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

The in vitro effects of prostaglandins E1 and F1alpha on the activity of cholesteryl ester synthetase and cholesteryl ester hydrolase activities of the pigeon aorta were examined. It was found that prostaglandin E1 markedly inhibited the cholesteryl ester hydrolase activity in the supernatant fraction and slightly inhibited the cholesteryl ester synthetase activity. Prostaglandin F1alpha, however, modestly stimulated the cholesteryl ester hydrolase activity both in the microsomal and in the supernatant fraction of the aorta. These observations strongly warrant further studies on the role of prostaglandins in atherogenesis.
Atherosclerosis 1977 May
PMID:Effect of prostaglandins E1 and F1alpha on the activities of cholesteryl ester synthetase and cholesteryl ester hydrolases of pigeon aorta in vitro. 1 25

In epididymal adipose tissue from rats, human serum antagonizes inhibition of basal lipolysis by nicotinic acid in vitro. Under similar conditions caffeine-stimulated lipolysis was unaffected by the presence of human serum. Very low density (VLDL), low density (LDL) and high density (HDL) lipoproteins were all found to antagonize the action of nicotinic acid on basal lipolysis. VLDL also antagonized prostaglandin E1 (PGE1)-inhibition of basal lipolysis in vitro. The fat cell membrane was suggested as the site at which human serum lipoproteins antagonize nicotinic acid or PGE1 antilipolytic action on basal lipolysis in vitro.
Atherosclerosis 1976 Oct
PMID:Modification of nicotinic acid and prostaglandin E1 antilipolytic action in vitro. 18 78

Individuals with familial hyperbetalipoproteinemia are at increased risk of premature atherosclerosis and thrombosis. Although there is controversy whether platelet survival is shortened or normal in this disease, several in vitro tests of platelet function are abnormal including a decreased threshold concentration for stimulation of aggregation by ADP, epinephrine and collagen and increased release of nucleotides to the same agents. These functional changes are accompanied by an increase of cholesterol to phospholipid ratio in the platelet membrane and in low density lipoprotein in individuals with type IIa hyperlipoproteinemia. Clofibrate and halofenate reverse some of the abnormalities in vitro and the former drug, when administered for 6 weeks to patients with type IIa hyperlipoproteinemia decreases platelet sensitivity to ADP and epinephrine. The platelet hypersensitivity to aggregating agents can be reproduced in vitro by increasing the cholesterol to phospholipid rather in normal platelets. These artificially hypersensitive platelets can be returned to normal by halofenate in vitro. Incorporation of cholesterol into platelet membranes increases the basal level of the membrane associated enzyme adenylate cyclase. However, the enzyme no longer responds to stimulation by prostaglandin E1, and this is associated with relative resistance of the platelet to inhibition by this pharmacologic agent. These functional alterations produced by cholesterol enrichment of platelet membranes occur is parallel with an increase in platelet membrane microviscosity suggesting that the more rigid membrane can alter the behavior of membrane associated enzymes and receptors. A correlation appears to exist between the ability of certain drugs to induce phase separation in model membranes and the potency in inhibitory platelet aggregation.
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PMID:Platelet function in hyperbetalipoproteinemia. 58 Sep 82

Although the effects of prostaglandins (namely PGE) on lipolysis are well known, there are few data about their action on the various serum lipids (cholesterol, phospholipids, triglycerides). We have no information about the action of these products on experimental atherosclerosis and the arterial lipids. In the present work, we found in rabbits fed an hyperlipidemic diet, or receiving adrenalin injections, or a sequential atherogenic treatment for a long course, that the treatment by PGE1 induces a decrease of the serum lipids, mainly in animals fed an hyperlipidemic diet. In the same experiment, we found also a decrease of the cholesterol level in aorta and in the connective tissue of sub-cutaneous granulomas. The interest of these findings is discussed in the light of present known data about the effect of prostaglandins on lipid metabolism.
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PMID:[Effect of prostaglandin PGE1 on blood and tissue lipids in rabbit experimental arteriosclerosis]. 77 49

The purpose of the investigation was to study the alterations in the lipid and lipoprotein content in the blood serum, the liver and the aortic wall of rats with experimentally induced salt, renal (Goldblatt) and adrenal-regeneration hypertension. The experiments were carried out on 59 Wistar rats (25 normotensive controls). It was established that both the serum and the liver lipid patterns vary in the three experimental models of hypertension. Thus, while in salt-induced hypertension no hyperlipidaemia and hyperlipoproteinaemia were established, in renal hypertension the serum lipid and lipoprotein levels were significantly increased in comparison to the controls. The cholesterol content in the liver was increased in all the three models of hypertension. The remaining lipid fractions were within normal ranges or a little decreased in salt-induced hypertension, while in renal and adrenal-regeneration hypertension their quantity was significantly increased. A two weeks' treatment with hypotensive prostaglandin E1 diminished the lipid and lipoprotein contents in the liver of rats with adrenal-regeneration hypertension, only cholesterol remaining unaltered. The blood serum level of free fatty acids increased in all the three models of experimental hypertension, as did the cholesterol and beta-lipoprotein level in the aortic wall. The alterations in lipid and lipoprotein metabolism established in this study are regarded as specific for the hypertensive process itself, since no histological alterations characteristic of atherosclerosis were observed.
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PMID:The action of arterial hypertension on lipid and lipoprotein metabolism. I. Salt, adrenal-regeneration and renal (Goldblatt) hypertension. 100 Sep 84

While some data suggest that Ca(2+)-mobilizing effects of low density lipoprotein (LDL) in platelets are mediated by a specific membrane receptor, the data about the nature of this lipoprotein-binding site are contradictory. This work was performed in order to assess possible involvement of apolipoprotein (apo) B,E receptor, present in most cell types. To answer the question we compared effects of LDL in normal platelets and those obtained from patients with homozygous familial hypercholesterolemia (HFH), characterized by absence of functional apo B,E receptors. We have found that in accordance with previous results LDL induced instant reversible elevation of free cytoplasmic calcium concentration ([Ca2+]i) in fura-2-loaded platelets. The effect was observed both in healthy and HFH groups. Neither half-maximal effective concentrations nor maximal effects of LDL differed significantly between two groups. Ca(2+)-mobilizing effects of lipoproteins were potentiated about 4-fold by epinephrine and completely blocked by prostaglandin E1 both in platelets of healthy and HFH subjects. The similarity of lipoprotein effects in control and HFH platelets is evidence that apo B,E receptor does not mediate the Ca(2+)-mobilizing activity of LDL in this cell type.
Atherosclerosis 1992 Oct
PMID:Platelets in patients with homozygous familial hypercholesterolemia are sensitive to Ca(2+)-mobilizing activity of low density lipoproteins. 133 52

The authors present their result of a two-year follow-up of 106 patients to whom an intra-arterial perfusion of prostaglandin E1 was administered, as limb salvage procedure. The patients were in the IIIrd and IVth stage of occlusive diseases by Fountain, and surgical reconstructions were not possible. All patients were divided into five groups: A--diabetic angiopathy (5), B--distal form of atherosclerosis (40), C--diabetic angiopathy and atherosclerosis (45), D--Burger disease (10) and E--adjuvant therapy in reconstruction with poor run-off (6). The Doppler sonographic and angiographic measurements were performed. After transcutaneous (16 cases), or intraoperative (90 cases) introduction of the catheter into superficial of profunda femoral artery, a continuous intraarterial administration of prostaglandin E1 was carried out in a dose of 10 nanograms/kg body weight/minute (total dosage 3000 nanograms). The patients were controlled immediately after the treatment, as well as 1, 3, 6, 12, 24 and 36 months after the treatment. In efficiency of the treatment was estimated on the following basis: elimination of rest pain, healing of trophic ulceration and demarcation of gangrenous processes. Our late results of intra-arterial administration of prostaglandin E1 proved to be a very successful limb salvage procedure. The treatment was more successful in a connections between the upper knee arterial net and pedal arterial arches were preserved.
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PMID:[Intra-arterial administration of prostaglandin E1 in occlusive arterial diseases]. 164 6

The blood levels of 6-keto-PGE1 alpha and thromboxane B2 were measured in the coronary sinus of 15 males during and just after a spontaneous myocardial ischemic episode. The comparison was made in 30 males with coronary heart disease in the presence of exercise-induced angina in whom coronary sinus blood samples were taken during myocardial ischemia provoked by pacing and 6 males suffering from cardialgias without signs of coronary atherosclerosis. The patients with spontaneous anginal attacks had lower baseline 6-keto-PGE1 alpha (179.0 +/- 47.8 pkg/ml) than those with exercise-induced angina (336.0 +/- 65.7 pkg/ml; p less than 0.1). This difference became greater during ischemia (165.0 +/- 49.0 and 350.0 +/- 69.5 pkg/ml, respectively, p less than 0.05) and just after its elimination (166.0 +/- 48.7 and 413.0 +/- 76.0 pkg/ml, respectively, p less than 0.05). Coronary sinus blood thromboxane B2 levels were not substantially different in the presence or absence of myocardial ischemia. Thus, a decrease in the prostacyclin-forming function of the coronary endothelium plays a definite role in the genesis of spontaneous myocardial ischemic episodes.
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PMID:[Coronary sinus blood thromboxane and prostacyclin in spontaneous myocardial ischemia]. 179 81

The effects of the stable prostacyclin analogue iloprost, prostaglandin E1 and prostaglandin F2 alpha on sterol synthesis were investigated in freshly isolated human mononuclear leukocytes. Incubation of cells for 6 h in a medium containing lipid-depleted serum led to a 3-fold rise in the rate of sterol synthesis from [14C]acetate or tritiated water. Iloprost and prostaglandin E1 added in increasing concentrations at zero time resulted in an inhibition of the synthesis of sterols, the suppression being 50 and 55% at a concentration of 1 mumol/1, respectively. Both prostaglandins yielded a sigmoidal log dose-effect curve. In contrast, prostaglandin F2 alpha had no influence on sterol synthesis up to a concentration of 1 mumol/1. The action of the prostacyclin analogue and prostaglandin E1 on the relative rate of sterol synthesis was not immediate, since the prostaglandins had no effect when given at 6 h to the incubation medium, and the incorporation of [14C]acetate into sterols was measured thereafter. The results suggest that prostacyclin and prostaglandin E1 affect cholesterol synthesis and therefore may play a role in the regulation of cellular cholesterol homeostasis and in the development of atherosclerosis.
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PMID:The prostacyclin analogue iloprost and prostaglandin E1 suppress sterol synthesis in freshly isolated human mononuclear leukocytes. 240 73

The antiplatelet action of PGE1 was the basic concept for introducing this substance into clinical therapy of atherosclerosis. However, in the meanwhile a variety of other mechanisms have been discovered, which might be of importance, especially concerning the long-term benefit seen after treatment with PGE1, such as stabilization of endothelial lining, reflected by a decreased number of circulating endothelial cells and a decreased thrombogenicity (potentiated by endogenous EDRF-release), an inhibitory action on smooth muscle cells of the vessel wall such as decrease in mitotic and proliferative activity associated with a diminished extracellular matrix formation, an increase in fibrinolytic capacity, beneficial effects on white and red blood cells and some beneficial effects on the lipid metabolism by decreasing the arterial wall cholesterol content and upregulation of LDL-receptors as well as a moderate drop in serum cholesterol, seen in severe hypercholesterolemics only. It is assumed, that especially the vascular effects together with the hypolipidemic actions of PGE1 might be of major importance underlying the long-term benefit.
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PMID:Pathomechanisms of atherosclerosis beneficially affected by prostaglandin E1 (PGE1)--an update. 269 1


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