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

Oxygen reactive species are normally formed in cells and play an essential part of the bactericidal activity of phagocytic cells. The damaging effect of these oxygen reactive species is prevented by the endogenous scavengers SOD, glutathione peroxidase, catalase, circulating transferrin, ascorbic acid, and membrane-bound alpha-tocopherol. However, when excess amounts of oxygen radicals and hydrogen peroxide are formed, as in reperfusion injury or trauma, the endogenous scavengers are insufficient to react with these active molecules. Lipid peroxidation is an important part of the formation of oxygen reactive species. Lipid peroxidation, especially peroxidation of LDL, may have a significant role in atherosclerosis. Thus dietary manipulation of PG and TX formation through either feeding cold water fish oils or plant oils containing high amounts of polyunsaturated fatty acids may be a two-edged sword. Also, the dietary manipulation of arachidonic acid through increasing its precursor linoleate may cause a decrease in the immune response as seen in animal experiments. The marine oils may be regarded as a natural aspirin in that formation of PGs of the bisenoic series will be replaced by the PGs of the trienoic series. This results in the formation of TXA3, which is biologically inactive, and PGI3, which is biologically active like PGI2. This may have no physiologic consequences but it is used to illustrate a possible mechanism for the postulated beneficial cardiovascular effects of these oils. The issues and the mechanisms are controversial and frequently highly speculative. The subject is a boon for the lipid biochemist and nutritionist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Free radicals, arachidonic acid metabolites, and nutrition. 212 35

Previous studies have shown that either fish oil or verapamil can attenuate the development of atherosclerosis in the lipid-fed rabbit. The present study was designed to evaluate the individual and combined effects of these two interventions on regression. Seventy New Zealand rabbits in seven groups (10 each) were fed a 0.3% cholesterol diet for 10 weeks. Control group C10 was then killed. Control group C20 was fed a 0.3% cholesterol diet and the other five groups were fed a normal diet for an additional 10 weeks. Group F in three treated groups received 2 ml/day of fish oil (Proto-Chol, eicosapentaenoic acid, 180 mg/ml and docosahexaenoic acid, 120 mg/ml) by gavage. Group V received verapamil, 2 g/1,000 ml drinking water, and group FV received both fish oil and verapamil for an additional 10 weeks. Group CF (control for fish oil) received 2 ml/day of water by gavage and group CV (control for verapamil) received water without gavage for an additional 10 weeks. The percent of aortic and pulmonary atherosclerosis was measured by planimetry of sudanophilic lesions. The percent of aortic lesions in the four control groups (C20, C10, CF and CV) was 57 +/- 22, 40 +/- 15, 40 +/- 14 and 33 +/- 25%, respectively. The fish oil or verapamil groups (F, V, FV) showed a significant reduction in aortic lesions: 15 +/- 17%, p less than 0.05; 16 +/- 12%, p less than 0.05; and 26 +/- 24%, p = NS, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regression of atherosclerosis in cholesterol-fed rabbits: effects of fish oil and verapamil. 213 76

Virologic findings reported in recent atherosclerosis literature may have profound implications. To assess them, we have viewed atherosclerosis in a broad biologic context and against a background of environmental, behavioral, and social change. Reasonable grounds exist, we believe, for regarding atherosclerosis as a chronic, low-grade infectious macroangiopathy which is aggravated by hypercholesterolemia and other recognized risk factors. There are probably multiple infective pathogens and transmission routes. The putative agents that initiate atherosclerosis might include ubiquitous viruses that produce clinically unapparent infections in many animal species. Pathways for their transmission to humans may include the food chain and contaminated water. Food-chain transmission may have been largely responsible for the parallel increases of meat consumption and mortality from coronary heart disease in the United States during the middle third of the century. It provides a hypothetical basis for considering thermal intervention as a heretofore unrecognized factor that may actually best account for the surprising reversal of climbing heart disease mortality rates. Improved sanitation and food hygiene as well as improvements in diet, lifestyle, and medical care may have shaped the downward mortality curve. The virus hypothesis may reconcile apparent epidemiologic conflicts and elucidate the natural history of atherosclerosis.
Atherosclerosis 1990 May
PMID:The natural history of atherosclerosis: an ecologic perspective. 219 39

Cardiovascular disease (CVD) accounts for nearly half the deaths, yearly, in the United States. The arterio(athero)sclerotic plaque is the principal lesion of CVD. The White Carneau (WC) pigeon is an animal model that has been employed extensively for studying CVD. Cholesterol (CHOL) feeding aggravates atherosclerosis in WC pigeons greater than 2 years old. In 1986, two reports appeared from a single laboratory claiming a direct effect of drinking chlorinated (Cl) water upon lipid levels and plaque development in young (less than 1 year) WC pigeons. These are the only reports of such direct effects, to date. Three months' exposure to 2 ppm or 15 ppm Cl in the drinking water, resulted in increased circulating CHOL levels in young male WC pigeons fed a normocholesterolemic (NC) diet in which Ca2+ levels were reduced. In addition, at both Cl concentrations there was a significant increase in plaque size, compared to controls. Pigeons in the 2 ppm group also exhibited elevated low density lipoprotein (LDL) levels after 3 months on the NC diet. These findings, if extrapolated to man, could have considerable public health consequences, since nearly 200 million people in the United States drink Cl water. We have carried out a similar set of studies but with strikingly different results. We used the same suppliers of pigeons and feed as did the authors of the 1986 reports and followed their approach where possible. Six month-old male WC pigeons drank water with 2 ppm or 15 ppm Cl (pH 8.5) and ate a NC diet with Ca2+ reduced to 80% of normal. At both 1 and 3 months, body weight, CHOL, triglyceride and LDL levels were unaffected by drinking Cl water. There was also no effect of Cl water on plaque size after 3 months. Thus, we found no evidence that drinking chlorinated water has any effect upon circulating lipid levels or upon the development of arteriosclerotic plaques, in this animal model.
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PMID:Ingestion of chlorinated water has no effect upon indicators of cardiovascular disease in pigeons. 221 28

In order to determine the effect of drag reducing polymers on the occurrence of atherosclerosis, the Guinea pigs were used as the experimental animals. The inhibitory effect of a drag reducing polymer (polyacrylamide) on atherosclerosis in the aortas of Guinea pigs on a high cholesterol diet (2%) was investigated over a period of 6 months. The aortas, livers, kidneys and lungs of the animals, which were separated into four experimental groups (control, polymer, cholesterol and cholesterol + polymer) were also investigated both macroscopically and light microscopically. The selected physiological parameters such as, plasma cholesterol levels, plasma hemoglobin, hematocrit and total lipid values were determined at regular intervals for each group. The results indicate that the atherosclerosis in aorta of the animals receiving the polymer injection is suppressed significantly and the drag reducing water soluble polymers may be effectively applied against atherosclerosis.
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PMID:Effects of drag reducing polymer on atherosclerosis. 227 57

A survey is given of the various "emotional" neuro-hormonal response patterns, organised at the limbic-hypothalamic level of the brain and specialised in dealing with the multiplicity of challenging environmental stimuli that all organisms, including man, have to cope with. Typically they involve all three efferent links of body control--i e, the somatomotor system, governing behaviour, the visceromotor (autonomic nervous) system, adjusting inner organs to suit behavioural response, and the hormonal system, adjusting metabolism, nutritional depots and water-electrolyte balance, again to provide optimal support for behavioural response. Special emphasis is put on the visceromotor and hormonal adjustment of the cardiovascular system, affecting blood pressure, cardiac output and blood flow distribution, particularly in stressful situations, where such responses as the "defence reaction", the "defeat reaction" and the "playing-dead reaction", are virtually the same in all species. It is discussed how in humans such age-old response patterns are also elicited by a variety of artificial or symbolic challenges typical of hectic modern society; and how, if provoked too often or too long, they may constitute crucial determinants of such serious cardiovascular disorders as hypertension and atherosclerosis. In this context, the defence and defeat reactions would seem to be particularly relevant, and the importance is stressed of animal studies of such complex systemic adjustments, for the understanding and hence future prevention of certain particularly serious disorders common in modern society.
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PMID:[Central nervous system control for maximal alertness in danger]. 227 23

This study is the first demonstration of preferential accumulation of a water soluble phthalocyanine dye in atheromatous plaques in the rabbit. Two groups of rabbits with diet-induced atheromatous plaques were killed 4 and 24 h following intravenous administration of copper phthalocyanine tetrasulfonate. Uptake of the dye by plaque-containing and normal appearing aortae was evaluated macroscopically and quantitatively by extraction of the dye from the tissues. The concentration of the dye in the atheromatous plaques was 2.6 and 1.7 times higher than in the normal vessel wall at 4 and 24 h, respectively. The concentration of the dye in normal appearing aortae in the 2 study groups was similar to that of aortae of control rabbits which were fed a normal diet and exposed to the dye for the same time periods. We conclude that copper phthalocyanine accumulates preferentially in atheromatous plaques in rabbits. These findings provide a basis for the utilization of phthalocyanines for plaque identification and for photodynamic therapy of atherosclerosis.
Atherosclerosis 1990 Oct
PMID:Preferential uptake of a water-soluble phthalocyanine by atherosclerotic plaques in rabbits. 228 94

As the intrinsic susceptibility to atherosclerosis differs among several taxonomic groups, the present studies were conducted to compare the angiotoxic responses of atherosclerosis-susceptible (quail) and -resistant (rat) animals to allylamine, a selective cardiovascular toxin. Japanese quail (125-150 g) and Sprague-Dawley rats (175-200 g) were gavaged daily for 1, 7, or 20 d with allylamine HCl (0.7, 7, and 70 mg/kg) or tap water. At the ultrastructural level, subchronic exposure of quail and rats to allylamine was associated with dose- and time-dependent disruption of the structural integrity of aortas. These alterations correlated with fluctuations in the nonprotein thiol content of avian and rodent vessels. Angiotoxicity was not associated with alterations in serum cholesterol content. At all times and doses tested, quail were more susceptible than rats to the angiotoxic effects of allylamine. Although the avian sensitivity to toxic insult was greater than that of rodents, quail aortic homogenates bioactivated allylamine to a lesser extent than rat homogenates. Collectively, these results suggest that the aortic sensitivity to toxic insult in avian and rodent species correlates with their intrinsic susceptibility to vascular injury.
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PMID:Comparative angiotoxic responses of avian and rodent species in vivo: implications in atherogenesis. 232 52

The influence of chronic ethanol intoxication upon vitamin D-induced damage of cardiovascular system in rats was examined. Eighty rats, divided into 16 groups according to sex and age, were intoxicated with ethanol as the only source of liquid. Control rats drank water only. After 6 months of ethanol intoxication, part of ethanol and part of water-drinking rats received 3 x 100,000 IU vitamin D/rat, in order to induce atherosclerosis and heart muscle necrosis. The results of the described experiment revealed that the degree of circulatory system damage after chronic ethanol intoxication and vitamin D treatment was dependent on the age of the animals at the beginning of the experiment. Ethanol intoxication intensified vitamin D-dependent heart muscle necrosis in young individuals. In old rats chronic alcohol intoxication diminished atherosclerosis induced by vitamin D.
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PMID:Effects of ethanol on the development of experimental atherosclerosis and cardionecrosis in rats. 239 Feb 5

High resolution 1H and 13C NMR spectroscopic measurements including 1H/13C 2D correlation and magnetic resonance imaging (MRI) studies, have been carried out on intact rabbit aortic tissues ex vivo using animals fed both normal and high cholesterol diets. The results show that 1H and 13C NMR spectroscopy can distinguish mobile lipids and can differentiate between normal triglyceride content and cholesterol-enriched lipids, in intact tissue, There were considerable differences in the level of deposition of cholesteryl esters in animals all fed on the same diet. Confirmation is presented of temperature-dependent differences in mobility and organization between the triglycerides found in control tissue and the cholesteryl esters found in aortas from high lipid diet animals. Water-suppressed MRI showed evidence of lipid accumulation in the aortas of high cholesterol diet rabbits. It is concluded that the hypercholesterolaemic rabbit model of atherosclerosis, coupled with such NMR methods, may offer a noninvasive method of monitoring disease development, allowing the evaluation of the effect of therapeutic agents on the progress of atherosclerosis.
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PMID:Lipid characterization in an animal model of atherosclerosis using NMR spectroscopy and imaging. 239 Apr 59


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