Gene/Protein Disease Symptom Drug Enzyme Compound
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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of variable doses of ethanol on plasma lecithin: cholesterol acyltransferase (LCAT) activity was examined in male, atherosclerosis-susceptible squirrel monkeys over a 12-month period. Primates were divided into three groups: 1) Controls fed isocaloric liquid diet; 2) Low Ethanol monkeys given liquid diet with vodka substituted isocalorically for carbohydrate at 12% of calories; and 3) High Ethanol animals fed diet plus vodka at 24% of calories. There were no significant differences between the treatments in serum glutamate oxaloacetate transaminase (SGOT), a measure of liver function. However, plasma LCAT activity (% esterification/min) measured in vitro was significantly reduced in High Ethanol monkeys while cholesterol esterification was elevated in the Low Ethanol group and intermediate in Controls. Similarly, the in vivo appearance of radiolabeled cholesteryl ester in high density lipoproteins (HDL) following the intravenous injection of 3H mevalonolactone was highest in the Low Ethanol primates, intermediate in Controls and significantly lower in monkeys fed the high alcohol diet. In vitro measurement of LCAT enzyme efficiency was similar for the three groups while substrate efficiency was lower in the High Ethanol treatment. Although LCAT activator (apoprotein A-I) was not markedly altered by dietary ethanol and the concentration of LCAT substrates (HDL free cholesterol and phosphatidyl choline) was significantly elevated in the High Ethanol group, subtle modifications in substrate-product composition may account for the observed reduction in cholesterol esterification. These include potential substrate and/or product LCAT inhibition resulting from increased concentrations of plasma free cholesterol, HDL lysophosphatidyl choline, and higher HDL2/HDL3 subfraction ratios, as well as alterations in HDL phospholipid fatty acid profiles in the High Ethanol group. Results from this study provide the first evidence of an anomalous enhancement in LCAT activity in nonhuman primates fed ethanol at 12% of calories and a marked depression in cholesterol esterification at the 24% dose which may be due to substrate alterations and product inhibition prior to overt biochemical evidence of liver dysfunction.
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PMID:Effect of ethanol on lecithin:cholesterol acyltransferase (LCAT) activity. 399 6

Forty-six elderly patients (mean age 60 years) suffering from diabetes mellitus (DM), or essential or arteriosclerotic hypertension (HT) were divided into 4 groups. Group 1 served as a control, group 2 was administered 1500 mg niceritrol, group 3 was administered 162 mg acetylsalicylic acid (ASA), and group 4 was administered both 1500 mg niceritrol and 162 mg ASA/day for 8 weeks. Niceritrol lowered serum levels of beta-lipoprotein and total cholesterol and increased HDL cholesterol, usually in 8 weeks. ASA did not affect the lipid-lowering effects of niceritrol. Platelet aggregation induced by epinephrine (1 microgram/ml), collagen (1 microgram/ml), and ADP (2 microM) was depressed in groups 2, 3 and 4. Degrees of depression were higher in groups administered ASA (groups 3 and 4) than in the group administered niceritrol alone (group 2). Plasma fibrinogen levels were lowered in groups administered niceritrol (groups 2 and 4) in 8 weeks. Apparent whole blood viscosity measured at shear rates of 37.6/s and 376/s was improved only in group 4 in 8 weeks, while hematocrit did not change during the study. Because flushing, the most frequent side effect of niceritrol, can be easily controlled by a low dose of ASA, and because the combination of the 2 drugs has some beneficial effects on blood rheology, this combination is considered worthwhile for treatment and prevention of atherosclerosis.
Atherosclerosis 1985 Apr
PMID:The effects on lipids, blood viscosity and platelet aggregation of combined use of niceritrol (Perycit) and a low dose of acetylsalicylic acid. 400 83

Platelet aggregation, [14C]serotonin release and platelet malondialdehyde production were determined in a patient with abetalipoproteinemia (ABL) and found to be normal. The patient demonstrated complete absence of apolipoprotein (apo) B and decreased apo A-I concentration in plasma. The high density lipoprotein (HDL) composition of plasma was abnormal, with an increased cholesterol/protein ratio, increased apo E levels and reduced apo C concentration. The patient's platelets, like platelets derived from a normolipidemic control, possessed receptors capable of binding lipoproteins. On incubating washed platelets derived from a control subject with HDL obtained from the ABL patient, an enhancement in platelet function was observed. A similar concentration of HDL derived from the control had the opposite effect, a depression of platelet function. Lipoprotein-deficient plasma (LPDP) derived from the patient, on the other hand, decreased platelet aggregation and [14C]serotonin release in comparison to the LPDP obtained from the control. The normal platelet function observed in the patient appears to be the result of the platelet-enhancing effect of an abnormal HDL, thus compensating for the absence of low and very low density lipoproteins from the patient's plasma which, when present, stimulate platelet function.
Atherosclerosis 1985 Nov
PMID:Platelet function in a case with abetalipoproteinemia. 408 61

In order to study the possible relation between blood viscosity and exercise ST segment depressions in hyperlipidemia the former was lowered by infusion of dextran and by treatment with clofibrate 1 g twice daily. Acute decrease of blood viscosity with dextran infusion in two cases increased the ST segment depressions during work. Nine subjects with asymptomatic hyperlipidemia, hyperfibrinogenemia and exercise ST segment depressions were treated with clofibrate in order to lower plasma fibrinogen and serum lipids. This did not influence the area of ST segment depression with either Frank leads or CH leads as determined by computer estimation. As the plasma fibrinogen level is of major importance for the blood viscosity it is concluded that the ischaemic ST segment depression seen in hyperlipidemia is not due to increased blood viscosity but more likely to a premature subclinical coronary atherosclerosis.
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PMID:Effect of blood viscosity decrease on exercise ST segment depressions in hyperlipidemia. 616 35

Sulocton effect was evaluated in 33 patients with symptoms of brain ischaemia during atherosclerosis. Thirty patients received the drug orally for 2 months in doses of 100 mg thrice daily. Three patients discontinued the treatment earlier (two of them discontinued it because of side effects). After two months of treatment a significant improvement was observed in such disturbances important for wellbeing and social contacts as: anxiety and fear, mood depression, disequilibrium of emotion, motivation and initiative. In many patients headaches, dizziness and gait disturbances disappeared or diminished. Sulocton was useful in the treatment of patients with cerebral atherosclerosis.
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PMID:[Evaluation of sulocton action in patients with atherosclerotic brain ischemia]. 629 59

The epidemiologic evidence that stress contributes to cardiovascular disease is reviewed. No one characterization of stress has been associated with all manifestations of cardiovascular disease, yet specific characterizations have been associated with particular manifestations of disease. Type A behavior pattern is a risk factor for coronary artery disease (CAD) and is correlated with the severity and progression of atherosclerosis demonstrated angiographically. Work overload with job dissatisfaction also predisposes to CAD. Socioeconomic disadvantage in a society of urbanization and industrialization increases the risk of hypertension and CAD, while chronic states of anxiety, depression, and helplessness are associated with angina and sudden death. Traumatic life events, especially involving loss of or threat to self-esteem, may precipitate sudden death in patients with preexisting CAD. There is evidence that the mechanism linking the experience of stress and the development of acute coronary events is exposure to sympathetic hyperarousal and a deficit in soothing. Research is needed to determine if work environments can be designed to minimize hyperarousal and provide protective outlets for individuals experiencing such arousal.
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PMID:Stress factors in the development of coronary artery disease. 638 69

We studied the effects of prostacyclin on the frequency, duration and severity of ischemic attacks in spontaneous angina. Twenty-seven patients who did not respond to 48 hours infusion of placebo, received after a two-day observation period, 48 hours infusion of prostacyclin at an average rate of 4.0 ng/kg/min. Prostacyclin decreased number of ischemic attacks in only one of four patients with Prinzmetal angina, and was without any effect in five other patients whose attacks were associated with increase in blood pressure and heart rate. However, in 12 of 18 patients with coronary atherosclerosis, whose attacks were characterized by ST-segment depression without increase in heart rate or blood pressure, and often occurred at night, prostacyclin consistently diminished both frequency of anginal attacks and nitroglycerin consumption. This improvement lasted from 10 days to 3 months. Healing of endothelial damage by prostacyclin could explain the favorable therapeutic response in this subset of patients with spontaneous angina.
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PMID:Treatment with prostacyclin of various forms of spontaneous angina pectoris not responding to placebo. 639 38

This volume details the history of vitamin B6, its chemistry and biochemistry, methods for the assessment of vitamin B6 status, and the clinical chemistry of the vitamin. Since its discovery and synthesis over 40 years ago, vitamin B6 has been implicated in a number of disease states. All approaches to the assessment of vitamin B6 status--direct measurement of blood levels, measurement of the excretion rate of the vitamin, measurement of the metabolites or abnormal metabolic products resulting from a deficient state, or measurement of some other process dependent on the concentration of the vitamin in the body--have significant technical or physiological problems. Dietary allowances vary for different age groups and situations. In the US, the National Academy of Sciences has recommended a daily dietary allowance of 2.2 mg for young adult males and 2.0 mg for young adult females. Additional allowances have been suggested for women during pregnancy and lactation, but not for users of oral contraceptives (OCs). Vitamin B6 deficiency can be either exogenous (when intake falls below the recommended dietary allowance) or conditioned (in cases where the physiologic requirement for the vitamin is higher than the dietary allowance). Conditioned deficiency arises in the following situations: defective intestinal absorption, defective cellular and intercellular transport, and impaired oxidtion or phosphorylation mechanisms in vitamin B6 metabolism. Studies aimed at assessing the abnormal tryptophan metabolism observed in some OC users have produced conflicting results. It appears that severe depression and impairment of glucose tolerance are the only important abnormalities encountered in OC users related to vitamin B6 deficiency. Abnormalities of tryptophan metabolism have been noted in patients with rheumatoid arthritis, some malignant diseases, liver disease, diabetes mellitus, atherosclerosis, and hyperkinetic syndromes.
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PMID:Clinical chemistry of vitamin B6. 639 13

Prognosis for the patient recovery from an acute myocardial infarction is related mainly to electrical instability, left ventricular function, residual ischemia, and extent of coronary atherosclerosis. Many procedures now exist that allow investigation of these various aspects of cardiovascular function and stratification of risk. No ideal marker of prognosis exists because prognosis is not related to a single factor, because the various determinants are often interdependent, and also because they are time dependent. Thus, the presence of ischemia may be particularly important in the first year when the risk is greater, whereas left ventricular function may be the most important factor thereafter. For this reason, an active strategy for detecting ischemia, by exercise testing or other means, may add to clinical observation. Exercise testing is a safe and noninvasive method that can provide information not only on residual ischemia but also on other aspects of cardiovascular function. Many parameters can be studied, such as ST segment elevation or depression, chest pain, ventricular arrhythmias, tolerance to exercise, completion or not of the test, and the heart rate and blood pressure responses. Some of these data are not specific and must be complemented by further investigation. Such as approach should allow an overall evaluation of the cardiovascular function of the patient and an assessment of risk, and help institute an optimal treatment.
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PMID:Exercise testing in the early period after myocardial infarction in the evaluation of prognosis. 640 5

Effort angina is the result of acute myocardial ischemia on exercise due to an imbalance between myocardial oxygen demand and supply. During exercise, ischemia is provoked by an increase in myocardial oxygen needs (tachycardia, increased blood pressure, etc.) which cannot be met by increased coronary blood flow. The commonest cause of insufficient flow is coronary atherosclerosis. Coronary spasm does, however, play a role, whether it occurs during exercise on normal or atheromatous coronary vessels. Classical anti-anginal therapy is directed towards a reduction in the intense adrenergic activity associated with exercise, and to the limitation of myocardial oxygen consumption. Calcium inhibitors which cause peripheral vasodilation, decrease ventricular wall tension and coronary resistance, are usually reserved for unstable or resistant angina. We studied 10 patients with stable effort angina for over 2 years with significant (greater than 70 per cent) atheromatous lesions on coronary angiography unsuitable for surgical treatment. The patients underwent a randomised double blind trial to compare the effects of propranolol, diltiazem and placebo. Exercise ECG was performed after a treatment period of one week, 3 hours after drug administration. The results showed a significant improvement of work capacity with propranolol and diltiazem as compared to placebo. Propranolol (160 mg/day) was more effective than diltiazem (180 mg/day) in 6 patients. In 4 cases, the improvement with diltiazem and propranolol was the same. The association of the two drugs in one open study in 5 patients was even more effective in 3 patients. The small number of patients studied makes it impossible to draw any firm conclusions. Although calcium inhibitors are the treatment of choice in coronary spasm and betablockers in effort angina, diltiazem exerts an anti-anginal effect by reduction of myocardial oxygen consumption without depression of myocardial contractility, as other workers have shown.
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PMID:[Are calcium inhibitors useful in the treatment of effort angina pectoris]. 640 53


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