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

We examined the hypothesis that impaired endothelium-dependent vasodilation in atherosclerosis is associated with decreased synthesis of nitrogen oxides by the vascular endothelium. The descending thoracic aortae of rabbits fed either normal diet, a high cholesterol diet for 2-5 wk (hypercholesterolemic, HC), or a high cholesterol diet for 6 mo (atherosclerotic, AS) were perfused in a bioassay organ chamber with physiologic buffer containing indomethacin. Despite a dramatic impairment in the vasodilator activity of endothelium-dependent relaxing factor (EDRF) released from both HC and AS aortae (assessed by bioassay), the release of nitrogen oxides (measured by chemiluminescence) from these vessels was not reduced, but markedly increased compared to NL. Thus, impaired endothelium-dependent relaxation in atherosclerosis is neither due to decreased activity of the enzyme responsible for the production of nitrogen oxides from arginine nor to arginine deficiency. Because the production of nitrogen oxides increased in response to acetylcholine in both hypercholesterolemic and atherosclerotic vessels, impairments in signal transduction are not responsible for abnormal endothelium-dependent relaxations. Impaired vasodilator activity of EDRF by cholesterol feeding may result from loss of incorporation of nitric oxide into a more potent parent compound, or accelerated degradation of EDRF.
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PMID:Diet-induced atherosclerosis increases the release of nitrogen oxides from rabbit aorta. 225 62

Investigations of nitrogen and protein metabolism with the stable isotope 15N were carried out on 11 patients with atherosclerosis and 7 healthy control subjects. After oral application of 3 g 15NH4Cl (95 At% 15N) per 70 kg body weight the incorporation of the isotope 15N in plasma proteins and blood cells and the 15N elimination in urine were followed up. Retardations of 15N elimination, an accelerated incorporation of 15N in fibrin and a retarded 15N incorporation in platelet protein were observed in patients with atherosclerosis. The described method enables complex assertions about protein metabolism of the whole body and so represents a possibility to evaluate objectively the influence of an intervention on metabolism.
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PMID:[Recording protein metabolism and cell proliferation with the stable isotope 15N]. 236 68

The liver participates in the turnover rate of free fatty acids (FFA) with a third. A severe disruption of liver function that occurs in cirrhosis leads therefore to a pathogenetic relevant hyperlipacidaemia respectively increases that. With regard to its clinical relevance a survey is given of the FFA metabolism of the liver. The factors are described which influence the FFA uptake by this organ. In this connection the metabolic fate of the FFA in dependence on the hormonal nutritive state is depicted. The author deals with the relation of the hepatic FFA metabolism to that of triglycerides, cholesterol, ketone bodies, carbohydrates, amino acids and insulin. The importance of these relatons for the caloric homeostasis and for the pathogenesis of various acute and chronic functional disturbances (ketoacidosis, negative nitrogen-balance, hyperlipoproteinaemia, hyperinsulinism, atherosclerosis) is described.
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PMID:[The metabolism of free fatty acids in the liver]. 266 56

We have used clamping of the aorta above the celiac axis (SC) in 30 of 431 elective resections of infrainguinal abdominal aortic aneurysms (AAA) during the past five years as an alternative to a difficult aortic cuff dissection. The results of SC clamping in these 30 patients are compared with the results of 379 routine aneurysm resections with infrarenal (IR) clamping and 22 additional aneurysm resections where the clamp was placed immediately above the renal arteries. These difficult cuff dissections occurred in 12 patients with inflammatory AAA, in 11 patients with juxtarenal AAA, and in seven patients with recurrent or noninfected false AAA of the proximal cuff. Patients with ruptured or suprarenal aneurysms and those undergoing combined operation for a visceral ischemic syndrome and an aneurysm were excluded from this study. Patients with SC clamping had similar operative mortality rates, comparable renal function, and frequency of cardiac events as patients with IR clamping. Blood loss was slightly higher in the SC group (p = 0.07) and serum aspartate amino transferase (AST) levels were three times higher than in the IR group; however, this was of no clinical significance. In contrast, those 22 patients whose aortas were clamped immediately above the renal arteries (AR) had higher perioperative mortality rates (2% IR, 3% SC vs 32% AR) and a higher incidence of kidney failure requiring dialysis (1% IR, 3% SC vs 23% AR). The mean values of serum creatinine and blood urea nitrogen were also significantly higher in the AR group when compared with both the IR and the SC groups (IR: 25 and 1.5 mg/dl, respectively; SC: 27 and 1.8 mg/dl; AR: 41 and 3.5 mg/dl). The single most important risk factor accounting for the differences between clamping above the celiac artery and clamping above the renal arteries was the presence of atherosclerotic debris in the nonaneurysmal, juxtarenal aortic segment. Clamping the aorta with juxtarenal atherosclerosis caused either atheroembolization to kidneys, legs, and intestine or injury to the aorta, renal arteries, or both; it was the cause of morbidity in all five cases of kidney failure requiring dialysis and accounted for all seven of the deaths in the AR group. SC clamping does not add risk to the patient undergoing resection of an infrarenal AAA and is the preferred method of achieving proximal control of the infrarenal aorta when a a hazardous cuff dissection is likely.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Results of supraceliac aortic clamping in the difficult elective resection of infrarenal abdominal aortic aneurysm. 291 Nov 32

Hypercholesterolemia was induced in New Zealand white rabbits by feeding them a 0.5% cholesterol-enriched rabbit chow for 2 wk. Half of the cholesterol-fed rabbits were given lovastatin, a potent inhibitor of hydroxymethylglutaryl-coenzyme A reductase (HMG-CoA reductase), the rate limiting enzyme in cholesterol biosynthesis, and the other half were given its vehicle (i.e., DMSO). At the end of 2 wk, the rabbits underwent experimental myocardial ischemia or a sham ischemia procedure. Ischemic animals fed the cholesterol-enriched diet for 2 wk experienced much greater cardiac damage than ischemic rabbits fed the control diet, despite the absence of any atherosclerosis. Lovastatin was shown to protect the ischemic rabbit myocardium by three different indices of ischemic damage: (a) maintenance of creatine kinase (CK) activity in the ischemic myocardium; (b) reduced loss of free amino-nitrogen containing compounds from the ischemic myocardium; and (c) blunting the rise of plasma CK activity. These effects were not due to differences in myocardial oxygen demand between the groups. Arteries isolated from animals fed the cholesterol-enriched diet developed defects in endothelium-dependent relaxation in both large vessels as well as coronary resistance vessels. Acute hypercholesterolemia increases the severity of myocardial ischemia while at the same time impairing endothelium-dependent relaxation. These deleterious changes can be significantly attenuated by treatment with lovastatin.
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PMID:Cardiovascular effects of acute hypercholesterolemia in rabbits. Reversal with lovastatin treatment. 291 50

Atherosclerosis was induced in New Zealand White rabbits by feeding them a 0.5% cholesterol-enriched rabbit chow for 10-12 wk. Half of the cholesterol-fed rabbits were given BM 13505, a specific thromboxane A2/endoperoxide (TxA2/PGH2) receptor antagonist, and the other half were given its vehicle (i.e., 2% Na2CO3). At the end of 10-12 wk, the rabbits underwent experimental myocardial ischemia or an identical sham operation, except that the coronary artery was not occluded. BM 13505 was shown to protect the ischemic rabbit myocardium by three different methods: 1) maintenance of myocardial tissue creatine kinase (CK) activity in the ischemic myocardium; 2) reduced loss of free amino nitrogen-containing compounds from the myocardium; and 3) blunting the rise of plasma CK activity. Part of the mechanism for these effects may be due to inhibition of platelet aggregation and blockade of the vasoconstrictor effect of TxA2. However, these protective effects were not due to differences in myocardial oxygen demand among the groups. Finally, BM 13505 exhibited an antiatherogenic effect by reducing the deposition of cholesterol in the aortic wall and by retarding plaque formation in coronary arteries. However, it does not achieve this antiatherogenic effect by lowering plasma cholesterol concentrations or by scavenging superoxide free radicals. Thus blockade of TxA2 receptors exerts a variety of beneficial effects that reduce the severity of ischemic damage resulting from myocardial ischemia.
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PMID:Cardioprotective actions of thromboxane receptor antagonism in ischemic atherosclerotic rabbits. 297 Feb 33

Soybean protein was exhaustively digested with endo- and exo-type microbial proteases and the effect of the digestible low molecular fraction (LMF) and the undigested high molecular fraction (HMF) on the serum cholesterol level was compared to that of the intact protein in rats given a cholesterol-enriched diet. The HMF, peptides relatively abundant in hydrophobic amino acids, was found to be substantially hypocholesterolemic when fed at the nitrogen level equivalent to that of the 20% soybean protein diet, and not only serum but also liver cholesterol levels were similar to those usually encountered in rats given diets free of cholesterol. There was a dose-dependent reduction of serum and liver cholesterol when casein was replaced stepwise with HMF. The cholesterol-lowering action could be attributable to an increased fecal steroid excretion.
Atherosclerosis 1988 Aug
PMID:The hypocholesterolemic action of the undigested fraction of soybean protein in rats. 306 66

Lipid, carbohydrate and protein metabolic parameters, such as triglycerides, total and alpha-cholesterol, total protein and albumin, urea nitrogen, creatinine, glucose and the activity of alanine and aspartate aminotransferases, alkaline phosphatase, total lactate dehydrogenase and creatine phosphokinase, were measured in 50 patients with obliterating atherosclerosis and 60 patients with arteritis. The latter showed more marked lipid metabolic disturbance, as compared to the former, as well as indirect signs of hepatic dysfunction.
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PMID:[Characteristics of metabolism in patients with arteriosclerosis obliterans and arteritis]. 323 41

We started a special follow-up system for women who had a history of severe toxemic pregnancy in our department since 1975. All medical records from 1956 to 1975 were reviewed and 468 deliveries with such disease were registered at that time. One hundred and ninety five deliveries (186 women) also were added from the prospective point of view until 1985. Among 654 patients, 374 women were available to address. I. The latter 186 women were divided into 7 groups: A1, A2, A3, A4, B1; and B2. The definitions of each group were as follows. A1: primipara with severe toxemia; A2: multipara that had a severe toxemia at the first time and then normal pregnancy (ies); A3: multipara that had a severe toxemia in the first pregnancy and then mild one(s); A4: multipara that repeated severe diseases; A5: multipara that had a severe toxemia and then unclassified type(s) of the disease; B1: multipara that had a normal pregnancy at the first time and then severe toxemia(s); B2: multipara that had a mild toxemia in the first pregnancy and then severe one(s). The percent of each group was 25, 24, 13, 15, 4, 6, and 12% respectively. Those women who had severe toxemia(s) were found to have hypertension, high levels of blood urea nitrogen, hyperhematocritemia, and hyperlipemia from the results of clinical and laboratory data. Consequently, they are a high risk group of atherosclerosis, because hypertension and hyperlipemia are main risk factors of that disease. II. Eighty percent of 374 women who had a history of severe toxemia from 1956 to 1985 was able to be followed up by us until 1987. Those women also were divided into the same groups as described above except A5, and checked up as to hypertension, hyperlipemia, body weight, and so on. The characteristic features were that the group A2 is in a well condition, and that many of group A4 are suffering from various diseases with regard to the remote prognosis. In conclusions, it was suggested that there may be four etiologic causes as to toxemia of pregnancy. The first is a disadaptation during pregnancy, and this seems to consist mainly of pregnancy induced hypertension. The second has various underlying diseases, such as chronic hypertension or renal disease, etc.. The third has a hypertensive trait which is manifested as the pregnancy advances. The fourth is considered to be related to biologic ageing.
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PMID:[Follow-up study on women suffered from severe toxemia of pregnancy]. 325 67

Smoking has been linked to the development and progression of atherosclerosis but the mechanism by which smoking exerts its deleterious effects remains unknown. This study was designed to examine in a systematic way the effects of nicotine and carbon monoxide on platelets, arterial walls, and the heart. Results of experiments designed to assess the effect of nicotine and carbon monoxide on the production of prostacyclin (PGI2) by the rabbit heart are reported. Animals exposed to carbon monoxide had the carboxyhemoglobin raised to at least 12% by breathing an atmosphere enriched with carbon monoxide. Nicotine was infused at 50 micrograms/kg/hr for 1 week. Nicotine was measured by gas/liquid chromatography. PGI2 was measured by radioimmunoassay of 6-keto-PGF1 alpha, and its biologic activity was assessed by inhibition of platelet aggregation. Nicotine is concentrated in the heart and blood vessel wall and causes a statistically significant reduction in PGI2 production. Carbon monoxide raised PGI2 production significantly in all chambers, and the combination of nicotine and carbon monoxide further raised PGI2 production. The difference between the effects of nitrogen and carbon monoxide alone and nitrogen and a combination of nitrogen and carbon monoxide was significant in all chambers. It is hypothesized that nicotine exerts a direct metabolic effect in lowering PGI2 production. Carbon monoxide may make the endothelial cell relatively hypoxic, a powerful stimulus of PGI2 production, or less likely exert a direct toxic effect on the endothelial cell.
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PMID:Prostacyclin production by the heart: effect of nicotine and carbon monoxide. 354 37


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