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Query: UMLS:C0020473 (
hyperlipidemia
)
15,891
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The present study evaluated indomethacin therapy--a nonsteroidal anti-inflammatory drug--on experimental
hyperlipidemia
and atherosclerosis in Rhesus monkeys. Twenty-four monkeys were divided randomly into four groups of six. Two groups received stock pellet diet and two were given an atherogenic diet for six months. After this period, one stock diet-fed group and one atherogenic diet-fed group were treated with oral indomethacin (2.5 mg) on alternate days for a further six months. Serum lipids and lipoproteins were markedly elevated in atherogenic diet-fed monkeys. Generally, indomethacin did not exert a hypocholesterolemic effect; however, liver cholesterol was decreased (P less than 0.05) in atherogenic diet-fed monkeys treated with indomethacin. High density lipoprotein cholesterol was increased in stock diet-fed, indomethacin-treated monkeys but not in atherogenic diet-fed, indomethacin-treated monkeys. Apoprotein A-I was not affected by indomethacin in either stock or atherogenic diet-fed monkeys; however, the drug produced a significant (P less than 0.01) reduction of serum thromboxane B2 in stock diet-fed monkeys, without restoring the 6-keto-
prostaglandin F1
alpha to pretreatment levels. A protective role of the drug was noted on both the extent and severity of aortic and coronary atherosclerosis.
...
PMID:Effect of indomethacin on serum lipids, lipoproteins, prostaglandins and the extent and severity of atherosclerosis in rhesus monkeys. 157 66
The acute effects of fatty meals (900 kcal) rich in saturated (cream) or n-3 polyunsaturated (cod liver oil, CLO) fatty acids on human umbilical vein endothelial cells (ECM) and platelet behavior were studied. The ECM were incubated for 24 hours at 37 degrees C with either plasma or chylomicrons (CM) obtained 3 hours after the meals. The ability of the ECM to inhibit platelet aggregation (PIA) and the release of prostaglandin I2 measured as 6-keto-
prostaglandin F1
alpha (6-keto-PGF1 alpha) were measured after 24 hours of incubation, after stimulation and after freezing and thawing. Similar studies were done with CM from a patient with type V hyperlipoproteinemia. The release of 6-keto-PGF1 alpha was increased by postprandial plasma and by CM obtained after both meals. Plasma collected after CLO, but not after cream, increased PIA, whereas CM derived from all sources studied stimulated the PIA of ECM. No consistent correlation could be established between the release of 6-keto-PGF1 alpha and PIA. Increased platelet aggregation in platelet-rich plasma was always observed during postprandial
hyperlipidemia
.
...
PMID:Effects of postprandial plasma and chylomicrons on endothelial cells. Differences between dietary cream and cod liver oil. 375 2
Lipid emulsions have been associated with changes in pulmonary function. Although these changes were related to the physical effects of the infusion-induced
lipemia
on gas exchange, several animal and human studies suggest that the impairment in pulmonary function observed with lipid infusions was mediated by prostaglandins. Prostaglandins are synthesized enzymatically from essential fatty acids. We studied the effects of two lipid emulsions, with different amounts of essential fatty acids (20% long-chain triacylglycerols [LCT] with 55% of linoleic acid and 7% of alpha linolenic acid in 100 g of emulsion, and a physical mixture of 20% medium-chain triacyglycerols [MCT] and LCT with 26% of linoleic acid and 4% of alpha linolenic acid in 100 g of emulsion), on plasma levels of eicosanoids in patients with acute respiratory distress syndrome (ARDS). Although in patients with ARDS, plasma levels of prostanoids were higher than the reference values, neither lipid emulsion, administered at the rate of 2 mg.kg-1.min-1 induced significant changes in the eicosanoids except for a decrease in systemic-pulmonary arterial 6-keto
prostaglandin F1
alpha difference.
...
PMID:Eicosanoids and fat emulsions in acute respiratory distress syndrome patients. 913 79