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

Leukocyte adhesion and other injury parameters have been studied in the aortic endothelium of Sprague-Dawley rats in two situations: (1) spontaneous pathology in conventional rats with antibodies to Mycoplasma pulmonis and/or Kilham or Sendai viruses, and (2) intravascular coagulation by thrombin administration in SPF rats. Adhesion (esterase (+) leukocytes/mm2) in SPF rats was 8 +/- 5 (n = 12). Adhesion in 38% of the conventional rats was 54 +/- 27 (n = 8), half of them being non-analyzed and the rest having antibodies to M. pulmonis and/or Kilham rat virus. In 19 rats with antibodies to M. pulmonis and/or Kilham or Sendai viruses, AgNO3 and hematoxylin staining of the aortic endothelium showed an increase in leukocyte adhesion, and the presence of argyrophilic cells, stigmata and granularity--severe endothelial lesions being observed in some cases. Adhesion in rats after 0.25, 1, 3 and 6 h of thrombin administration (30 units/100 g) was not different from controls. Adhesion after 24 h was 108 +/- 53 (n = 10) and 60 +/- 59 (n = 10), and 22 +/- 20 (n = 10) in rats treated with thrombin plus heparin or hirudin, respectively. Thrombin produced endothelial lesions at all times studied, and these included membrane blebs, platelet and erythrocyte adhesion and alterations in the pattern of endothelial esterase activity.
Atherosclerosis 1992 Apr
PMID:Effect of spontaneous pathology and thrombin on leukocyte adhesion to rat aortic endothelium. 159 Aug 26

This report describes a new method for obtaining whole mount preparations of rat thoracic aorta which allows the study en face of the complete surface of the endothelium. A comparative study of the different techniques utilized for silver staining of endothelium has been performed. Included is the description of an apparatus for perfusion fixation of rat aorta which allows sequential perfusion of several fluids at a constant pressure. Conditions for perfusion fixation at physiological pressure and flow and for optimal nuclear staining and silver staining of the interendothelial junctions have been studied. The method is rapid and easy to perform and, in the same preparation, allows by optical microscopy the study of the most commonly described parameters for the characterization of normal and injured endothelium. Qualitative aspects of the endothelial lesions found in rats with antibodies to Mycoplasma pulmonis are presented.
Atherosclerosis 1987 May
PMID:Methodological approaches for the study of the aortic endothelium of the rat. 244 Apr 56

Adhesion of leukocytes to the aortic endothelium was studied in specific pathogen-free (SPF) and conventional rats and in SPF rats with diet-induced hypercholesterolemia. Nonspecific esterase activity with alpha-naphthyl acetate as substrate was used to characterize the adhered cells. Phagocytic activity was determined by injecting i.v. 0.1-0.4 ml/100 g doses of Monastral blue B (MbB). Adhesion in SPF rats was 8 +/- 4 esterase (+) cells/mm2. Adhesion in conventional rats was of the same order except in 2 cases with antibodies to Mycoplasma pulmonis and Kilham rat virus, where adhesion was 44 and 68 esterase (+) cells/mm2, respectively. For all MbB doses studied, phagocytic activity arose in a percentage of the adherent cells, ranging from 5 to 85%. Rats fed the hyperlipidic diet for 15 days developed severe hypercholesterolemia and adhesion was drastically increased to 200-700 esterase (+) cells/mm2. Results indicate that: (1) spontaneous pathology in rats may produce an increased adhesion of leukocytes to the endothelium, and (2) phagocytic activity is only expressed in a fraction of the esterase (+) cells adhered to the endothelium.
Atherosclerosis 1989 Jan
PMID:Adhesion of leukocytes to the aortic endothelium of conventional, specific pathogen free (SPF) and hypercholesterolemic SPF rats. 293 Jun 16

The purpose of this study was to determine whether the free cholesterol of hypercholesterolemic low density lipoprotein from cholesterol-fed nonhuman primates has a greater potential for surface transfer to cell membranes than does the free cholesterol of normal low density lipoprotein. The low density lipoproteins were isolated from normal and hypercholesterolemic rhesus and cynomolgus monkeys, incubated with membranes from Acholeplasma laidlawii, a mycoplasma species devoid of cholesterol in its membranes, and the mass transfer of free cholesterol determined by measuring membrane cholesterol content. Since these membranes neither synthesize nor esterify cholesterol, nor degrade the protein or cholesterol ester moieties of low density lipoprotein, they are an ideal model with which to study differences in the cholesterol transfer potential of low density lipoprotein independent of the uptake of the intact low density lipoprotein particle. When added at an equivalent particle concentration, there was greater enrichment of membranes with free cholesterol from hypercholesterolemic low density lipoprotein. Hypercholesterolemic low density lipoprotein, however, contains more cholesterol per particle than normal low density lipoprotein; yet calculations on the basis of equivalent free cholesterol content showed no difference in either the rate or extent of free cholesterol transfer from normal or hypercholesterolemic low density lipoprotein. This was true for the transfer of at least 90% of the free cholesterol from both lipoproteins. These studies indicate that, even though there are marked differences in the cholesterol composition of normal and hypercholesterolemic low density lipoproteins, this does not result in a greater chemical potential for surface transfer of free cholesterol. Consequently, if a difference in the surface transfer of free cholesterol is responsible for the enhanced ability of hypercholesterolemic low density lipoprotein to promote cellular cholesterol accumulation and, perhaps, also atherosclerosis, it must be the result of differences in the interaction to the hypercholesterolemic low density lipoprotein with the more complicated mammalian cell membranes, rather than differences in the chemical potential for cholesterol transfer.
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PMID:Cholesterol transfer from normal and atherogenic low density lipoproteins to Mycoplasma membranes. 729 88

Chlamydia pneumoniae causes respiratory tract infections, and it is transmitted by air and fomites. It is probably more frequent than it is described, due to asymptomatic or mild symptomatic patients. They respond to macrolides, tetracyclines and quinolones, though patients may recover slowly. An increase of the incidence of pneumonia, caused by Chlamydia pneumoniae, is shown in recent multicenter surveys, being even more frequent than Streptococcus pneumoniae and Mycoplasma pneumoniae. Recently it has been demonstrated an association between coronary artery disease and atherosclerosis with Chlamydia pneumoniae infection. Special attention must be paid to the cardiovascular complications of Chlamydia pneumoniae. We describe six clinical cases of Chlamydia pneumoniae pneumonia in which two of them suffered from ischemic artery disease as a complication of the infection.
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PMID:[Chlamydia pneumoniae pneumonia]. 1042 Sep 52

Chlamydia pneumoniae, a bacterial respiratory tract pathogen, has been associated with atherosclerosis in humans. C. pneumoniae infection of the respiratory tracts of rabbits fed a noncholesterol diet induced changes of atherosclerosis of the aorta in 6 (26.1%) of 23 animals after a single inoculum at 3 months. Multiple inocula given three times within 6 weeks resulted in grade III atherosclerosis in 8 (34.8%) of 23 rabbits, with an additional 5 (21. 7%) showing increased myxoid changes in the intima-media junction and exhibiting 8 (34.8%) focal periaortitis. Control animals inoculated with carrier broth (n = 24), HEp-2 cells (n = 12), or another respiratory pathogen, Mycoplasma pneumoniae (n = 32), produced no changes of atherosclerosis after 3 months. The histological changes were dissimilar (fewer foam cells) from those of rabbits fed a 0.5% cholesterol diet but were highly similar to or indistinguishable from changes in rabbits fed a 0.15% cholesterol diet (similar to that of humans). Proinflammatory cytokines and tissue growth factors were more consistently detected in cholesterol-induced aortic lesions than those induced by C. pneumoniae. These data are compatible with de novo induction of atherogenesis by C. pneumoniae in rabbits and suggest that C. pneumoniae may be important in the pathogenesis of atherosclerosis in humans.
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PMID:De Novo induction of atherosclerosis by Chlamydia pneumoniae in a rabbit model. 1053 Dec 66

Chlamydia pneumoniae is strongly implicated in the pathogenesis of atherosclerosis in human beings. Animal models are important to help establish causality, to understand the mechanism of infection induced atherogenesis, to examine interaction of other factors or variables, to explore treatment regimens and their efficacy, and to help develop a vaccine for prevention. To date, the rabbit model is the only animal model shown to develop de novo atherosclerotic changes with C pneumoniae infection. However, the mouse model may be useful to show enhancement with other factors such as hypercholesterolemia and to explore pathogenic mechanisms. In our studies, we have shown that C pneumoniae respiratory infection in the rabbit results in early atherosclerotic changes in 26% with single inoculation and in 35% after triple inoculation, but sham infection or infection with Mycoplasma pneumoniae does not result in similar changes. Early treatment (5 days after inoculation) with 30 mg/kg per day azithromycin once every 6 days was 87% effective in preventing atherosclerotic changes, but delayed treatment (6 weeks after inoculation) was ineffective. Further studies are needed with longer or more aggressive regimens or possible combination of agents to determine whether it is possible to reverse preformed lesions. An effective vaccine for prevention of C pneumoniae -induced pneumonia and possibly atherosclerotic lesions in human beings would have tremendous application and would circumvent the shortcomings of antibiotic therapy.
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PMID:Value of animal models for Chlamydia pneumoniae-related atherosclerosis. 1053 61

Italian investigations have shown an association between Chlamydia pneumoniae infection and atherosclerosis. With the use of several diagnostic techniques, including serology, a microimmunofluorescence test, and nucleic acid amplification methods, a temporal association was found between acute C. pneumoniae reinfection and acute myocardial infarction, suggesting that an acute infection superimposed on a chronic or latent infection may trigger the onset of acute myocardial infarction. C. pneumoniae but not Helicobacter pylori or Mycoplasma pneumoniae was found in atherosclerotic plaques of abdominal aortic aneurysms and the carotid artery. A reverse transcriptase-polymerase chain reaction process confirmed the presence of viable C. pneumoniae in carotid atheromas. Nucleic amplification of peripheral blood mononuclear cells may enable the identification of subjects carrying C. pneumoniae in the vascular wall. Macrolide treatment reduced fibrinogen and C-reactive protein plasma levels and C. pneumoniae burden in patients with atherosclerotic diseases.
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PMID:Chlamydia pneumoniae detection in atherosclerotic plaques in Italy. 1102 90

The association of Chlamydia pneumoniae infection with the complications of atherosclerosis, cardiovascular disease, and stroke are well established. C. pneumoniae infection of New Zealand White rabbit respiratory tract can result in early changes of atherosclerosis of the aorta that are not produced by sham infection or by Mycoplasma pneumoniae (which result in similar lung pathology). Early institution of antimicrobials with antichlamydial activity (azithromycin, clarithromycin, moxifloxacin, and doxycycline) within 5 days of infection can largely prevent the aortic lesions (75%-85% efficacy). Early treatment is also effective in suppressing the IgG antibody response to C. pneumoniae. However, delayed treatment (6 weeks after infection) with azithromycin was ineffective in aborting vascular changes but clarithromycin was partially effective (62.5% reduction). These studies support but do not prove that C. pneumoniae can cause atherosclerosis. Antibiotics are potentially useful in this model, but the optimum dose and duration of therapy or use of combination of agents remain to be determined.
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PMID:Antibiotics effects in a rabbit model of Chlamydia pneumoniae-induced atherosclerosis. 1083 50

Polymerase chain reaction (PCR) and immunohistochemistry (IHC) have been used to detect Chlamydia (C.) pneumoniae in vascular tissues. Discrepancies between the results of these two methods have frequently been reported. However, the correlation between PCR and IHC has not been analyzed yet. This study assesses the correlation between the detection of C. pneumoniae by PCR and IHC in 45 atherosclerotic and 50 non-atherosclerotic tissue specimens. Also, the presence of Mycoplasma (M.) pneumoniae in these 95 specimens was investigated. Correlation was found between the detection of C. pneumoniae by PCR and IHC in the atherosclerotic tissues. Both tests were positive in 10 specimens and negative in 17 specimens (p = 0.003). There was no significant correlation between PCR and IHC in non-atherosclerotic specimens (p = ns). M. pneumoniae was detected, by PCR, in one atherosclerotic specimen.The results show correlation between PCR and IHC in the detection of C. pneumoniae in atherosclerotic tissues, emphasize the association between C. pneumoniae and atherosclerosis, and support the specificity of the association between C. pneumoniae and atherosclerosis.
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PMID:Correlation between detection methods of Chlamydia pneumoniae in atherosclerotic and non-atherosclerotic tissues. 1133 79


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