Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of ischemic heart disease is significantly lower in southwestern American Indians than in Caucasians. To investigate this difference, the metabolism of low density lipoprotein apoprotein (apo-LDL) and plasma lipoprotein cholesterol composition were studied in 10 southwestern American Indians and 5 Caucasian controls. The plasma concentration of LDL cholesterol in American Indians was 88 +/- 5 mg/dl (mean +/- SEM) and 111 +/- 7 mg/dl in Caucasians. The corresponding values of apo-LDL concentrations were 53 +/- 3 mg/dl and 77 +/- 4 mg/dl, respectively. Conversely, high density lipoprotein cholesterol (HDL) concentrations were significantly higher in American Indians (56 +/- 4 mg/dl) than in Caucasians (37 +/- 3 mg/dl). There were no statistically significant differences in the biological half-life of apo-LDL, calculated from the second exponential of the plasma die-away curve (3.06 +/- 0.15 days vs. 3.45 +/- 0.11 days), the fractional catabolic rate of apo-LDL (0.432 +/- 0.01 vs. 0.411 +/- 0.01), or the fraction of total exchangeable apo-LDL in the intravascular space (70 +/- 1 vs. 67 +/- 3%). As derived from the absolute catabolic rate under steady-state conditions, the synthetic rate of apo-LDL in American Indians was, however, significantly lower than in Caucasians (334.6 +/- 7.8 mg/m(2) per day vs. 507.2 +/- 6.7 mg/m(2) per day; P < 0.001). These data indicate that the lower levels of plasma LDL cholesterol and apo-LDL in American Indians are due to a reduced rate of apo-LDL synthesis rather than to differences in fractional catabolic rates. These differences, in combination with higher HDL cholesterol levels, may contribute to the lower prevalence of ischemic heart disease in American Indians.
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PMID:Low density lipoprotein metabolism and lipoprotein cholesterol content in southwestern American Indians. 22 Mar 52

Conditioned medium from human monocyte-macrophages incubated under various conditions was tested for its ability to stimulate fibrinogen mRNA levels in the hepatoma cell line HepG2. Recombinant human interleukin-6 (IL-6) stimulated fibrinogen mRNA levels 4.4-fold over control levels; this response was blocked by an anti-IL-6 antibody. Conditioned medium from 3-day-cultured monocyte-macrophages produced a slight stimulation of fibrinogen synthesis in HepG2 cells which was enhanced when the monocyte-macrophages had been treated with lipopolysaccharide (LPS). This stimulation was blocked by the anti IL-6 antibody. The cytokines, interleukin-1 (IL-1) and tumour necrosis factor (TNF) were also detected in the conditioned medium from the 3-day-cultured monocyte-macrophages. Monocyte-macrophages were cultured for 17 days and then incubated with acetylated low density lipoprotein (AcLDL) for 48 h. Such cells were 'foamy' in appearance and showed a 4-fold increase in apoE mRNA and a 10 to 50-fold increase in apoE secretion. This increase in apoE production was suppressed by almost a third when cells were coincubated with AcLDL and LPS. Conditioned medium from these 17-day-cultured AcLDL-treated human monocyte-macrophages did not stimulate fibrinogen mRNA synthesis in HepG2 cells, nor did the conditioned medium contain detectable levels of cytokines. These results suggest that cytokine production from foam cells in the atherosclerotic lesion is unlikely to be a major contributing factor in determining the elevated fibrinogen levels seen in the plasma of patients with IHD.
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PMID:Cytokine production by cholesterol-loaded human peripheral monocyte-macrophages: the effect on fibrinogen mRNA levels in a hepatoma cell-line (HepG2). 193 38

The purpose of the present study was to evaluate the influence of obesity on ischaemic heart disease frequency in a well-documented type II diabetic population. To eliminate one of the possible sources of variability for plasma lipid concentrations, only subjects showing the apoprotein E phenotype, indicative of homozygosity for the epsilon 3 allele (i.e. an E3/E3 genotype), have been recruited. A larger prevalence of ischaemic heart disease was noticed among obese patients as compared to non-obese or merely overweight subjects according to a higher frequency of hypertension and to higher triglyceride concentrations. These results corroborate the hypothesis of a common pathogenesis of the major cardiovascular risk factors.
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PMID:Relationships between obesity and ischaemic heart disease in type II diabetic subjects homozygous for the apoprotein E3 allele. 195 96

In 62 patients with diabetes mellitus type II, 22 patients with obesity I degree and 40 patients with normal body mass (28 with ischemic heart disease and 12 without ischemic heart disease) the blood sugar profile and the composition of the high density lipoproteins (HDL) were examined. In decompensated diabetes mellitus type II reduction of cholesterol and phospholipid contents of HDL and of apoprotein A were found. With compensation of the carbohydrate metabolism the composition of HDL becomes normal. In the obese diabetics the changes of these indices are more pronounced. In diabetic patients with ischemic heart disease the cholesterol and phospholipid contents and that of apoprotein A in HDL are lower than those in diabetic patients without ischemic heart disease. These data show that changes of HDL in diabetes mellitus favor the development of atherosclerosis changes.
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PMID:[Changes in the high-density lipoprotein level in patients with diabetes mellitus type II]. 228 7

The authors studied the effect of anaprilin monotherapy (dose: 160-200 mg/daily for 10 months) on the level of atherogenic apolipoproteins (apo A, apo B) and fractions of plasma cholesterol in 34 patients with ischemic heart disease, stable exertion angina pectoris (class 2-3). It was established that changes in the plasma lipid and apoprotein spectrum result in an increase of apo B, decrease of apo 1, increase of apo B/apo A1, decrease of high-density lipoprotein cholesterol (HDLCS) and a different dynamics of HDLCS/apo A1. The established changes in the lipid metabolism are of atherogenic character.
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PMID:[The effect of propranolol on the apoprotein spectrum of the blood plasma in patients with ischemic heart disease]. 233 43

Lipid metabolism indices were followed up in 62 patients with diabetes mellitus type II and in 20 healthy persons as controls. An increase of serum triglycerides, very low density lipoproteins and low density lipoproteins, a decrease of high density lipoproteins and cholesterol in the upper reference range were found. Following diabetes compensation these indices became normal. In decompensated diabetes apoprotein A increased, apoprotein B decreased. Diabetes compensation lead to normalization of these indices. A comparative study of these indices in diabetics with and without ischemic heart disease was carried out. It showed a considerable decrease of the high density lipoproteins and a parallel increase of the very low density lipoproteins and low density lipoproteins in the diabetics with ischemic heart disease. The results of the study lead to the conclusion that criterion for diabetes compensation should be not only the blood sugar normalization bur also the correction of the lipid fractions changes.
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PMID:[Lipoprotein and apoprotein changes in type-2 diabetes mellitus]. 321 33

The interaction of mouse peritoneal and human pericardial macrophages with lipoprotein (LP)-antibody (Ab) immune complex isolated from the serum of ischemic heart disease (IHD) patients has been studied. It is shown that the Ab of the autoimmune complex belongs to IgG class, and the antigen is the LP with d less than 1.063 g/ml. Incubation of mouse peritoneal macrophages with such complex led to the activation of [14C]oleic acid incorporation into cholesteryl esters by 2.5-2.8-fold, in comparison with the experiments where macrophages were incubated with free apoprotein (apo) B-containing LP isolated from the same serum. Incubation of human pericardial macrophages with autologous LP-Ab immune complex led to the transformation of macrophages into foam cells. These data lead to the conclusion that formation of LP-Ab autoimmune complexes may play an important role in the formation of atherosclerotic lesions of the arteries.
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PMID:Accumulation of cholesteryl esters in macrophages incubated with human lipoprotein-antibody autoimmune complex. 321 80

Serum apolipoprotein and lipoprotein concentrations, fatty acid spectra of various lipids, dietary habits and common risk factors for ischaemic heart disease were studied in 73 and 77 randomly selected, 50-year-old healthy men in Naples and Stockholm, respectively. Mean serum cholesterol concentration was higher in Stockholm than in Naples men (6.23 vs. 5.47 mmol/l, p less than 0.001) as were low (LDL) (4.08 vs. 3.57 mmol/l, p less than 0.001) and high (HDL) (1.40 vs. 1.25 mmol/l, p less than 0.001) density lipoprotein fractions. Mean serum triglyceride concentrations did not differ. Mean apolipoprotein B and C-I concentrations were higher in Stockholm men (1,116 vs. 1,020 mg/l, p less than 0.05 and 96 vs. 79 mg/l, p less than 0.01, respectively). Stockholm men derived significantly more of their calories from fat (38 vs. 28%, p less than 0.001) and the dietary fat had significantly lower polyunsaturated-to-saturated fatty acid ratio (P/S-ratio 0.29 vs. 0.51, p less than 0.001), and less from carbohydrate (44 vs. 49%, p less than 0.001) than Naples men, respectively. Mean caloric intake and mean weight/height index did not differ. Stockholm men had higher blood pressures, but there were more smokers among Naples men. The higher fat intake in Stockholm men may offer an explanation of the differences seen in lipoprotein and apoprotein concentrations and compositions but other factors, such as genetic influences cannot be excluded. A greater cholesterol flux through the plasma compartment in Stockholm men may be one important factor contributing to the higher incidence of ischaemic heart disease in this population.
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PMID:Serum apolipoproteins, lipoproteins and fatty acids in relation to ischaemic heart disease in northern and southern European males. 334 2

There is a very high probability that lipoprotein metabolism plays a central role in the etiology of coronary heart disease. In sedentary persons one way to favorably alter lipoprotein metabolism and possibly delay the progression of coronary atherosclerosis is by an increase in their habitual physical activity. More physically active persons tend to have lower plasma triglycerides and very low density lipoprotein concentrations, and a greater high-density lipoprotein mass due to higher concentrations of the subfraction HDL2 and apoprotein A-I. Plasma low-density lipoprotein concentrations usually are not significantly reduced by exercise unless accompanied by weight loss, but there may be important changes in the distribution among the low-density subfractions. These exercise effects are most likely mediated by alterations in the activity of enzymes involved in the synthesis, transport and catabolism of the various lipoproteins including lipoprotein lipase, hepatic lipase and lecithin: cholesterol acyltransferase. In healthy persons as well as in patients with ischemic heart disease, diabetes and renal failure, an increase in moderate-intensity, endurance-type activity requiring an expenditure of approximately 4 MJ (1,000 kcal) per week usually produce favorable lipoprotein changes. Above this level a dose-response relationship exists, with greater changes occurring up to energy expenditures of 19 MJ (4,500 kcal) per week.
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PMID:The influence of exercise training on plasma lipids and lipoproteins in health and disease. 353 12

Changes in the content of lysophosphoglycerides in a crude plasmalemmal fraction of canine heart during short-term ischemia (occlusion of the left descending coronary artery for 8 min) have been studied in the presence and in the absence of phosphocreatine and phosphocreatinine. In the control experiments without PCr or PCr-nine ischemia caused significant elevation of the content of LPG: that of lysophosphatidylcholine was increased by 83% and that of lysophosphatidylethanolamine by 168%. Intravenous administration of PCr and PCr-nine in doses of 300 mg/kg completely prevented accumulation of LPG in the ischemic zone. Because of the well-known arrhythmogenic properties of LPG, the inhibitory effect of PCr and PCr-nine on the elevation of their concentration in the ischemic zone may be closely related to the antiarrhythmic action of PCr and PCr-nine in acute myocardial ischemia.
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PMID:Effect of phosphocreatine and related compounds on the phospholipid metabolism of ischemic heart. 371 64


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