Vascular Wall Structure Research Articles

Relationship between homocysteine and thrombotic disease.

Hyperhomocysteinemia is a condition which, in the absence of kidney disease, indicates a disrupted sulfur amino acid metabolism, either because of vitamin deficiency (folate, B12 and B6) or a genetic defect. Epidemiologic evidence suggests that mild hyperhomocysteinemia is associated with increased risk of arteriosclerotic disease and stroke. The relationship between hyperhomocysteinemia and thrombosis has been investigated in 10 studies involving a total of 1200 patients and 1200 controls. Eight of these studies demonstrated positive association with odds ratios that ranged from two to 13. This association was enhanced by including a methionine loading test. There is some evidence which suggests that hyperhomocysteinemia and activated protein C resistance have synergistic effect on the onset of thrombotic disease. Recent studies with animal models for mild hyperhomocysteinemia provided encouraging results in the understanding of the mechanism that underlies this relationship between mild elevations of plasma homocysteine and vascular disease. These animal models pointed to the possibility that the effect of elevated homocysteine is multifactorial, affecting both the vascular wall structure and the blood coagulation system.

Vascular endothelial cell regulation of extracellular matrix collagen: role of nitric oxide.

Endothelium-derived products have been implicated in the regulation of vascular wall structure through their effects on extracellular matrix metabolism. The purpose of this study was to further understand the paracrine mechanisms underlying endothelial cell regulation of extracellular matrix metabolism by testing the hypothesis that endothelium-derived nitric oxide decreases the concentration of soluble collagens derived from vascular smooth muscle cells (VSMCs). Porcine coronary endothelium and VSMCs were grown under a coculture configuration to assess the paracrine effects of nitric oxide produced by the endothelium on VSMC collagen types I and III. Endogenous endothelial cell nitric oxide production was blocked with N(omega)-nitro-L-arginine methyl ester. Collagen type I and type III were quantitatively measured using an enzyme-linked immunosorbent assay method. The endothelium elicited a time-dependent increase in the concentration of soluble VSMC-derived collagen type I; in contrast, collagen type III was decreased. After inhibition of nitric oxide production, there was a marked increase in both collagen types I and III concentration. These results demonstrated that endothelium-derived nitric oxide differentially alters collagen subtypes produced by VSMCs. The data support the hypothesis that nitric oxide functions via a paracrine mechanism to decrease VSMC collagen types I and III concentration, a finding consistent with an integral role for the endothelium in modulating extracellular matrix metabolism.

Endothelial Cell Injury in Cardiovascular Surgery: An Overview

In the last decade the endothelium has been shown to play a major role in regulating membrane permeability, lipid transport, vasomotor tone, coagulation, inflammation, and vascular wall structure. These critical endothelial cell functions are extremely sensitive to injury in the form of hypoxia, exposure to cytokines, endotoxin, cholesterol, nicotine, surgical manipulation, or hemodynamic shear stress. In response to injury endothelial cells become activated, tipping the balance of endothelial-derived factors to disrupt barrier function, and enhance vasoconstriction, coagulation, leukocyte adhesion, and smooth muscle cell proliferation. Although these responses likely exist as protective mechanisms, if the stimuli are severe the responses may become excessive, resulting in damaged tissue, impaired organ function, and an abnormal fibroproliferative response. Recent discoveries in the field of vascular biology have led to an expanded understanding of many of the complications of cardiovascular operations. Because of the wide impact endothelial cell dysfunction has on patients with cardiovascular disease, issues pertaining to endothelial biology are in the forefront of research that will affect the current and future practice of cardiothoracic surgery.

Factors controlling growth and matrix production and matrix production in vascular smooth muscle and glomerular mesangial cell

The vasculature wall is an active, integrated organ composed of endothelial cells and vascular smooth muscle cells, as well as other cell types depending on the specific vascular segment (e.g. fibroblasts in many vascular regions). The vascular wall is not static; the vascular components (cells and extracellular matrix) dynamically increase, decrease or reorganize, or both, in response to physiological and pathological stimuli. The vascular smooth muscle cells are the final common pathway for many of these dynamic changes in vascular wall structure. In the renal glomerulus, however, the glomerular mesangial cells-a cell phenotypically related to the vascular smooth muscle cells-also participate. Although sometimes beneficial, changes in vascular or glomerular structure often lead to cardiovascular (e.g. atherosclerosis, restenosis, intimal hyperplasia) and renovascular (e.g. glomerulosclerosis) diseases. Consequently, much effort has been expended to elucidate the mechanisms that control growth and extracellular matrix production by vascular smooth muscle cells and glomerular mesangial cells. The purpose of this review is to discuss recent developments.

Effects of Angiotensin-Converting Enzyme Inhibitors on the Heart and Vessels in Clinical and Experimental Hypertension

The primary aim of antihypertensive therapy is to reduce blood pressure. Whatever their mechanisms of action, almost all the antihypertensive drugs currently available can be considered to achieve this goal. However, the most common complications of hypertension (myocardial infarction, thrombolytic stroke and sudden cardiac death) are related to structural cardiovascular changes rather than being directly related to blood pressure elevation. Thus, it would appear logical that an optimum antihypertensive drug should also prevent and reverse the cardiovascular abnormalities associated with hypertension before irreversible damage occurs. The different classes of antihypertensive drug are in fact largely successful in preventing or reversing these target abnormalities, in particular cardiac and vascular abnormalities. In hypertensive patients, angiotensin-converting enzyme (ACE) inhibitors appear to be particularly effective in achieving this goal, probably because they alter vascular wall and cardiac structure, irrespective to some extent of the haemodynamic changes they produce. ACE inhibitors may have particularly beneficial effects on left ventricular mass because of their favourable interference with growth factors; an increased production of bradykinin, and hence of nitric oxide, may add further benefit. ACE inhibitors also prevent and/or reduce reactive perivascular and interstitial growth, as well as fetalisation of cardiac myocytes. Furthermore, in common with calcium channel antagonists and nitrates, ACE inhibitors improve arterial compliance, and thus decrease cardiac load. Indirect evidence suggests that a reduction in left ventricular hypertrophy during antihypertensive therapy reverses the pathological consequences of an increased left ventricular mass, although further studies are needed to assess the true clinical impact of these treatment-induced changes in the morbidity and mortality of hypertensive patients.

Vascular wall thickness in hypertension: the perindopril regression of vascular thickening European community trial: Protect

A high prevalence of increased intima/media thickness of the arterial wall has been documented in hypertension. These alterations in vascular wall structure may be potent determinants for the promotion of the development of atherosclerosis. Direct histologic data from animal models of hypertension, and indirect data from hypertensive patients, have demonstrated a marked regression of increased intima/media thickness by angiotensin-converting enzyme (ACE) inhibition. Long-term effects of ACE inhibition on structural wall changes in humans have not been examined. Therefore, a multicenter, randomized, double-blind European trial was designed to compare the effects of the ACE inhibitor perindopril and the diuretic hydrochlorothiazide in slowing or reversing progression of increased intima/media thickness of carotid and femoral arteries in hypertensive patients. A total of 800 patients at 17 clinical centers in 7 European countries, aged 35-65 years, with hypertension and ultrasonographically proven intima/media thickness > or = 0.8 mm of the common carotid artery will be randomly assigned to receive in a double-blind fashion either perindopril or hydrochlorothiazide and will be followed for 24 months. High resolution duplex sonography will be used to quantify intima/media thickness at baseline and twice a year during follow-up. A change of 0.1 mm of intima/media thickness from baseline is considered to be detectable, and the standard deviations of the changes from baseline are expected not to be higher than 0.2 mm. The primary endpoint of the study is the comparison of changes in intima/media thickness of the common carotid artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Vascular wall thickness in hypertension: the perindopril regression of vascular thickening European community trial: Protect

A high prevalence of increased intima/media thickness of the arterial wall has been documented in hypertension. These alterations in vascular wall structure may be potent determinants for the promotion of the development of atherosclerosis. Direct histologic data from animal models of hypertension, and indirect data from hypertensive patients, have demonstrated a marked regression of increased intima/media thickness by angiotensinconverting enzyme (ACE) inhibition. Long-term effects of ACE inhibition on structural wall changes in humans have not been examined. Therefore, a multicenter, randomized, double-blind European trial was designed to compare the effects of the ACE inhibitor perindopril and the diuretic hydrochlorothiazide in slowing or reversing progression of increased intima/media thickness of carotid and femoral arteries in hypertensive patients. A total of 800 patients at 17 clinical centers in 7 European countries, aged 35–65 years, with hypertension and ultrasonographically proven intima/media thickness ≥0.8 mm of the common carotid artery will be randomly assigned to receive in a doubleblind fashion either perindopril or hydrochlorothiazide and will be followed for 24 months. High resolution duplex sonography will be used to quantify intima/media thickness at baseline and twice a year during follow-up. A change of 0.1 mm of intima/media thickness from baseline is considered to be detectable, and the standard deviations of the changes from baseline are expected not to be higher than 0.2 mm. The primary endpoint of the study is the comparison of changes in intima/media thickness of the common carotid artery. Secondary endpoints include comparison of the effectiveness of the two treatments on left ventricular mass, posterior wall thickness, intraventricular septal thickness, left ventricular end-diastolic diameter, and comparison of the 2 treatments on ultrasonographically determined thickness of the intima/media complex of the common femoral artery. Further analyses will assess the relation between intima/ media thickness changes and the changes of blood pressure, heart rate, low and high density lipoprotein cholesterol, triglycerides, and glucose. The study is designed to assess the impact of antihypertensive therapy on early pathological vascular wall changes and to clarify whether this is due to a drug-specific action or only dependent on the blood pressure lowering effect.

Expression of basement membrane and endothelial cell adhesion molecules in vascular malformations of the brain: Preliminary observations and working hypothesis

Little is known about the pathogenesis and subsequent cellular biologic behaviour of human cerebral vascular malformations. Innovative therapeutic strategies will depend on more fundamental understanding of structural and functional lesion biology. We have freeze-processed four specimens of arteriovenous malformation (AVM), two cavernous malformations (CM), and resected cortex from one case of Sturge-Weber disease (SWD) for immunohistochemical studies. Probes of vascular maturity and cellular adhesion were examined, including Factor 8 related antigen (F8RAG), laminin, fibronectin, and adhesion molecules VCAM, ELAM and ICAM-1 (CD 54). Sections of the same lesions were permanently fixed and stained using Haematoxylin and Eosin, and MOVAT Pentachrome stain for identification of vascular wall structures. A double antibody staining battery was utilized with ultraviolet fluorescent microscopy, and was analysed by an observer blinded to the antibody and lesion type. All malformations showed strong expression on their luminal endothelial surface for F8RAG. There was no expression of ELAM in any lesion. Two AVMs expressed VCAM on the endothelial surface of some vessels. ICAM-1 was expressed faintly within two AVMs. The CMs expressed fibronectin within the endothelium and subendothelial matrix, and both lesions were devoid of laminin expression. The AVMs and the SWD vessels stained for laminin, while none of the AVMs expressed fibronectin. These preliminary observations are consistent with the hypothesis that AVMs and SWD represent more mature vessels, consistent with possible lesion genesis during early phases of embryonic vascular development (dysvasculogenesis). In contrast, CMs represent immature vessels devoid of laminin and other features of mature vessels, consistent with ongoing dysangiogenesis within a fibronectin rich matrix. Further studies should be aimed at better elucidation of these biologic probes, and correlation with specific lesion behaviour.

Intervascular Smooth Muscle Fibers and Muscular Bolsters in Nasal Swell Bodies of Humans

There is strong clinical evidence that the cavernous tissue (swell bodies) of nasal mucosa plays an important role in congestion of the nose. Still, the complex mechanisms responsible for the unique behavior of these vessels have not yet been identified, and even the morphology of these structures is still a matter of controversy. The present study was performed on nasal mucosal specimens from inferior turbinates of humans by means of histology and transmission electron microscopy. Besides the evaluation of the vascular wall structure of the nasal swell bodies, special attention was given to two morphological peculiarities: intervascular smooth muscle fibers and muscular bolsters. Intervascular smooth muscle fibers are composed of bundles of smooth muscle cells varying in diameter between 14 and 35 microns; they are attached to the muscular coat of the vessels of the cavernous tissue. Muscular bolsters are distinct protrusions of the vascular wall in nasal swell bodies; they are found not only at the transition between different vessels, but also irregularly within the course of veins of the cavernous tissue. The authors report on their understanding of the functional significance of intervascular smooth muscle fibers and muscular bolsters within the cavernous tissue for swelling mechanisms in the nose and discuss their results in light of the literature.

The morphology of endonasal cavernous tissue with special reference to muscular cushion formation. A light and transmission electron microscopy study

Nasal "cavernous" tissue is widely accepted as a key structure for the tumefactive mechanism inside the nose; still there is no common understanding of the structural composition of this special tissue. In the present paper the authors demonstrate the results of their histological and transmission electronmicroscopic findings in human nasal "cavernous" tissue, especially referring to the structural and ultra-structural pattern of the so-called muscular pads or "cushion". Serial sections revealed that these structures occur at the transition of communicating vessels; their muscular coat shows a different and irregular pattern, compared to the vascular wall structure of other parts of nasal "cavernous" tissue. Ultrastructural examination confirmed the impression of a variable and complex orientation of smooth muscle cells within the muscular "cushions". The cytoplasmic components, however, were the same as in other smooth muscle cells of nasal "cavernous" tissue. Localisation and structure of muscular "cushions" imply their functional significance for tumescence of the nasal mucosa in a variety of rhinological disorders. Therefore, the authors suggest to include these special features in therapeutic considerations on the treatment of congested nose. Evaluation of the neurovegetative regulation of this tissue could be a step in the right direction.

Carotid arterial compliance in patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy

Conduit artery distensibility affects the pulsatile component of afterload and may contribute to impaired left ventricular function in patients with congestive heart failure (CHF). The objectives of this study were to (1) determine whether arterial distensibility is reduced in patients with CHF, and (2) determine whether decreased arterial compliance is related to an abnormality in vascular wall structure (i.e., wall thickness or excessive levels of circulating neurohumoral vasoconstrictors, or both). The study participants included 40 patients with CHF secondary to idiopathic dilated cardiomyopathy and 33 age-matched healthy volunteers. High-resolution ultrasonography was performed to directly visualize the common carotid artery and measure its diameter and wall thickness. Its elastic properties were determined by relating changes in arterial diameter to changes in pressure generated with each heart beat. Carotid artery distensibility was less (14.1 ± 1.1 vs 25.3 ± 1.6 10−6 · N−1 · m2, p < 0.001) and Young's modulus of elasticity was greater (3.99 ± 0.51 vs 2.29 ± 0.23 105 · N · m−2, p < 0.005) in patients with CHF than in normal subjects. Also, carotid artery wall thickness was increased in patients with CHF. When the entire population was considered, age, wall thickness, and plasma norepinephrine and aldosterone concentrations correlated inversely with distensibility, whereas age and plasma norepinephrine concentration correlated directly with elasticity. Among normal subjects, only age correlated inversely with distensibility; among patients with CHF, only plasma norepinephrine concentration correlated with elasticity. It is concluded that carotid artery distensibility is reduced in patients with CHF. Sympathetic nervous system activity may contribute actively to decreased arterial compliance in patients with CHF by increasing vascular tone in medium-sized arteries.

Site-specific, structural and ultrastructural characteristics of endonasal cavernous tissue exemplified by the inferior turbinate in man. Light and transmission electron microscopy study

The cavernous tissue of the nose has been studied morphologically for now more than 150 years. Even though the majority of new findings was already described in the second half of the last century and is associated with scientists like Kölliker, Kohlrausch and Zuckerkandl. The vascular structures, usually described as "cavernous tissue" or "swell bodies" are located in different parts of the nasal mucosa, but mainly in the inferior turbinate. In the present paper the author demonstrates the results of his studies on the structure and ultrastructure of smooth muscle components of nasal swell bodies based on light - and transmission-electron microscopic findings. Light microscopic observations already reveal the differences in vascular wall structure between areas adjacent to the epithelium and those parts of the vessels located in the deeper parts of the tunica propria. Ultrastructural examination shows differences in size and density of smooth muscle cells in different parts of the cavernous tissue; it also demonstrates the variant appearance of the basal lamina of these muscle cells. The results are discussed and compared with the appropriate literature.

Vascular wall thickness in hypertension

A high prevalence of increased intima/media thickness of the arterial wall has been documented in hypertension. These alterations in vascular wall structure may be potent determinants for the promotion of the development of atherosclerosis. Direct histologic data from animal models of hypertension, and indirect data from hypertensive patients, have demonstrated a marked regression of increased intima/media thickness by angiotensinconverting enzyme (ACE) inhibition. long-term effects of ACE inhibition on structural wall changes in humans have not been examined. Therefore, a multicenter, randomized, double-blind European trial was designed to compare the effects of the ACE inhibitor perindopril and the diuretic hydrochlorothiazide in slowing or reversing progression of increased intima/media thickness of carotid and femoral arteries in hypertensive patients. A total of 800 patients at 17 clinical centers in 7 European countries, aged 35-65 years, with hypertension and ultrasonographically proven intima/media thickness ~0.8 mm of the common carotid artery will be randomly assigned to receive in a doubleblind fashion either perindopril or hydrochlorothiazide and will be followed for 24 months. High resolution duplex sonography will be used to quantify intima/media thickness at baseline and twice a year during follow-up. A change of 0.1 mm of intima/media thickness from baseline is considered to be detectable, and the standard deviations of the changes from baseline are expected not to be higher than 0.2 mm. The primary endpoint of the study is the comparison of changes in intima/media thickness of the common carotid artery. Secondary endpoints include comparison of the effectiveness of the two treatments on left ventricular mass, posteriorwall thickness, intraventricular septal thickness, left ventricular end-diastolic diameter, and comparisonof the 2 treatments on ultrasonographitally determined thickness of the intima/media complex of the common femoral artery. Further analyses will assess the relation between intima/ media thickness changes and the changes of blood pressure, heart rate, low and high density lipoprotein cholesterol, triglycerides, and glucose. The study is designed to assess the impact of antihypertensive therapy on early pathological vascular wall changes and to clarify whether this is due to a drug-specific action or only dependent on the blood pressure lowering effect. (Am J Cardioll995; 7650E64E)

Effects of angiotensin-converting enzyme inhibition with perindopril on hemodynamics, arterial structure, and wall rheology in the hindquarters of atherosclerotic mini-pigs

The effects of ACE inhibition with perindopril on the atherosclerosis-induced impairment of arterial flow were investigated via histopathologic studies, hemodynamics, and vascular rheology of hindlimb arteries in 7 adult Pitman-Moore mini-pigs (7 months of age) fed for 4 months with an atherogenic diet and perindopril (at the daily oral dose of 4 mg, which induced a continuous 70% inhibition of serum ACE activity), versus 7 atherogenic and 7 control animals. Major fibroproliferative fatty lesions with medial intimalization were observed in the abdominal aorta. Atherosclerosis impaired the function of both capacitance and resistance hindlimb arteries. In atherogenic minipigs, blood pressure (BP) increased significantly due to increased hindlimb peripheral resistance (HPR) and aortic input impedance, although aortic blood flow was not affected. Altered aortic wall rheology revealed that the stiffness of the aorta was markedly increased due to increased wall tension and reduced viscoelasticity, the viscous component being reduced in the arterial wall. Perindopril significantly opposed these alterations by reducing BP, HPR and input impedance and by returning parietal stiffness to control values by increasing aortic compliance. Angiotensin converting enzyme (ACE) inhibition significantly prevented the development of atherosclerosis in the abdominal aorta by decreasing the cross-sectional area of lesions and the presence of lipid-laden cells, as well as by preventing alteration and fragmentation of elastic laminae. In conclusion, ACE inhibition with perindopril showed a significant preventive action on atherosclerosis-induced-deleterious effects on vascular wall function and structure in mini-pig arteries.

Intraluminal ultrasound imaging through a balloon dilation catheter in an animal model of coarctation of the aorta.

Controversy still exists over the optimal balloon size, extent of vascular disruption, and long-term results of balloon dilation therapy for coarctation of the aorta. Intravascular ultrasound imaging has been used in patients with coronary artery disease to provide further insight into the anatomy of atherosclerotic lesions and the results of angioplasty and atherectomy. Initial observations of the results of balloon dilation of coarctations with intravascular ultrasound imaging have shown prominent dissections of the inner vascular layers that are often not detected by angiography. The purpose of this study was to test a new transballoon catheter ultrasonic imaging system capable of on-line direct visualization of lumen diameter and vessel wall structure for imaging before, during, and after dilation in an acute animal model of aortic coarctation. Abdominal aortic coarctations were created surgically in three 14-19-kg mongrel dogs by using Teflon gauze ties. The 6.8F ultrasound balloon catheter was placed percutaneously in the right femoral artery through a 9F sheath. Ultrasound imaging allowed measurement of the coarctation diameter, characterization of the vessel wall structure, localization of the stenosis, and placement of the midportion of the balloon at the narrowest area. Imaging through the balloon was performed through several dilations (five to eight per animal), and after balloon deflation, it provided information on postdilation diameter, intimal tears, long-segment dissections, and intramural thrombi, findings that were confirmed at postmortem examination. The results of this study demonstrate that imaging with a new intraballoon ultrasound device is feasible during inflation to therapeutic dilation pressures; it allows visualization of the changes in diameter and vascular wall structure after serial dilations without having to recross the obstructed area. Adaptation to larger balloon sizes and lower frequencies should make this system applicable to interventional catheterizations in patients with congenital cardiac and vascular lesions.

Experimental Steroid-Induced Osteonecrosis in Adult Rabbits With Hypersensitivity Vasculitis

Osteonecrosis (ON) was experimentally induced in rabbits by employing a combined protocol of hypersensitivity vasculitis and administration of high-dose corticosteroids. Thirty-five adult rabbits were used: five were injected twice with horse serum (Group A), five were injected three times with methylprednisolone acetate (Group B), 20 were treated with a combination of horse serum and methylprednisolone acetate (Group C), and five were used as a control (Group D). Both femurs of each rabbit were obtained one to five weeks after the final treatment and were histologically examined. There was no evidence of ON in Groups A, B, and D, whereas vasculitis was prominent in the femurs of Group A rabbits. In Group C, 14 of 20 specimens (70%) showed histologic evidence of ON in the femoral metaphysis: seven showed marrow necrosis and seven marrow and trabecular necrosis. Intramedullary hemorrhage was detected in eight animals. All specimens that showed ON or marrow necrosis revealed arteriopathy (i.e., severe damage to the vascular wall structure of arterioles). These findings were similar to those observed in early ON of clinical materials. The authors conclude that arteriopathy plays an important role in the pathogenesis of ON.

Alzheimer's disease as a capillary dementia.

In addition to the well known structural stigmata which accompany the senile dementia of Alzheimer, attention is called to the presence of a group of robust changes which affect the fine vessels (capillaries, capillary arterioles and capillary venules), particularly of the cerebral cortex. These alterations include irregular pouches and excrescences on the vessels (a "lumpy-bumby" appearance), general thickening of the basement membrane, loss of the fine perivascular neuronal plexus which seems to invest each vessel, no matter how small, and the appearance of pits or lacunae in the vessel walls of about one half of the Alzheimer patients studied. None of these changes have been seen in a group of approximately age-matched, non-demented controls. Much of this perivascular neural plexus originates within a few specific subcortical fields, especially the locus ceruleus and the nucleus basalis of Meynert and basal forebrain area. These also happen to be included among those brain areas which experience the most marked neuronal atrophy or loss in Alzheimer's disease. Since there is some evidence suggesting that surgically induced vascular denervation in myocardium produces dramatic changes in vascular wall structure we wonder whether neuronal pathology developing initially in these subcortical areas may not play a significant role in the development of the characteristic neuropathology in Alzheimer's disease. These speculations emphasize the possible importance of a failing blood brain barrier in the development of the disease.

Morphological changes of microvessels in the brain with Alzheimer's disease.

The pathological changes of microvessels in the cerebral cortex in Alzheimer's disease were examined at the ultrastructural level. With transmission electron microscopy (TEM), the endothelial cells of many capillaries and their pericytes exhibited atrophy and swelling with a narrowed lumen. The capillary basal laminas were thickened and tortuous. After isolation of the microvessels by ultrasonic treatment and collagenase digestion, the vascular wall structure was viewed by scanning electron microscopy (SEM). Most of the terminal arterioles had smooth muscle cells with an irregular shape and arrangement and often showed a series of focal constrictions. In some areas, the capillaries were arrayed in a bundle and terminated with tapered ends. Associated with the microvessels were fine filaments which may represent amyloid fibrils. The findings indicate that diffuse atrophy and the deletion of nerve cells in the cerebral cortex might be caused, at least partly, by a circulatory disturbance through the pathomorphologically changed microvessels.

Molecular perspectives of vascular wall structure and disease: the elastic component.

In 1974 more than 50 percent of all deaths in the United States were caused by the major cardiovascular diseases [I]. Thus the ancient dictum that man is as old as his arteries is even more applicable to longevity in our modern Western society. With past analytical developments utilized in biomedical research, the primary site within the vascular wall of two of the three major degenerative processes has been identified as the elastic fiber. This has led to an extension of the above statement. It is true that we have the age of our arteries. This means more or less that we have the age of their elastic fibers [2]. More recently, composite elements of the elastic fiber have been described in molecular detail [3, 4]. These molecular descriptions provide an understanding of the mechanism of pathological calcification of the elastic fiber [5] and of deleterious lipid deposition in this essential dynamic component of vascular wall [6]; they provide an understanding of the importance of temperature in the formation and repair of elastic fiber [7]; and they may provide a molecular rationale for relating elevated sodium chloride levels to elevated blood pressures [7]. The molecular perspectives derive from physicochemical methods and concepts applied in studying the structure and disease of vascular wall elastic fiber.

The effect of indomethacin and ASA on [formula omitted] induced white platelet arterial thrombus formation

White platelet thrombus formation in a branch of the mesenteric artery of the rat induced by electrical current application followed by ADP superfusion can be inhibited by Aspirin and indomethacin topically applied. This phenomenon could result from the decrease of the cyclooxygenase-like activity present in the vascular wall structures.