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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We first supplied the rats with sucrose which accelerates the synthesis of the very low density lipoprotein (VLDL). After 5 weeks ingestion, we investigated the effects of the long-term endurance exercise on the concentration of the endogenous cholesterol and on the accumulation of the cholesterol ester on the arterial wall, with the emphasis on lipid metabolism, especially on lipoprotein metabolism. The concentrations of triglyceride and VLDL in sucrose-ingested group were significantly higher than control. As to the aortic wall, the total amount of cholesterol ester was increased (almost twice). Regular endurance exercise over long period after serum and hepatic lipids had already reached a high level did not reduced the triglyceride in the liver but in serum. It showed be emphasized that the exercise reduces triglyceride and VLDL-cholesterol, and to this extent does contribute to alleviation of hyperlipidemia and to prevention or moderation of arteriosclerosis.
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PMID:[How does endogenous and exogenous cholesterol influence the lipoprotein metabolism. Effects of long-term endurance exercise, and accumulation of cholesterol ester on the aortic wall]. 403 19

A total of 594 patients admitted for cerebrovascular disease (CVD) and for peripheral vascular disease (PVD), were examined in a study aimed at clarifying by a simple, inexpensive out-patient method, a) the relationship existing between the different locations of the vascular disease: brain, lower limbs, coronaries; b) the prevalence in the patients studied of risk factors such as hypertension, hyperlipidaemia and diabetes, and of migraine. The results were as follows: a) of the patients admitted for CVD, 44% also presented arteriosclerosis in other locations; this figure was 32% for PVD cases; b) hypertension was found in 38.5% of CVD and 27% of PVD cases; diabetes in 11.5% of CVD and in 18% of PVD cases; hyperlipidaemia in 31% of CVD and 24% of PVD cases; migraine in 11% of CVD and 1% of PVD cases.
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PMID:Validity of out-patient screening in arteriosclerosis to identify multiple lesions. 406 67

A report is presented of a patient surviving four years with a human cardiac allograft. The allograft arteries showed marked graft arteriosclerosis with intimal fibrocellular proliferation. The arteriosclerotic lesions occurring in the larger epicardial vessels were strikingly similar to spontaneous atherosclerosis. The relationship of the long-term survival to the use of a permanent transvenous pacemaker and of the development of severe vascular lesions to acute rejection and hyperlipemia are discussed.
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PMID:A study of human cardiac allograft in a patient with four-year survival. 458 96

In concluding this eclectic review, I believe that we can say with certainty that coronary atherosclerosis has its origins in childhood, at least by age 10 and possibly earlier. Endothelial changes follow lipid accumulation, but, with present methods, there is no evidence that endothelial injury precedes lipid accumulation. Proliferation is a prominent feature of accelerated experimental atherosclerosis, but we do not see evidence that proliferation is a major feature of early naturally occurring human atherosclerosis. The prominence of the monocyte-macrophage in the earliest detectable lesions of atherosclerosis in childhood justifies the current interest in monocyte biology. Hyperlipidemia, in the sense of the average high levels common in our population, seems almost certain to contribute to accelerated atherogenesis in children, but conclusive proof is still lacking. Mild hypertension in children, or even the high range of normal blood pressure, may accelerate the transition of innocuous childhood fatty streaks to more ominous fibrous plaques. The putative relationship of adult coronary heart disease risk factors to the childhood lesions of atherosclerosis is largely based on extrapolation from adult data. Direct evidence bearing on these relationships, however difficult to obtain, would be helpful in designing and promoting effective preventive regimens for children.
Arteriosclerosis
PMID:George Lyman Duff memorial lecture. Persistent problems in the pathogenesis of atherosclerosis. 608 24

Partial or complete occlusion of the internal carotid artery is a familiar consequence of severe atherosclerosis seen in the elderly. Complete obstruction of both internal carotids is rare, particularly in the young or middle-aged. The rapid onset of bilateral internal carotid occlusion would be expected to produce devastating neurological sequelae and probably not be compatible with survival. We present a case of a young man with complete obstruction of both internal carotid arteries whose presenting symptoms were those of a visual field cut. The history suggests that the carotid occlusion occurred as a result of blunt trauma. The patient had no known predisposition to vascular abnormalities (no history of hypertension, hyperlipidemia, signs of systematic arteriosclerosis or vasculitis, and an unremarkable family history for vascular abnormalities). Computerized tomography revealed an infarct in his right parietal lobe. Angiography demonstrated complete occlusion of both internal carotid arteries and the right posterior communicating artery and failed to disclose the development of extensive collatorals, adding further evidence to the acuteness of the occlusion. The patient was followed by noninvasive studies and in the subsequent year showed marked neurological and ophthalmological improvement.
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PMID:Complete bilateral internal carotid artery occlusion in a young man. 622 81

Widespread arteriosclerotic lesions were detected by histological examinations of rats killed at seven or nine weeks after an intrarenal (ir) injection of nickel subsulfide (Ni3S2, 5 mg per rat). Arteriosclerotic plaques were readily visualized by administering hematoporphyrin derivative (HPD) iv to rats at 24 hours before sacrifice. At necropsy, the major arteries were inspected under ultraviolet light, revealing patches of intense HPD-fluorescence in the arterial endothelium of Ni3S2-treated rats, but not in control rats. Consistent with previous reports, the Ni3S2-treated rats developed pronounced erythrocytosis; blood hematocrit values averaged 70 +/- 4 percent at seven weeks after ir injection of Ni3S2 (P less than 0.001 vs corresponding value of 49 +/- 2 percent in vehicle controls). At seven weeks, blood platelet counts averaged 17 percent lower and serum glucose concentrations averaged 23 percent lower in Ni3S2-treated rats than in controls; serum lipids, lipoproteins, non-protein nitrogen constituents, electrolytes, proteins, and enzymes were not significantly affected. Body weights and systolic blood pressures of rats at two, four, and six weeks after ir injection of Ni3S2 did not differ from corresponding values in controls. Addition of egg yolk to the diet caused mild hypercholesterolemia, but it did not enhance the incidence or severity of arterial lesions in Ni3S2-treated rats. These findings exclude hypertension and hyperlipidemia as pathogenic factors in Ni3S2-induced arteriosclerosis.
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PMID:Studies of the pathogenesis of arteriosclerosis induced in rats by intrarenal injection of a carcinogen, nickel subsulfide. 623 39

The present investigation was designed to examine the influence of dietary fibers with differing soluble fiber compositions upon the metabolism of lipids in a hyperlipemic animal model, the Zucker fatty rat. The response to fiber was examined using a diet supplemented with cellulose, oat bran, or pectin which have a soluble/insoluble fiber ratio of 0:100, 33:66, and 100:0, respectively. These fibers provided 10% of the total diet weight; the control diet contained no fiber. A rapid increase in plasma triglyceride concentration was observed in all animals given fiber-supplemented diets in correlation with the increased carbohydrate content of the defined diets relative to the prestudy diets. This increase in plasma triglyceride was due to increased production of triglycerides with no change in the rates of clearance. The plasma total cholesterol levels were relatively constant on all diets. However, after 7 weeks on the pectin-supplemented diet, rats showed a 39% elevation in HDL and a 44% reduction in LDL concentration. This diet also resulted in reduced weight gain, in spite of a caloric intake equivalent to the control diets. Our data suggest that the ability of dietary fiber to alter plasma lipoproteins might be predictable from the soluble fiber composition or the pectin content of a given dietary fiber in this model of genetic endogenous hyperlipemia.
Arteriosclerosis
PMID:Dietary fiber and lipoprotein metabolism in the genetically obese Zucker rat. 632 36

In studies concerning risk factors for cardiovascular diseases, a number of reports have emphasized the influence of lipids, but the role of dietary minerals other than sodium has been less studied. However, epidemiological studies have suggested that dietary intake of magnesium and potassium may be involved in such pathogenesis. Studies of the influence of magnesium deficiency on arteriosclerosis include its effect on the initial lesion, altered metabolism of elastin, proliferation of collagen, calcification, lipid metabolism, platelet aggregation and hypertension. Magnesium and potassium metabolism are closely related and magnesium is required for maintaining the level of cellular potassium. As a consequence, magnesium and potassium deficiency frequently occur together and potassium deficiency may be an aggravating factor in pathogenesis. The development of the initial lesion in the arterial wall may be facilitated by loss of cellular magnesium and potassium. Experimental magnesium deficiency induces arterial damage, a loss of magnesium and potassium and an increase in the calcium and sodium content of the cell. Experimental models that have been used to produce cardiovascular lesions induce similar changes and losses of major intracellular cations may affect the main metabolic processes of the cell. This report summarizes the experimental evidence that magnesium deficiency may affect several different stages involved in arteriosclerosis and that potassium deficiency may exacerbate this. Magnesium deficiency results in vascular calcification. Experiments indicate that elastin is the site of the initial calcification and the metabolism of elastin is altered. This vascular lesion then brings about an increase in the collagen content of the wall. Low magnesium status could probably affect this process by slowing collagen resorption and lead to an irreversible accumulation of connective tissue. Results showing a different distribution of the various types of lipoprotein during experimental magnesium deficiency strongly suggest that lipid exchange between the vessel walls and blood can be modified. Severe magnesium deficiency in weanling rats produces a marked hypertriglyceridemia, a decrease in the percentage of cholesterol transported by HDL lipoprotein and a reduction in LCAT activity. The decreased clearance of circulatory triglycerides appears to be the major mechanism contributing to hyperlipemia. Magnesium deficiency could therefore contribute to accumulation of vascular lipid. Magnesium and potassium depletion have also been reported in diabetes and the vascular implications of this should be considered.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of magnesium and potassium in the pathogenesis of arteriosclerosis. 639 44

A supraphysiologic (greater than 95th percentile) rise in plasma lipids in pregnancy may serve as a marker for "prelipemia" in the same way that gestational diabetes is a marker for prediabetes. To qualify as prelipemic, subjects with an abnormal lipid rise antepartum must return to normal postpartum but may have other identifying characteristics. This paper describes the antepartum-postpartum changes of lipoprotein lipids and apoproteins at 34 to 38 weeks of gestation and 6 and 20 weeks postpartum in 23 subjects with physiologic and six subjects with supraphysiologic plasma lipid increases during pregnancy. These results are compared to measurements in 23 nonpregnant controls matched for weight, age, and race. In subjects with a physiologic antepartum lipid rise, postpartum total triglyceride and very low density lipoprotein (VLDL) lipids (cholesterol and triglyceride) and apo B returned to baseline within 6 weeks. In contrast, low density lipoprotein (LDL) showed a slow postpartum decline in lipids and apo B with elevations remaining at 20 weeks postpartum. High density lipoprotein (HDL) cholesterol concentrations, elevated in pregnancy, remained elevated at 6 weeks postpartum, but fell to baseline by 20 weeks postpartum. HDL triglyceride and apo A-l concentrations, both elevated in pregnancy, returned to baseline by 6 weeks postpartum. A supraphysiologic triglyceride rise in pregnancy was associated with a slower return of total triglycerides and VLDL to baseline, reduced HDL cholesterol ante- and postpartum, atypical changes in LDL cholesterol during pregnancy and postpartum, and evidence of hyperlipidemia among family members. Two subjects with hypercholesterolemia in the nonpregnant state showed no marked exaggeration of total or LDL cholesterol concentrations in pregnancy. The data support the hypothesis that a supraphysiologic rise in plasma triglyceride concentrations in late pregnancy may serve as a marker of prelipemia. Proof of the hypothesis requires further investigation and longer follow-up.
Arteriosclerosis
PMID:Physiologic and supraphysiologic increases in lipoprotein lipids and apoproteins in late pregnancy and postpartum. Possible markers for the diagnosis of "prelipemia". 643 54

Plasma low density lipoprotein (LDL) kinetics and their relation to plasma very low density lipoprotein (VLDL) and LDL composition were determined in patients with familial combined hyperlipidemia (FCHL) of varying lipoprotein phenotypes. In both Type II and IV subjects, LDL apolipoprotein B (apo B) synthesis was greater than normal. In Type IV, the VLDL triglyceride/apo B ratio was normal and almost all of the LDL apo B was derived from VLDL. LDL cholesterol/apo B ratio was diminished and LDL apo B fractional catabolic rate (FCR) was sufficiently increased to prevent a rise in plasma LDL concentration. In Type II, VLDL triglyceride/apo B was reduced and 14% to 50% of the LDL was formed by direct synthesis. LDL cholesterol/apo B was normal and LDL apo B FCR was lower than in Type IV subjects. In four patients whose plasma lipid levels became normal with carbohydrate restriction and intake of a fibric acid derivative, plasma VLDL and LDL composition and LDL kinetic measurements remained unchanged. By contrast, VLDL triglyceride-apo B decreased and direct LDL synthesis increased in four patients whose phenotype changed to Type IIa. LDL cholesterol/apo B also increased and LDL FCR declined. Among patients with FCHL, significant correlations between VLDL triglyceride/apo B, LDL apo B derived by direct synthesis, LDL cholesterol/apo B, and LDL apo B FCR were found. Thus, increased apo B synthesis is a characteristic feature of FCHL. The phenotypic expression is determined by the availability of triglyceride for hepatic coupling to apo B which could influence the source, composition, and removal rate of circulating LDL. Despite normalization of their plasma lipid levels, some patients continued to show the compositional and kinetic features of FCHL.
Arteriosclerosis
PMID:Low density lipoprotein metabolism in familial combined hyperlipidemia. Mechanism of the multiple lipoprotein phenotypic expression. 650 36


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