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At least 325 records · Page 18Linked to original sources
PubMed2004

Microvascular endothelial cell activation is present in the umbilical placental microcirculation in fetal placental vascular disease.

OBJECTIVE: Fetal growth restriction is associated with an abnormal umbilical artery Doppler study. A vascular disease is present in the fetal umbilical placental microcirculation. We hypothesized that the local production of factors that are injurious to microvessel endothelium is responsible for this vascular disease and that endothelial cell activation is a feature of this. Because the expression of the cell adhesion molecules is associated with endothelial cell activation, we isolated endothelial cells from the microvessels of the umbilical placenta and examined them for evidence of gene expression of cell adhesion molecules. STUDY DESIGN: Endothelial cells from the microcirculation of human placenta were isolated and purified with collagenase digestion and extraction with superparamagnetic beads that were coated with monoclonal antibody against CD31. Microvessel endothelial cells were isolated from the placentae of 13 women with a normal pregnancy and delivery at term and 10 placentas with umbilical placental vascular disease that was defined by abnormal umbilical artery Doppler study. Total RNA was extracted from isolated endothelial cells. The messenger RNA expressions of cell adhesion molecules (intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and platelet endothelial cell adhesion molecule-1) were assessed by semiquantitative reverse transcription-polymerase chain reaction. RESULTS: Microvessel endothelial cells from the fetal placentae of pregnancies that were complicated by umbilical placental vascular disease showed an enhanced expression of intercellular adhesion molecule-1 messenger RNA (2.12+/-0.45 vs 0.92+/-0.25) and platelet endothelial cell adhesion molecule-1 messenger RNA (4.29+/-0.87 vs 2.41+/-0.42) in comparison to normal pregnancies. There was no significant difference in expression of vascular cell adhesion molecule-1 messenger RNA (1.55+/-0.37 vs 1.68+/-0.38). CONCLUSION: We have shown that vascular disease in the fetal umbilical placental circulation is associated with an increase in the expression of intercellular adhesion molecule-1 and platelet endothelial cell adhesion molecule-1 by microvessel endothelial cells. We postulate that locally released factors cause injury and activation to microvessel endothelial cells. In this regard, the process in the fetus is similar to that of atherothrombotic vascular disease of later life.

Adult↗
PubMed1997

Cell adhesion molecules and insulin-like growth factor-1 in vascular disease.

PURPOSE: Recent advances in the understanding of the biologic mechanisms of vascular diseases suggest that multifactorial stimulation of the endothelial cell and its subsequent adhesion to leukocytes is a prerequisite to the formation of atherosclerotic and restenotic lesions. As leukocyte-endothelial cell interaction is coordinated by a variety of cell adhesion molecules (CAMs), we hypothesized that the expression of certain CAMs is up-regulated in the vasculature of patients who have peripheral vascular disease. In addition, we proposed that insulin-like growth factor-1 (IGF-1) increases monocyte-endothelial adhesion by means of upregulation of these CAMs. METHODS: Using immunohistochemical techniques, the expression of intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, and P-selectin was examined in human vascular disease specimens. Normal aortas obtained from the organ retrieval system were studied as control specimens. Adhesion studies between human umbilical vein endothelial cells (HUVECs) incubated with IGF-1 and purified human blood monocytes labeled with 51chromium were completed. Western blotting and flow cytometry were performed to show CAM expression on IGF-1-treated HUVECs. RESULTS: Of the CAMs, ICAM-1, P-selectin, and E-selectin were distinctly increased in diseased specimens when compared with control specimens (p < 0.05). Adhesion studies showed an increase in monocyte-endothelial cell adhesion of as much as 40% to 45% (p < 0.01) over baseline, with peak adherence occurring 4 hours after treatment with IGF-1. IGF-1 increased adherence in a dose- and time-dependent manner. The threshold concentration of IGF-1 that induced increased adhesion was 20 ng/ml, with a maximum effect occurring at 150 ng/ml. This increased adhesion was attenuated by pretreatment with IGF-I receptor antibody, as well as with genistein and herbimycin-A, which are potent and selective tyrosine kinase inhibitors. Increased adhesion correlated with an increase in the expression of CAMs on the surface of the HUVECs. An additive effect on adhesion was observed between IGF-1 and tumor necrosis factor-alpha (TNF-alpha) and endothelin-1 (ET-1). Finally, immunohistochemical analysis of human vascular disease specimens revealed an increased expression of IGF-1 receptors as compared with control specimens (p < 0.05). CONCLUSIONS: These results suggest that IGF-1 may be important in the pathogenesis of peripheral vascular disease by increasing endothelial cell-monocyte adhesion by means of an increase in the expression of ICAM-1 and VCAM-1.

Aorta↗
PubMed1991

Long-term antiplatelet therapy for the prevention of vascular disease.

OBJECTIVE: To estimate the effects of prolonged antiplatelet therapy on the primary and secondary incidence of vascular disease. DATA SOURCES: Twenty-five randomised trials in 29,000 patients with a history of vascular disease (the Antiplatelet Trialists' Collaboration) and two randomised trials in 27,000 individuals without a history of vascular disease (the British doctors' and American physicians' studies). STUDY SELECTION: The Antiplatelet Trialists' Collaboration obtained data from all randomised trials of secondary prevention completed before January 1988. The British doctors' and American physicians' studies are the only two completed randomised trials of primary prevention. DATA EXTRACTION: Data from the secondary prevention trials were provided by the Antiplatelet Trialists' Collaboration. Data from the primary prevention trials were extracted from the final published reports of these studies. DATA SYNTHESIS: In the secondary prevention trials, antiplatelet therapy reduced the rate of vascular disease by about 15% and the incidence of non-fatal myocardial infarction and stroke by about 30%. In the American physicians' study, but not the British doctors' study, the incidence of non-fatal myocardial infarction was also reduced. In neither primary prevention trial was there evidence of reduced rates of non-fatal stroke or vascular death; overall, fatal or disabling strokes were slightly more frequent among those assigned aspirin. CONCLUSIONS: For patients with a history of vascular disease, the benefits of antiplatelet therapy appear to outweigh any risks. Among 100 such patients, antiplatelet therapy for two years would prevent one death and two major non-fatal events. The balance of benefits and risks for individuals without a history of vascular disease is less clear because there is no firm evidence of a net reduction in either vascular death or disabling non-fatal vascular events among those treated with aspirin.

Aspirin↗
PubMed2004

Depression in older persons with versus without vascular disease in the open population: similar depressive symptom patterns, more disability.

BACKGROUND: Clinical studies suggest that vascular depression presents with typical symptom patterns. The aim of the present study is to examine whether depressed older persons in the open population with and without vascular disease show different symptom patterns. METHODS: In the Longitudinal Aging Study Amsterdam (LASA), a depressed cohort with (n=114) and without (n=292) vascular disease was identified. Depression was measured using self-reports (CES-D). Vascular disease was confirmed or ruled out using a combination of self-reported data, medication use and reports from general practitioners. RESULTS: No significant differences were found in depressive symptom patterns, in symptom clusters nor individual items of the CES-D. Depressed subjects with vascular disease showed much more disability than those without vascular disease. Age of onset of depression did not show statistically significant difference. CONCLUSIONS: From our study in the open population, there is no evidence to support the hypothesis that depressed older persons with vascular disease have a distinct depressive symptom profile, but they do show more disability.

Activities of Daily Living↗
PubMed1995

[Expression of bc1-2 protein in collagen vascular diseases with pulmonary interstitial involvement].

Expression of bc1-2 protein was studied immunohistochemically in 25 patients with collagen vascular diseases and in 10 patients with idiopathic interstitial pneumonia. The collagen vascular diseases included rheumatoid arthritis (n = 9), progressive systemic sclerosis (n = 9), polymyositis/dermatomyositis (n = 4), Sjögren's syndrome (n = 2), and systemic lupus erythematosus (n = 1). All 35 patients underwent open lung biopsy; cellular infiltration, fibrosis, and lymphoid aggregation were scored according to Cherniack's classification. T lymphocytes (CD43: DFT-1) and B lymphocytes (CD20:L-26) were also evaluated. Expression of bc1-2 protein was dominant in T lymphocytes infiltrating the alveolar interstitium and in B lymphocytes in the mantle zone of lymphoid follicles. In collagen vascular diseases, the degree of expression of bc1-2 protein in those T lymphocytes was closely related to the alveolar lymphocyte infiltration score. However, these findings were not marked in the patients with idiopathic interstitial pneumonia, and were not related to the underlying disease in the patients with collagen vascular diseases. The expression of bc1-2 protein in T lymphocytes was not related to fibrosis or to lymphoid aggregation. Expression of bc1-2 protein in B lymphocytes did not correlate with pathological scores or with underlying disease. Bc1-2 protein has been recognized as an oncogene that suppresses apoptosis. Marked expression of bc1-2 protein in T lymphocytes from patients with collagen vascular diseases indicates that oversuppression of apoptosis may be related to the pathogenesis of pulmonary interstitial involvement in these conditions. Further clinicopathological studies focusing on apoptosis in collagen vascular diseases and in idiopathic interstitial pneumonia are needed.

Apoptosis↗
PubMed1995

The activated megakaryocyte-platelet-system in vascular disease: focus on diabetes.

Vascular diseases and related complications still represent the main cause of death. In diabetes neuropathy, nephropathy, retinopathy and disturbed nutritive tissue perfusion result from reduced capillary microcirculation. These disturbances are diabetes specific, whereas macroangiopathy does not differ structurally from atherosclerotic lesions of non-diabetic subjects, but leads to accelerated cerebral, coronary and peripheral artery disease. Occurrence of life terminating thrombotic events which are superimposed to those vascular lesions is increased. Thus, morbidity and mortality of diabetes depend mainly on vascular complications. Normal blood flow is a prerequisite of adequate organ perfusion and results from vasomotion, plasma components, corpuscular blood elements, vascular architecture and the undisturbed interaction of these components at the endothelial interface. Functional thromboresistance of the endothelial layer is reduced in the diabetic state. Increased intravascular thrombin generation, reduced fibrinolytic potential and hyperactive platelets lead to a prethrombotic state. This thrombotic diathesis raises the permanent danger of acute flow disruption. Activated platelets operate by three mechanisms: 1. microembolization of the capillaries; 2. local progression of preexisting vascular lesions by secretion of constrictive, mitogenic, and oxidative substances; and 3. trigger of the prognosis limiting arterial thrombotic event. We were able to show that the increased functional properties of diabetic platelets result from the primary release of larger platelets with enhanced thromboxane formation capacity and increased numbers of functional glycoprotein receptors GPIB and GPIIB/IIIA which are synthesized in the megakaryocytes. The megakaryocyte-platelet system is turned on in diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗
PubMed2004

C-reactive protein and microalbuminuria differ in their associations with various domains of vascular disease.

C-reactive protein (CRP) and microalbuminuria (MA) have been identified as risk markers for cardiovascular disease (CVD). We questioned whether CRP and MA are similar markers of vascular disease in different regions of the vascular tree like the heart, kidneys and extremities or if they differ in their relationships with these vascular beds. Baseline levels of CRP and urinary albumin were measured in 6669 non-diabetic participants in the Prevention of Renal and Vascular ENdstage Disease (PREVEND) study, a Dutch cohort derived from the general population. We defined three domains of vascular disease; coronary heart disease (myocardial infarction or infarct pattern on the ECG), renal insufficiency (creatinine clearance <60 ml min(-1)) and peripheral artery disease (ankle brachial index <0.9 or lower limb revascularisation). The prevalence of an elevated CRP (27.7 vs. 17.9%) and MA (17.5 vs. 10.4%) were increased in subjects with vascular disease as compared with subjects without CVD. The prevalence of an elevated CRP was equal in subjects with either coronary heart disease, renal insufficiency or peripheral artery disease (28.4 vs. 29.5 vs. 26.0%, NS), whereas MA was most prevalent in subjects with coronary heart disease (22.5 vs. 12.8 vs. 14.9%, P<0.05). Using multivariate analyses, CRP was independently associated with all three domains of vascular disease, whereas MA was independently associated with coronary heart disease only. In addition, we found synergistic contributions of an elevated CRP and older age to the risk of vascular disease in all three domains. Thus, CRP and MA are risk markers for vascular disease, each showing a different risk profiling for different vascular beds.

Adult↗
PubMed1993

Thromboxane A2 and prostacyclin biosynthesis in children and adolescents with pulmonary vascular disease.

BACKGROUND: The pathogenesis of pulmonary vascular disease in children with congenital heart disease is incompletely understood. Thromboxane (TX) A2 and prostacyclin (PGI2) have opposing effects on platelet aggregation and pulmonary vascular smooth muscle. An imbalance in their biosynthesis could contribute to the progressive increase in pulmonary vascular resistance seen in older untreated patients with pulmonary hypertensive congenital heart disease and the thrombotic complications they may develop. METHODS AND RESULTS: We investigated TXA2 and PGI2 biosynthesis in 15 young children (0.2 to 2.25 years old) with congenital heart disease with increased pulmonary blood flow and potentially reversible pulmonary vascular disease by measuring urinary excretion of 2,3-dinor-TXB2 and 2,3-dinor-6-oxoprostaglandin (PG) F1 alpha and compared the findings with those in 16 healthy children (0.5 to 2.8 years old). 2,3-Dinor-TXB2 excretion was greater in the patients than in control subjects (1253 +/- 161 versus 592 +/- 122 ng/g creatinine; P < .001). Excretion of 2,3-dinor-6-oxo-PGF1 alpha was 452 +/- 54 compared with 589 +/- 95 ng/g creatinine in control subjects. In 5 patients who underwent successful cardiac surgery > or = 1 year later excretion of 2,3-dinor-TXB2 decreased from 1100 +/- 298 to 609 +/- 131 ng/g creatinine (P < .05), a value comparable to those in 5 healthy children of similar age (749 +/- 226 ng/g creatinine). We also compared 15 patients (11 to 23 years old) with advanced irreversible pulmonary vascular disease with 19 healthy control subjects (10 to 23 years old). The ratio of TX to PGI2 metabolite excretion was greater in the patients than in control subjects (3.5 +/- 0.6 versus 2.0 +/- 0.3; P < .05). CONCLUSIONS: There is increased 2,3-dinor-TXB2 excretion in children with congenital heart disease and a high pulmonary blood flow that may reflect an imbalance in biosynthesis of TXA2 and PGI2 in the pulmonary vascular bed. The imbalance may contribute to the progressive development of increased pulmonary vascular resistance and persists in older patients whose heart defects are uncorrected.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Detection of reversible platelet aggregates in the blood of smokers and ex-smokers with peripheral vascular disease.

OBJECTIVE: To demonstrate that smoking increases platelet aggregation in vivo, that smoking cessation reverses platelet aggregation and that this explains, in part, why smoking perpetuates the development of peripheral vascular disease. DESIGN: Prospective case-control study involving three groups of patients: smokers with peripheral vascular disease, ex-smokers with peripheral vascular disease and smokers with peripheral vascular disease who quit smoking during the study. SETTING/PARTICIPANTS: Fourteen smokers and seven ex-smokers, new patients with confirmed peripheral vascular disease, attending the vascular clinic at Fremantle Hospital between February and November, 1988. INTERVENTIONS: Blood samples taken weekly from all subjects for five weeks. Week 1 was taken as the baseline before smoking cessation in the six smokers who were assigned to stop smoking during the study. MAIN OUTCOME CRITERIA: Platelet aggregate ratio, an indicator of in-vivo platelet aggregability where an increase in platelet aggregate ratio suggests a decrease in platelet function. RESULTS: Only three of six smokers stopped smoking for the duration of the study. Median platelet aggregate ratios were: smokers = 0.85 (range, 0.79-0.92) v. non-smokers = 0.93 (range, 0.91-1.00). The difference was statistically significant P less than 0.0002. The difference in platelet aggregate ratios between smokers and quitters was not statistically significant. CONCLUSIONS: This study demonstrated an increase in platelet aggregability in smokers compared to ex-smokers but there was no clear evidence that platelet function was fully reversed after only four weeks cessation of smoking. The data suggested that platelet function of the ex-smokers had fully reversed to normal over a longer period. This could explain the decreased incidence of complications of peripheral vascular disease in ex-smokers. The small number of patients able to quit smoking impeded this study.

Adult↗
PubMed1995

Ankle-arm blood pressure index as a marker for atherosclerotic vascular diseases in hemodialysis patients.

The ankle to arm blood pressure index (AABI) has been recently found to be a strong predictor of cardiovascular and overall mortality in several populations. The test, which is a noninvasive marker for lower extremity vascular disease (when the index is < 0.9), is an office procedure that is simple to perform. The purpose of this study was to evaluate the AABI in hemodialysis patients. One hundred seventy-seven hemodialysis patients were studied, of which the AABI could be measured in 142. The AABI was then compared in patients with and without coronary artery disease, cerebrovascular disease, and peripheral vascular disease. In patients with or without coronary artery disease, the AABI was, respectively, 0.87 +/- 0.03 and 1.03 +/- 0.02 (P < 0.0001). For cerebrovascular disease, the mean AABI for patients with or without disease was, respectively, 0.82 +/- 0.04 and 1.00 +/- 0.02 (P < 0.0004). In patients with or without peripheral vascular disease, the mean AABI was, respectively, 0.75 +/- 0.04 and 1.02 +/- 0.02 (P < 0.0001). The mean AABI was 0.86 +/- 0.03 in patients with any of the three diseases compared with 1.07 +/- 0.02 in patients without any vascular disease (P < 0.0001). Thirty-eight percent of patients had an AABI of less than 0.9; 24% were less than 0.8 and 11% were less than 0.7.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

The role of nitric oxide and other endothelium-derived vasoactive substances in vascular disease.

Alteration in the release and action of endothelium-derived vasoactive factors is responsible for changes in vascular reactivity early in the course of vascular disease. These factors include nitric oxide, eicosanoids, endothelium-derived hyperpolarizing factor, endothelin, and angiotensin II. Because endothelial dysfunction occurs at early stages of disease, it may reflect physiological changes that, if allowed to become chronic, are responsible for changes in vascular structure and growth and adhesivity to platelets and leukocytes, ultimately leading to atherosclerosis and thrombosis. Each of the major risk factors predisposing to vascular disease are associated with endothelial cell dysfunction, suggesting a direct etiologic link between the effects of the risk factors on the endothelium and their propensity to accelerate vascular disease. Restoration or replacement of endothelium-derived factors such as nitric oxide and prostacyclin, which impede the progression of vascular disease, or preventing the action of mediators such as vasoconstrictor eicosanoids, angiotensin II, or endothelin, which accelerate the progression of vascular disease, has become a useful paradigm in the treatment and prevention of vascular disease. Thus, understanding the physiology of endothelium-derived vasoactive factors is a necessary part of every physician's education.

Angiotensin II↗