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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of dietary fish oil (rich in n-3 polyunsaturated fatty acids (PUFA], corn oil (rich in n-6 PUFA) and coconut oil (low in n-3 and n-6 PUFA) on the induction of atherosclerosis by serum sickness in rabbits was investigated over a 12-month period. Dietary fish oil led to a significant increase in the level of eicosapentaenoic acid (EPA) in all platelet phospholipid fractions and to a significant reduction in the level of platelet phosphatidylethanolamine arachidonic acid (AA). In aortic total phospholipids, rabbits given fish oil showed a significant reduction in AA and a significant increase in EPA. Rabbits given fish oil showed significantly lower collagen-induced platelet thromboxane A2 release and aortic production of 6-keto-PGF1 alpha. Serum total immune complex levels and anti-horse serum IgG levels were not influenced by diet. There was a significant reduction in total aortic atherosclerosis in fish oil-fed animals compared with coconut oil fed animals.
Atherosclerosis 1988 Jul
PMID:Effect of polyunsaturated fatty acids of the n-3 and n-6 series on lipid composition and eicosanoid synthesis of platelets and aorta and on immunological induction of atherosclerosis in rabbits. 321 57

In order to examine the effect of corticosteroids on coronary atherogenesis in collagen diseases, an experimental study of serum sickness was performed. Forty-two rabbits were divided into four groups (Groups A-D). Group B, C and D rabbits received four intravenous injections of bovine serum albumin (250 mg/Kg) at 16-day intervals. Groups A, C and D rabbits were fed ad libitum cholesterol supplemented diet (1%) 16 days after the last injection. Group D rabbits received subdermal injections of prednisolone (1 mg/Kg) three times per week in the same period. After 124 days, all rabbits were sacrificed. Serum cholesterol and phospholipid increased in Group A, C and D rabbits. Group A rabbits showed intimal foam cell proliferation. Group B rabbits showed slight fibrous intimal thickening. The coronary arteries of Group C rabbits showed fatty-proliferative intimal thickening and an increase in the incidence of vascular lesions (13.9% of the coronary arteries as compared with 11.7% for Group A and 8.4% for Group B). The coronary lesions of Group D showed the same pattern as those of Group C, but the incidence of lesions was 6.0%. It was concluded that prednisolone did not augment immunologically induced atherosclerosis.
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PMID:An experimental study of atherosclerosis as a sequela of coronary arteritis. 344 99

The role of mononuclear cells in antibody-mediated endothelial cell damage and vascular diseases is not well understood when compared to our understanding of the role of neutrophil-mediated endothelial injury in vascular diseases. Thus we initiated these in-vitro studies to investigate the interactions of leukocytes (neutrophils and mononuclear cells) with vascular endothelial cells in the presence and absence of antiendothelial cell antibodies (anti-red blood cell antiserum-anti-RBC). Cultured endothelial cells were isolated from bovine pulmonary artery. The effects of unfractionated and fractionated human leukocytes (neutrophils, mononuclear cells, or lymphocytes) on endothelial cell viability was examined both quantitatively (51Cr release) and qualitatively (electron microscopy). Results from these studies indicated that the interactions of mononuclear cells and lymphocytes with antibody-coated endothelial cells resulted in a significant endothelial cell lysis within 1 to 6 hours of reactions. Neutrophils, on the other hand, failed to induce significant endothelial cell damage compared to mononuclear cells and lymphocytes when tested under similar conditions. In the absence of anti-RBC antibodies, all cell types (neutrophils, mononuclear cells, or lymphocytes) did not produce detectable endothelial damage. Additionally, the effectiveness of mononuclear cells to injure antibody-labeled endothelial cells was confirmed by ultrastructural examination. Similar studies, utilizing leukocytes obtained from patients with atherosclerosis disease, were also undertaken. In these studies we found that, again, only mononuclear cells and lymphocytes wer capable of inducing damage to endothelial cells precoated with antibodies. In summary, our results demonstrate the ability of mononuclear cells and lymphocytes to induce significant damage to antibody-coated endothelial cells. This finding suggests a major role of mononuclear leukocytes in vascular endothelial destruction in diseases that are characterized by the presence of circulating autoantibodies in serum and the adhesion of mononuclear cells to the vascular wall. Such diseases include vasculitis, allograft rejection, serum sickness, and perhaps atherosclerosis particularly in patients with autoimmune diseases.
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PMID:Influence of anti-endothelial cell antibodies on the interactions of leukocytes with vascular endothelial cells in vitro. 391 99

We determined the effect of chemotactic peptides FMLP and C5a, postulated to be relatively selective activators of phagocytes, on the thoracic aorta of rabbits subjected to experimental pathologies that allowed infiltration by leukocytes, i.e., dietary atherosclerosis and serum sickness. Aortic ring tissues isolated from hypercholesterolemic rabbits, precontracted or not by phenylephrine, exhibited a rapid and relatively sustained (10 to 20 min) contractile response when challenged by FMLP (10 nM and above); precontracted tissues also responded to C5a (2.5 nM and above). Aortic rings from rabbits with serum sickness (13 days post-BSA injection) exhibited brief contractions that were often followed by a relaxation in phenylephrine-precontracted tissues. In both models, tissues from normal weight-matched animals were not consistently responsive to these peptides. The cyclooxygenase inhibitor indomethacin extensively reduced the contractile effect of either peptide on precontracted aortic rings in both models. Chemotactic peptide-induced increased prostanoid secretion was evident only in the fluid bathing atherosclerotic aortic rings. Morphologic correlations included the demonstration of cells positive for the RAM-11 macrophage marker and the C5a receptors in tissues from rabbits with hypercholesterolemia (numerous clusters of cells) or serum sickness (modest infiltration). Control aortic rings responded to FMLP by a significant contraction if cultured for 2 h in the presence of resident peritoneal cells (84% macrophages), but not in the presence of a high density of PBL (less than 0.5% monocytes). Infiltrating or adherent macrophages in the blood vessel wall confer to some phagocyte activating peptides the role of eicosanoid-dependent vasoconstrictor agents.
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PMID:Pathologic leukocyte infiltration of the rabbit aorta confers a vasomotor effect to chemotactic peptides through cyclooxygenase-derived metabolites. 861 69

The normal vascular wall contains resident leukocytes, notably tissue macrophages (histiocytes) and mast cells, that confer a rapid, eicosanoid-dependent vasoconstrictor response to agonists typical of leukocytes, such as the complement-derived anaphylatoxin C5a or the formylated peptide f-Met-Leu-Phe (isolated organ methodology). The eicosanoid-dependent vasomotor response is even more intense in pathologies that involve leukocyte infiltration of the blood vessel wall, such as atherosclerosis and serum sickness in the rabbit. The leukocyte compartment of the blood vessel is the likely source of vasoactive mediators (eicosanoids, radicals, cytokines) of physiopathological importance, with possible application in cardiac ischemia, lupus nephritis, vasculitides, and graft rejection. This line of investigation may be compared to the discovery and characterization of endothelium-dependent vasomotor responses. However, the problem is experimentally more demanding: histological correlations, experiments based on leukocyte depletion, reconstitution, and enrichment are useful approaches to document this form of circulatory control.
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PMID:Evidence for vascular tone regulation by resident or infiltrating leukocytes. 893 61

This report traces the development of our knowledge about immune-complex arteritis from the early 20th Century to the present time. The emphasis is on the work which began with the seminal observations of serum sickness by Longcope, MacKenzie, and Rich, to the pathogenetic studies of serum sickness arteritis in rabbits by several groups including the outstanding contributions by Dixon and coworkers concerning the role of circulating immune complexes. This work was followed by investigations of the relationship to atherosclerosis revealed by the sustained studies by Minick et al. on serum sickness arteritis in hypercholesterolemic rabbits. This pioneering research work has more recently been of pivotal value in understanding the arteritis observed in certain primate species such as the cynomolgus and the nemestrina, in human lupus erythematosus, and in organ transplantation arteritis. More recently it has become apparent that one of the microscopic hallmarks of this type of immune complex injury is the concentic micro-architecture of the inflammatory arterial lesions, for which, when they are also lipid containing, we have coined the term artheroarteritis. The contributions of the neoantigens from glycosylated LDL and oxidized LDL to the development of this type of atheroarteritis are considered. New frontiers in this area of research are being opened by the PDAY study which offers new opportunities to link circulating immune complexes and new antigens to arheroarteritis with its accelerated stenotic arterial lesion development.
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PMID:Atheroarteritis: a combined immunological and lipid imbalance. 911 26

The work that stimulated a series of experiments, conducted to determine the relationship between vasectomy and atherosclerosis in nonhuman primates, is summarized along with results in 2 nonhuman primate species. Attention is directed to the following: immunologic injury and atherosclerosis; immunologic responses to vasectomy; effects of atherogenic diet and vasectomy; and the effects of vasectomy alone. Using rabbits as the animal model, early workers found that inducing both immunologic serum sickness and hyperlipoproteinemia caused more extensive atherosclerosis than did hyperlipoproteinemia alone and that the resulting lesions more closely resembled those of human beings in both morphologic characteristics and anatomic location. The mechanism by which immunologic injury exacerbates atherosclerosis still remains unclear, but studies focusing on injury to the vascular endothelium as an important mechanism in atherogenesis are currently of considerable interest. Sperm agglutination, sperm immobilization, and immunofluorescence have all been used to demonstrate circulating free antisperm antibodies after vasectomy. Such antibodies occur in about 50% of vasectomized men and in vasectomized males of several animal species. It is unclear why circulating free antisperm antibodies have not been found in all vasectomized men and male animals. The development of an antibody response to sperm antigen in vasectomized rhesus monkeys has been shown to correlate with high sperm counts before vasectomy and similar observations have been made in studies of men. Results in nonhuman primate species showed that vasectomized monkeys developed more extensive and severe atherosclerosis than did nonvasectomized monkeys of the same age and dietary history. In 2 species of monkeys, the effect of vasectomy on atherogenesis seemed to be present whether the animals were hyperlipoproteinemic or had plasma lipid concentrations in the normal range. The presumed mechanism of atherosclerosis exacerbation is persistent antibody production after vasectomy in response to sperm antigens. The continuing leakage of soluble sperm antigens favors antigenemia and the development of circulating immune complexes, which in turn damage the vascular endothelium. The exact mechanism remains unclear. The accumulated data to show that vasectomy is a risk factor for atherosclerosis in 2 species of nonhuman primates.
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PMID:Does vasectomy increase the risk of atherosclerosis? 1231 10