Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aortic localization of diet-induced fatty streaks in relation to focal increases in intimal permeability was evaluated in cynomoglus monkeys. Animals fed a hypercholesterolemic diet and studied at 10, 15, and 100 days had increasing intensity of Evans blue dye uptake. The overlap of fatty streaks with areas of dye intake increased as the areas of dye uptake enlarged, but all hypercholesterolemic groups showed some fatty streaks not topographically related to areas of dye uptake or flow instability. Because the upper thoracic aorta tended to show more advanced fatty streak formation dissociated from evident permeability change or hydraulic instability, it is suggested that mechanical factors associated with the geometric configuration of the descending thoracic aorta may have a significant role in the localization of some hypercholesterolemic fatty streaks.
Atherosclerosis 1978 Dec
PMID:The relation of hypercholesterolemic fatty streaks to intimal permeability changes shown by Evans blue. 10 62

In 64 patients with ischemic strokes that occurred on the background of atherosclerosis (33) and a combination of atherosclerosis with arterial hypertension (31) using the dilution method of Evans's blue the authors studied indices of general hemodynamics compared to rheoencephalographic data. Twenty similar patients without signs of brain circulation disturbances and 20 healthy persons were taken as control groups. In 69% of the patients with ischemic strokes deep disturbances of general hemodynamics were observed. An increase of tonus, a decrease of elasticity of cerebral vessels and deficit of pulse blood repletion were determined rheoencephalographically. Insufficiency of general hemodynamics in conditions of changed autoregulation of brain circulation promotes development of ischemic disorders of brain circulation and unfavourably influences the course and outcome of the stroke.
 ...
PMID:[State of general and cerebral hemodynamics in patients with ischemic strokes]. 42 64

Parameters of the general and cerebral hemodynamics were examined in 45 patients with cerebral circulation disturbances developed in the presence of atherosclerosis (30 patients) and atherosclerosis plus arterial hypertension with cardiac arrhythmias (15 patients) and without the latter (72 patients). The examinations were carried out with the use of the Evans blue dilution method (T-1824) and rheoencephalography. Shifts in the general and the cerebral hemodynamics were revealed in the patients with and without cardiac arrhythmias, these shifts being more pronounced in patients with atherosclerosis complicated with the heart ischemic disease and cardiac arrhythmia. In the course of complex treatment which included cardiotonics and beta-adrenoblocking agents the parameters of the general hemodynamics got better along with the clinical improvement.
 ...
PMID:[General hemodynamic features in the cerebral circulatory disorders of patients with atherosclerosis and atherosclerosis combined with arterial hypertension accompanied by heart rhythm disorders]. 49 32

In comparing the indices in 105 patients with diabetes and in 75 healthy persons a possibility was revealed of significant disturbances of the contractile function of the myocardium also in young patients with diabetes without any clinico-instrumental signs of coronary atherosclerosis. This proves the significane not only of atherosclerotic changes in the development of myocardial pathology in diabetes, but alos of the metabolic ones. Against the opinion of some authors, when given in the usual therapeutic doses insulin failed to lead to negative shifts in the phasic structure of the left ventricle systole in diabetics. For the first time investigations of hemodynamics by the method of diluted Evans blue demonstrated an increase in the plasma volume and of the circulating blood mass, and a decrease of circulation velocity in diabetes.
 ...
PMID:[The contractile capacity of the myocardium, the effect of insulin on it and indices of central hemodynamics in patients with diabetes mellitus]. 113 69

Repeated endothelial cell injury has been suggested as an initiating factor in atherogenesis. Dying or dead endothelial cells have been shown to make significant contributions to the local enhancement of transendothelial macromolecular transport. Since cigarette smoking is one of the major risk factors for atherosclerosis, we examined the hypothesis that smoking accelerates atherogenesis by increasing the frequency of endothelial cell death and hence transendothelial macromolecular transport. Sixteen male Sprague-Dawley rats were given nicotine at a weight-adjusted dose of 5 mg/kg body wt per day in their drinking water over a period of 6 weeks. A group of 16 age-matched male Sprague-Dawley rats not exposed to nicotine and maintained over the same time period served as the control group. In en face preparations of thoracic aorta, immunoglobulin G-containing dying or dead endothelial cells were identified by the indirect immunoperoxidase method, and endothelial leakage to Evans blue-albumin (EBA) complexes (5 minutes after intravenous injection) was visualized by fluorescence microscopy. The results showed that in nicotine-treated rats, 51% of dead endothelial cells were associated with EBA leakage, which was responsible for 57% of total EBA leaky foci. Both the frequency of endothelial cell death (0.94 +/- 0.11% versus 0.40 +/- 0.04%, p < 0.0001 by two-tailed, unpaired Student's t test) and the number density of EBA leaky foci (6.45 +/- 1.23/mm2 versus 3.30 +/- 0.49/mm2, p < 0.05 by two-tailed, unpaired t test) were significantly greater in nicotine-treated rats than in control rats.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Long-term nicotine exposure increases aortic endothelial cell death and enhances transendothelial macromolecular transport in rats. 142 90

There are focal areas in the aorta with an enhanced endothelial permeability to macromolecules, as indicated by the focal uptake of the protein-binding azo dye Evans blue in vivo. These areas exhibit high rates of endothelial cell turnover and a number of structural characteristics in en face endothelial morphology. To determine the relationship of endothelial cell death to macromolecular leakage at the level of individual endothelial cells, thoracic aortas of 12 adult male Sprague-Dawley rats were studied at 3 to 5 minutes after intravenous administration of Evans blue-albumin (EBA). Leakage of EBA around individual endothelial cells in en face preparations of the aorta was visualized by fluorescence microscopy. Dying or dead endothelial cells were identified by indirect immunoglobulin G (IgG) immunocytochemistry. Although endothelial cell death is uncommon in normal aortic endothedium (i.e., an average frequency of 0.48%), a high percentage (63%) of IgG-containing dying or dead endothelial cells was found to be associated with EBA leakage. These dying or dead endothelial cells were responsible for 37% of total EBA leaky foci. The results suggest that, in addition to mitotic endothelial cells, the dying or dead endothelial cells also make significant contributions to the local enhancement in aortic endothelial permeability. The present findings lend further support to the "cell turnover-leaky junction" hypothesis for the localization of atherosclerosis.
 ...
PMID:Role of dying endothelial cells in transendothelial macromolecular transport. 169 53

Evans blue dilution and ultrasound dopplerography was used to examine 170 atherosclerosis patients with initial manifestations of insufficient cerebral blood supply (77 patients) and transient disorders of the cerebral blood circulation (93 patients) with occlusive and stenotic involvements of the major brain arteries. The authors revealed characteristic aspects of responses of the systemic-hemodynamic mechanisms in initial manifestations of insufficiency of the cerebral blood supply and transient disorders of the cerebral blood circulation with stenosis and occlusions of the major brain arteries and without involvement of the brain vessels. Treatment aspects are discussed.
 ...
PMID:[Cardiogenic disorders of the systemic hemodynamics in lesions of the major cerebral arteries]. 194 36

Leaky endothelial junctions associated with cell turnover have been suggested to be a hydrophilic pathway for the transport of macromolecules across the vascular endothelium. To demonstrate focal increases in endothelial permeability, the occurrence of localized uptake of macromolecules in the rat thoracic aorta was studied at various time periods after intravascular administration of Evans blue-albumin (EBA) complexes. With fluorescence microscopy, EBA uptake in the rat thoracic aorta was visible either as discrete spots or as larger areas in both en face and cross-sectional preparations. The average size of EBA leaky spots increased with dye circulation time, indicating that there is a continuous influx of macromolecules through the transiently leaky junctions in these foci with subsequent diffusion in the vessel wall. There was heterogeneity in EBA spot size distribution, suggesting that endothelial cells undergoing turnover in different phases of the cell cycle might exhibit different extents of junctional leakage to macromolecules. The technique of [3H]thymidine labeling autoradiography was applied to en face preparations of the rat thoracic aorta for identifying replicating endothelial cells. The correlation of EBA leakage with [3H]thymidine-labeled endothelial cells was determined. Only 26% of endothelial cells with nuclear incorporation of [3H]thymidine were shown to be associated with EBA leaky foci. This lack of correlation suggests that alterations in endothelial junctional permeability accompanying cell turnover might occur only in some limited time periods of the cell cycle, e.g., the mitotic (M) phase, rather than the whole period of [3H]thymidine labeling.
Atherosclerosis 1990 Dec
PMID:Temporal and spatial changes in macromolecular uptake in rat thoracic aorta and relation to [3H]thymidine uptake. 210 86

Atherosclerotic lesions are characterized by lipid infiltration in regions with high rates of endothelial cell turnover. The present investigation was designed to elucidate the route of macromolecular transport across vascular endothelium. The aorta and vena cava of male Sprague-Dawley rats were perfusion-fixed after the intravenous injection of Evans-blue albumin (EBA) or horseradish peroxidase (HRP). Fluorescence microscopic examination of en face preparation of the aorta stained with hematoxylin allowed the identification of endothelial cells that underwent mitosis, together with the localization and quantification of fluorescent spots for EBA leakage. The HRP specimens were subjected to histochemical treatment, and HRP leakage was seen as brown spots under the light microscope. Silver nitrate stain was added in both EBA and HRP studies to outline cell boundaries and to visualize stigmata, stomata, and dead cells. In the aorta, almost every dividing cell showed junctional leakage to albumin and HRP, with clustering of leaky spots around the branch orifices. Time-dependent studies showed gradual increases in the diameter and number of these heterogeneously sized leaky spots, which finally fused to sizes corresponding to the "blue areas" for EBA or "brown areas" for HRP. Compared with arteries, veins had fewer mitotic cells, but more dead cells and diffuse dye-staining areas, indicating a more rapid transport of macromolecules. The leaky spots in the artery were associated mainly with mitotic cells, dead cells, and stigmata, whereas those in the vein occurred primarily at regions with dead cells. These results suggest that the preferential association of the enhanced transport of macromolecules with mitosis in the arterial as compared to venous endothelium and the differential behavior in transmural transport between arteries and veins may form the basis for the predilection of atherosclerosis in arteries.
 ...
PMID:Macromolecular transport across arterial and venous endothelium in rats. Studies with Evans blue-albumin and horseradish peroxidase. 218 Mar 95

Leaky endothelial junctions occurring during cell turnover have been postulated to be a major pathway for enhanced lipoprotein transport across the vascular endothelial layer, which leads to the development of atherosclerosis. Because hypertension has been well documented as one of the major risk factors for atherosclerosis, we explored the possibility that hypertension accelerates atherogenesis by increasing the turnover of endothelial cells and hence the transendothelial macromolecular permeability. The investigations were performed on thoracic aortas of 10 male 3-4-month-old spontaneously hypertensive rats and eight male age-matched Wistar-Kyoto normotensive rats. In en face preparations of aortic specimens, mitotic endothelial cells were identified by hematoxylin nuclear staining; dying or dead endothelial cells containing cytoplasmic immunoglobulin G were detected by indirect immunoperoxidase technique; and endothelial leakage to Evans blue-albumin conjugate was visualized by fluorescence microscopy. The number of leaky foci per unit endothelial surface area in spontaneously hypertensive rats was found to be approximately three times that in Wistar-Kyoto control rats; the frequencies of both endothelial cell mitosis and death in spontaneously hypertensive rats were also approximately three times the corresponding values in Wistar-Kyoto rats. These findings indicate that hypertension in spontaneously hypertensive rats is accompanied by increased endothelial cell turnover and an attendant enhancement of permeability to macromolecules.
 ...
PMID:Transendothelial macromolecular transport in the aorta of spontaneously hypertensive rats. 237 48


1 2 3 4 5 6 7 Next >>