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

The effects of dietary fat-induced lipemia on arterial oxygen tension and plasma lactate, cholesterol, and triglyceride levels were examined in 11 male subjects (average age 60) with a diagnosis of arteriosclerotic coronary vascular disease and angina pectoris. All subjects were alternately fed three isocaloric formula meals consisting of 100 g of cream fat, 100 g of saffola oil, and an isocaloric nonfat cornstarch control meal. Resting values of arterial blood gases and plasma lactate, triglyceride, and cholesterol were measured before (fasting) and at 3 and 5 hr postprandially. Both types of dietary fat produced significant postprandial decreases in plasma lactate, significant increases in plasma triglyceride and cholesterol levels, and no significant changes in arterial oxygen tension. The control meal had no effect upon any value except to transiently increase the plasma lactate. The role of postprandial lipemia in the atherosclerotic process is discussed and a hypothesis for the plasma cholesterol elevation due to dietary fats is presented.
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PMID:Dietary fat-induced postprandial lipemia: effect on arterial oxygen saturation and plasma lactate, triglyceride, and cholesterol levels in subjects with angina pectoris. 738 9

The purpose of this study was to examine the effect of one bout of low-intensity exercise on the lipemic response to a high-fat meal. Twelve (six women, six men) normolipidemic adults aged 25.8 +/- 1.2 years (mean +/- SEM) took part in two trials. In the exercise trial, subjects walked for 2 hours on a treadmill at 30.9% +/- 1.6% of maximal oxygen uptake (VO2 max) 15 hours before ingestion of the test meal. In the control trial, subjects rested the day before the test meal. After a 12-hour fast, blood samples were obtained by venous cannulation before ingestion and hourly after ingestion for 6 hours. Serum was analyzed for triacylglycerol (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and HDL2-C, apolipoproteins (apos) A-I and B, free fatty acids (FFA), free glycerol, glucose, and insulin. TG values were corrected for free glycerol. Fasting serum TG and peak TG concentrations were lower (Wilcoxon, P < .05) for the exercise trial than for the control trial (0.74 +/- 0.03 v 0.92 +/- 0.08 and 1.98 +/- 0.18 v 2.59 +/- 0.32 mmol.L-1, respectively). The total lipemic response (area under the TG/time curve, normalized to the 0-hour level) was 31% +/- 7% lower in the exercise trial (4.28 +/- 0.66 v 6.46 +/- 1.08 mmol.L-1.h, P < .01). No differences were found between trials in the other parameters. These results show that a single bout of low-intensity exercise reduces the extent of postprandial lipemia in normolipidemic young adults. One possible mechanism is enhanced lipoprotein lipase (LPL) activity in the exercised skeletal muscle.
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PMID:The effect of a single bout of brisk walking on postprandial lipemia in normolipidemic young adults. 802 6

Two key events in the atherogenic cascade are the focal influx and accumulation of low-density lipoprotein (LDL) cholesterol at arterial sites having a predilection for atherosclerotic lesion development and the recruitment of blood monocytes to these lesion-prone sites. Both processes are enhanced in the setting of hyperlipidemia and dyslipoproteinemia. The monocytes recruited to the endothelial surface subsequently migrate to the subendothelial space under the directed guidance of chemoattractants, such as monocyte chemotactic protein-1 and oxidatively modified LDL. These cells then undergo activation-differentiation to become macrophages. At the same time, LDL, and probably other lipoproteins such as the small dense LDL particles and lipoprotein (a), traverse the endothelium and undergo oxidative modification by reactive oxygen species. These oxidatively modified lipoproteins are recognizable by the non-down-regulating macrophage scavenger receptor. Their uptake by these receptors results in the formation of the foam cell characteristic of early-stage atherosclerosis. As monocyte recruitment and lipoprotein influx continue, the lesion grows and develops into the fatty streak. Subsequent foam cell necrosis due to the influence of cytotoxic oxidatively modified LDL and increased collagen synthesis by intimal smooth muscle cells lead to the established atherosclerotic lesion referred to as the fibrous plaque. As our understanding of the mechanisms involved in the pathogenesis of atherosclerosis has evolved over the past few years, novel strategies for intervention in the atherogenic process have emerged.
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PMID:A modern view of atherogenesis. 843 61

We evaluated the preoperative and intraoperative general condition of 33 pediatric kidney recipients. Eighteen patients were anaesthetized with lumbar epidural anaesthesia. Ten patients were with nitrous oxide-oxygen-halothane, 5 cases were with NLA. Preoperatively many children had cardiovascular and metabolic complications. For example 39% of patients had history of hypertension. Sixty-seven percent of patients were found to have cardiomegaly (cardio-thoracic ratio > 50%) with chest X-ray film. Seven of 9 patients undergoing echocardiogram had abnormality of cardiac wall motion, valvular impairment, pericardial effusion. In forty-eight percent of patients, hyperlipidemia was found. During operation we could not maintain the cardiovascular stability following intratracheal intubation and manipulation of vena cava or abdominal aorta under NLA or nitrous oxide-oxygen-halothane anesthesia. Epidural analgesia inhibited the cardiovascular fluctuation following these surgical stresses. We concluded that epidural analgesia is the best anaesthesia for pediatric renal transplantation and phentolamine or PGE1 are useful to maintain cardiovascular stability and transplanted kidney function.
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PMID:[Anaesthetic management of pediatric renal transplantation for chronic renal failure]. 843 61

An antioxidant defense system consisting of enzymes and non-enzymatic compounds prevents oxidative damage of lipoproteins in the plasma. When the activity of this system decreases or the reactive oxygen species (ROS) production increases, an oxidative stress may occur. Since fatty acids and triglyceride-rich emulsions can stimulate leukocytes to produce ROS, it is conceivable that raised plasma triglyceride-rich lipoproteins such as very low density lipoprotein (VLDL) may overload the antioxidant system. To test this hypothesis, we selected 14 patients with combined hyperlipidemia (HLP), in whom low density lipoprotein (LDL) and VLDL levels are elevated, as well as 18 hypercholesterolemic patients (HCH) with increased LDL levels and 19 controls (NL) to examine the trend for an imbalance between the production of oxidative species and the antioxidant defense system as challenged by increased plasma lipids. With this goal, plasma lipoprotein lipid fractions were determined and correlated with the release of ROS by leukocytes monitored by luminol-enhanced chemiluminescence. Plasma beta-carotene, alpha-tocopherol, lycopene and the lipoprotein lipid hydroperoxides were determined by high pressure liquid chromatography with electrochemical detection. HLP had lower plasma superoxide dismutase (SOD) activity (0.04 and 0.11 U/mg protein; P < 0.05) as well as lower concentrations of lycopene (0.1 and 0.2 nmol/mg cholesterol; P < 0.05) and beta-carotene (0.8 and 2.7 nmol/mg cholesterol; P < 0.05) in the plasma, as compared with NL. Moreover, HLP showed the highest ROS production by resting mononuclear leukocytes (MN) among the three study groups. When the results of the subjects of the three groups were taken together, the plasma triglyceride concentration was positively correlated to ROS release by resting polymorphonuclear leukocytes (PMN, r = 0.38, P = 0.04) and MN (r = 0.56, P < 0.005). Moreover, ROS release by resting MN was positively correlated with VLDL (r = 0.47, P = 0.02) and LDL (r = 0.57, P = 0.01) triglycerides. There was also a positive correlation between ROS release by stimulated PMN and VLDL (r = 0.44, P = 0.03) as well as LDL (r = 0.53, P = 0.01) triglycerides. High density lipoprotein (HDL) cholesterol showed a negative correlation with ROS release by resting MN (r = -0.48, P = 0.02) and resting PMN (r = -0.49, P = 0.01). VLDL susceptibility to copper (II) oxidation was not different among the three groups. Regarding LDL, there was an increased oxidizability in HLP group.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Evaluation of oxidative stress in patients with hyperlipidemia. 854 56

Recently, expired gas analysis(EGA) during exercise testing is broadly performed. It has been recognized that anaerobic threshold(AT) and maximal oxygen uptake(VO2 max) may be useful in identifying one's exercise tolerance. AT especially has a good correlation with endurance capacity. In the field of sports medicine, the purposes of EGA are: 1) evaluation of endurance exercise capacity. 2) decision of intensity and frequency for exercise training, and 3) prevention of overtraining syndrome. In the clinical fields, EGA is frequently performed with cardiovascular patients, for example, myocardial infarction(MI), and congestive heart failure(CHF). The purposes are: 1) decision of intensity for exercise therapy with the patients of old MI. 2) evaluation of exercise capacity with the patients' of CHF. 3) index of exercise therapy for hypertension, hyperlipidemia, and diabetes, and 4) evaluation of drug effects including vasodilators and cardiotonics.
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PMID:[Expired gas analysis--focused on VO2 max and anaerobic threshold]. 874 88

During the last decade, our understanding of the role of nitric oxide for central renal functions has greatly been enhanced. We know now that nitric oxide is produced in renal arteries, macula densa, glomeruli, and tubules by different NO-synthases. Nitric oxide contributes to physiological regulation of renal blood flow, renal autoregulation, tubuloglomerular feedback, renin release, pressure natriuresis, and tubular function. The physiological role of nitric oxide can be modulated by a variety of pathophysiological influences, such as dyslipidemia, diabetes mellitus, hypertension, specific drugs, or radiocontrast agents. In this article, the possible interactions between nitric oxide and atherogenic lipoproteins with regard to important renal functions and development of glomerulosclerosis have been stressed. Atherogenic lipoproteins impair endothelium-dependent, nitric oxide-mediated dilations of renal arteries. The underlying mechanism involves formation of reactive oxygen species which inactivate nitric oxide. Lipoproteins induce formation of oxygen radicals not only in arteries, but also in glomeruli and juxtaglomerular cells, causing, e.g., stimulation of renin release. Although interactions between lipoprotein and nitric oxide take place at different levels, they finally may contribute to renovascular hypertension. Future studies will have to prove that treating hyperlipidemia has a positive influence on nitric oxide-mediated renal functions.
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PMID:Impact of nitric oxide on renal hemodynamics and glomerular function: modulation by atherogenic lipoproteins? 881 12

Repeated episodes of exaggerated postprandial lipemia may hasten the progression of atherosclerosis. The purpose of this study was to compare the lipemic response to a high-fat meal in trained and untrained women in the presence and absence of the acute effects of exercise. Nine endurance-trained and thirteen untrained women aged 40.4 +/- 3.3 and 43.8 +/- 4.3 y (mean +/- SD), with maximal oxygen uptake of 50.3 +/- 5.9 and 31.7 +/- 3.6 mL.kg-1.min-1, and a body mass index (kg/m2) of 22.2 +/- 0.9 and 22.9 +/- 2.3, respectively, underwent two trials, each over 2 d. Subjects did not exercise during the 2 d leading up to a trial. On day 1 they either walked for 90 min at 60% of maximal oxygen uptake (exercise), or refrained from exercise (control). On day 2 venous blood and expired air samples were obtained in the fasted state and for 6 h after consumption of a high-fat meal (1.70 g fat, 1.65 g carbohydrate, and 0.25 g protein/kg fat-free mass). Exercise decreased lipemia as determined by the mean (+/-SEM) area under the plasma triacylglycerol concentration versus time curve: trained, 6.96 +/- 0.48 compared with 4.87 +/- 0.33 mmol.h/L; untrained, 8.36 +/- 0.83 compared with 7.01 +/- 0.79 mmol.h/L (control and exercise trials, respectively, both P < 0.05). Lipemia differed significantly between groups in the presence of this acute effect of exercise but not in its absence. Exercise decreased insulinemia in trained women (543 +/- 25 compared with 433 +/- 24 pmol.h/L, P < 0.01) but had no effect in untrained women (592 +/- 34 compared with 585 +/- 47 pmol.h/L). Total oxidation of fat over the 6-h postprandial period was enhanced by exercise, and to a similar degree in each group of women.
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PMID:Acute effects of exercise on postprandial lipemia: a comparative study in trained and untrained middle-aged women. 902 40

Lycopene is one of the major carotenoids in Western diets and is found almost exclusively in tomatoes and tomato products. It accounts for about 50% of carotenoids in human serum. Among the common dietary carotenoids lycopene has the highest singlet oxygen quenching capacity in vitro. Other outstanding features are its high concentration in testes, adrenal gland and prostate. In contrast to other carotenoids its serum values are not regularly reduced by smoking or alcohol consumption but by increasing age. Remarkable inverse relationships between lycopene intake or serum values and risk have been observed in particular for cancers of the prostate, pancreas and to a certain extent of the stomach. In some of the studies lycopene was the only carotenoid associated with risk reduction. Its role in cancer risk reduction still needs to be clarified. Patients with HIV infection, inflammatory diseases and hyperlipidemia with and without lipid lowering treatment may have depleted lycopene serum concentrations. Before embarking on large-scale human trials the distribution of lycopene and its biological functions need to be further evaluated.
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PMID:The potential role of lycopene for human health. 910 Feb 11

New evidence suggests an interaction between hyperlipidemia, activation of the renin-angiotensin system, and atherosclerotic disease. In patients with atherosclerosis and hyperlipidemia, coronary endothelial dysfunction is usually diffuse and affects vasomotor tone, platelet activity, thrombosis, fibrinolysis, and regulation of inflammatory cells. Angiotensin II, an important oxidant, alters the binding of low-density-lipoprotein (LDL) cholesterol to its receptors and increases endothelial uptake of LDL. Endothelial dysfunction is worsened by the suppression of nitric oxide production and/or release via angiotensin II-associated degradation of bradykinin and oxygen free radical production, resulting in inadequate vasorelaxation. Therapy with angiotensin-converting enzyme (ACE) inhibitors appears to eliminate these untoward effects and may ameliorate the tendency for myocardial infarction associated with elevated plasma levels of angiotensin II. Although the role of ACE inhibitors in the prevention and/or treatment of coronary artery disease in patients without left ventricular dysfunction remains to be established, the capacity of ACE inhibition to correct endothelial dysfunction offers promise. The ability of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors to improve endothelial function, prevent the progression of coronary atherosclerosis, reduce the incidence of ischemic events, and improve survival is well known. Potentially, ACE inhibitors may have an additive or synergistic effect on the development of atherosclerosis and the clinical consequences of this disease when used in combination therapy with lipid-lowering strategies.
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PMID:The potential use of angiotensin-converting enzyme inhibitors in patients with hyperlipidemia. 912 18


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