic tone impairment remained unchanged in vinblastine and mAb RP-3-treated rats. Postischemic Kir2.x-dependent relaxation impairment was not prevented in neutropenic conditions. The fully relaxation of smooth muscle response to sodium nitroprusside was similar in all groups. 5. Our results evidenced the dissociate prevention of pharmacologically induced neutropenia on postischemic vascular endothelial and smooth muscle impairment. The selective endothelial protection by neutropenia is parallel to a neuroprotective effect suggesting a possible relationship between the two phenomena.

Animals↗

PubMed1996

Cardiovascular syndromes X, endothelial dysfunction and insulin resistance.

Cardiac Syndrome X (microvascular angina) and the more recently described metabolic Syndrome X (an epidemiological association between insulin resistance and atheroma, dyslipidaemia, and hypertension) may have more in common than the chance of their common sobriquet, in view of evidence that microvascular angina too is characterised by insulin resistance and endothelial dysfunction. The implications are discussed.

Endothelium, Vascular↗

PubMed1992

Endothelial dysfunction caused by University of Wisconsin preservation solution in the rat heart. The importance of temperature.

The superiority of the University of Wisconsin solution over routinely used crystalloid cardioplegic solutions for myocardial preservation has been demonstrated in animal studies. We have investigated the effect of the University of Wisconsin solution at different temperatures on endothelial function by examining its influence on 5-hydroxytryptamine- and nitroglycerin-induced increase in coronary flow in the isolated rat heart. Thirty-eight rat hearts were perfused on a modified Langendorff preparation. In the control experiments, there was no significant difference in the percentage increase in coronary flow induced by 5-hydroxytryptamine and nitroglycerin after 30 minutes of perfusion with Krebs-Henseleit buffer (n = 6). Continuous infusion of the University of Wisconsin solution for 30 minutes at 4 degrees C or at 10 degrees C did not alter the 5-hydroxytryptamine or nitroglycerin response. However, infusion at 15 degrees C reduced the 5-hydroxytryptamine-induced vasodilation, while at 20 degrees C the 5-hydroxytryptamine response was converted to vasoconstriction without a significant change in nitroglycerin effect (15 degrees C, 5-hydroxytryptamine, before: 30.2% +/- 1.5%, after: 6.0% +/- 1.0%, nitroglycerin, before: 28.8% +/- 1.3%, after: 31.2% +/- 1.8%; 20 degrees C, 5-hydroxytryptamine, before: 32.2% +/- 2.5%, after: -23.8% +/- 3.6%, nitroglycerin, before: 30.3% +/- 1.9%, after: 33.5% +/- 1.7%). Coronary vascular resistance in the control experiments rose from 55.0 +/- 2.5 cm H2O/ml/gm/min to 58.4 +/- 2.3 cm H2O/ml/gm/min (p = not significant). The increase after University of Wisconsin solution infusion at 4 degrees C and at 10 degrees C was similarly not significant. Coronary vascular resistance increased significantly following infusion of University of Wisconsin solution at 15 degrees C (p < 0.001) or at 20 degrees C (p < 0.01). We conclude that University of Wisconsin solution produces temperature-dependent endothelial dysfunction in the isolated rat heart.

Adenosine↗

PubMed2004

Endothelial dysfunction in patients with chronic periodontitis and its improvement after initial periodontal therapy.

BACKGROUND: Recent epidemiological data suggested that there is a relationship between periodontal health and atherosclerotic coronary heart disease. Although hypothetical models were proposed, the exact mechanism of this association has not been clarified. The aim of this study is to investigate whether there is an endothelial dysfunction in patients with chronic periodontitis and, if present, whether recovery is possible with therapy. METHODS: The study groups consisted of 28 patients (mean age: 45.5 +/- 8.6 years) with chronic periodontitis and without any atherosclerotic vascular disease, and 26 healthy controls (mean age: 43.7 +/- 6.8 years). Cardiovascular risk factors were investigated in both groups. Brachial artery responses to reactive hyperemia (endothelium-dependent dilatation [EDD]) and sublingual nitroglycerin (endothelium-independent dilatation [EID]) were measured using high-resolution vascular ultrasound in both groups. Measurements were taken before and after initial periodontal therapy in the periodontal patients. RESULTS: There was no significant difference between the groups with regard to cardiovascular risk factors. In the baseline measurements, EDD and EID were significantly impaired in patients with chronic periodontitis when compared with the controls (8.4% +/- 4.0% versus 19.4% +/- 8.1%, P<0.0001; 13.3% +/- 6.3% versus 29.5% +/- 10.0%, P<0.0001 for EDD and EID, respectively). After non-surgical periodontal therapy, EDD and EID improved significantly (from 8.4% +/- 4.0% to 17.7% +/- 5.7%, P<0.0001; and from 13.3% +/- 6.3% to 24.9% +/- 7.3%, P<0.0001 for FMD and EID, respectively). The EDD and EID changes in the controls were insignificant. CONCLUSION: This study showed that endothelial functions were impaired in patients with chronic periodontitis and that they improve following initial periodontal therapy.

Arteriosclerosis↗

PubMed1999

SOD1 rescues cerebral endothelial dysfunction in mice overexpressing amyloid precursor protein.

Peptides derived from proteolytic processing of the beta-amyloid precursor protein (APP), including the amyloid-beta peptide, are important for the pathogenesis of Alzheimer's dementia. We found that transgenic mice overexpressing APP have a profound and selective impairment in endothelium-dependent regulation of the neocortical microcirculation. Such endothelial dysfunction was not found in transgenic mice expressing both APP and superoxide dismutase-1 (SOD1) or in APP transgenics in which SOD was topically applied to the cerebral cortex. These cerebrovascular effects of peptides derived from APP processing may contribute to the alterations in cerebral blood flow and to neuronal dysfunction in Alzheimer's dementia.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1998

Pancreatic transplantation reverses endothelial dysfunction in experimental diabetes mellitus.

BACKGROUND: There is insufficient evidence whether transplantation of the whole pancreas can reverse vascular complications associated with diabetes. In this study we investigated whether pancreatic transplantation in experimental diabetes reverses established defects in endothelium-dependent relaxation. METHODS: Streptozotocin-induced diabetic rats underwent whole-pancreas transplantation after 12 weeks of disease. Endothelial function was evaluated 4 weeks after transplantation and compared with that of control- and age-matched diabetic animals. Blood was taken for analysis of glucose, insulin, total glycosylated hemoglobin, and plasma amino acid levels. Descending thoracic aortas were isolated, sectioned into rings, and mounted in isolated tissue baths. In precontracted rings, endothelium-dependent relaxation to acetylcholine was performed and compared with endothelium-independent relaxation to nitroglycerin as a control. RESULTS: Pancreatic transplantation normalized the increases in glucose and total glycosylated hemoglobin levels and the decrease in serum insulin levels. Diabetes resulted in impaired relaxation to acetylcholine without altering relaxation to nitroglycerin. Pancreatic transplantation completely restored the defective relaxation to acetylcholine without altering the relaxation to nitroglycerin. CONCLUSIONS: These results suggest that pancreatic transplantation selectively improved endothelium-dependent relaxation as opposed to a generalized improvement in vascular smooth muscle reactivity. Furthermore, these studies suggest for the first time that one aspect of vascular complications (i.e., endothelial dysfunction) is amenable to this surgical intervention.

Acetylcholine↗

PubMed2001

Current strategies and perspectives for correcting endothelial dysfunction in atherosclerosis.

The vascular endothelium synthesizes and releases a spectrum of vasoactive substances such as nitric oxide and endothelin. In atherosclerosis, the delicate balance between endothelium-derived factors is disturbed. Endothelin acts as the natural counterpart to endothelium-derived nitric oxide, which exerts vasodilating, antithrombotic and antiproliferative effects, and inhibits leukocyte adhesion to the vascular wall. Besides its blood pressure increasing effect in man, endothelin also induces vascular and myocardial hypertrophy, which are independent risk factors for cardiovascular morbidity and mortality. The derangement of endothelial function in atherosclerosis is likely to be caused in part by genetic factors, but is also due to cardiovascular risk factors. Endothelial dysfunction in atherosclerosis is crucial for the development of the disease process in the vasculature and is therefore an important therapeutic target. However, the efficacy of pharmacotherapy aimed at an improvement in endothelial function depends on the individual risk factor profile of the patient.

Adrenergic beta-Antagonists↗

PubMed1998

[Prevention and therapy of vascular damage and endothelial dysfunction with hypocholesteremic agents].

Several recent pieces of clinical evidence have demonstrated that reduction of cholesterol levels positively affects outcomes in both primary and secondary prevention of atherosclerotic vascular disease. The mechanism for the beneficial effects of cholesterol-lowering interventions has been attributed to decreased progression or actual regression of plaques as a consequence of reduced circulating LDL concentrations. Other mechanisms can be hypothesized, including a "stabilizing" effect on plaques, which would decrease chances of rupture, and an improvement of endothelial dysfunction, which would slow-down the progression of the disease. This review is aimed at offering an update on such mechanisms. The hypothesis of a direct action of cholesterol-lowering agents, in particular of statins, on endothelial functions, independently of LDL-lowering effects, will be discussed.

Anticholesteremic Agents↗

PubMed2006

The metabolic syndrome and endothelial dysfunction: common highway to type 2 diabetes and CVD.

Due to global lifestyle changes, obesity (the main driver of type 2 diabetes and cardiovascular disease ) is reaching pandemic proportions. The metabolic syndrome, which is regarded as a prediabetic state, is characterized by a concurrence of interrelated cardiovascular risk factors, including abdominal obesity, insulin resistance, hypertension, dyslipidemia, and glucose intolerance. Endothelial dysfunction (ED) is common in the metabolic syndrome and is associated with increased risk for T2D and CVD. This review focuses on the mechanisms linking ED to the metabolic syndrome, T2D, and CVD, and the possible therapies that may improve ED and reduce T2D and CVD risk.

Cardiovascular Diseases↗

PubMed1998

Impaired release of tissue plasminogen activator from the endothelium in Graves' disease - indicator of endothelial dysfunction and reduced fibrinolytic capacity.

BACKGROUND: Patients with hyperthyroidism have increased plasma levels of von Willebrand factor (vWF). Changes in tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1), another two endothelium-derived proteins and modulators of blood fibrinolytic activity, have not been reported in hyperthyroidism. METHODS: The release of t-PA by vascular endothelial cells after venous occlusion, basal blood concentrations of t-PA, PAI-1 and vWF were studied in 33 patients with hyperthyroidism, with most of them followed up 30 days after iodine radiotherapy. RESULTS: Compared with control subjects, both the basal t-PA levels in plasma and the increase in t-PA levels with venous occlusion were significantly decreased in patients (P < 0.001), whereas plasma PAI-1 and vWF levels were increased greatly (P < 0.001). At follow-up, patients with normal plasma free thyroxine (T4) and total tri-iodothyronine (T3) showed similar plasma levels of t-PA, PAI-1, vWF and release of t-PA from endothelial cells as the control subjects (P > 0.05). In those with persistent elevated T4 or T3 levels, however, the basal plasma t-PA level and the released t-PA from endothelial cells during venous occlusion were significantly lower than in the control subjects (P < 0.001 and P < 0.005), and blood concentrations of PAI-1 and vWF did not return to the normal range (P < 0.001 and P < 0.001). In all patients, serum thyroid hormone concentrations were inversely correlated with basal plasma t-PA (T4: r = -0.549, P < 0. 001; T3: r = -0.463, P < 0.001) and released t-PA by endothelial cells (T4: r = -0.505, P < 0.001; T3: r = -0.450, P < 0.001) but strongly correlated with plasma PAI-1 (T4: r = 0.613, P < 0.001; T3: r = 0.577, P < 0.001) and vWF (T4: r = 0.457, P < 0.001; T3: r = 0. 564, P < 0.001). CONCLUSION: Hyperthyroid patients may experience vascular endothelial dysfunction and reduced fibrinolytic activity in blood.

Adult↗

PubMed2006

Endothelial dysfunction in Buerger's disease and its relation to markers of inflammation.

BACKGROUND: Buerger's disease (BD) is a segmental occlusive vascular disease. The aim of this study was to detect functional changes in brachial artery and asymptomatic morphological changes in extra-cranial carotid arteries not affected by the disease process and to assess markers of inflammation and endothelial damage. MATERIALS AND METHODS: Fourteen patients in the remission phase of BD and the same number of age- and sex-matched healthy controls were included in the study. The capability of endothelium-dependent (flow-mediated) and endothelium-independent dilation of the brachial artery and intima-media thickness of the carotid arteries were measured using high-resolution ultrasound. Laboratory parameters of endogenous fibrinolytic activity, inflammation and endothelial dysfunction were also measured. RESULTS: Patients with BD had a diminished capability of endothelium-dependent vasodilation and higher levels of some circulating markers of inflammation, such as leukocytes, C-reactive protein, intercellular adhesion molecule-1 and E-selectin. Intercellular adhesion molecule-1 levels were related to some of the inflammatory markers (sedimentation rate, C-reactive protein, alpha2-globulins and fibrinogen), while E-selectin was correlated with decreased endogenous blood fibrinolytic activity. Endothelium-dependent vasodilation was in negative correlation with the relative share of neutrophil granulocytes. There were no significant differences in intima-media thickness between patients with BD and controls. CONCLUSIONS: Our study has expressed generalized functional arterial disorder in patients with BD not accompanied by any measurable morphological changes of the carotid arterial wall. Functional deterioration of brachial artery could be related to increased levels of various inflammatory markers--the process which is most probably the basic pathogenetic mechanism of the disease.

Adult↗