Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ELISA using the test systems and a complex of equipment manufactured by Flow Company was employed to study over time the content of fibronectin, fibrinogen, products of its degradation and myoglobin in 178 patients suffering from coronary heart disease (stable and progressive angina pectoris, acute myocardial infarction). The concentration of myoglobin, fibronectin, fibrinogen and products of its degradation was established to depend on the gravity of coronary heart disease and the tame elapsed since the disease onset. In patients with progressive disease, there was an increased consumption of fibronectin which may be due both to its expenditure during blood coagulation and fulfillment of angioprotective function because of exacerbation of systemic atherosclerosis.
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PMID:[The content of fibronectin, fibrinogen, its degradation products and myoglobin in patients with ischemic heart disease]. 209

Transitional metals, particularly iron, markedly potentiate oxidant damage to isolated cell organelles. However, determining the probable importance of iron in damage to intact cells is difficult because of our inability experimentally to increase the cell content of this transition metal. We now report that heme is a uniquely effective iron delivery vehicle, capable of loading large amounts of potentially reactive iron into intact cells. We find that endothelial cells in vitro rapidly incorporate free heme and this heme-loading sensitizes endothelium to oxidant-mediated cytotoxicity caused by hydrogen peroxide, the hypoxanthine/xanthine oxidase system, or phorbol-stimulated PMN. Although the precise mechanism of the heme-aggravated cytotoxicity is not yet known, it closely parallels amplified lipid peroxidation in endothelial cell membranes suggesting the importance of lipid injury. Hemopexin, by complexing heme, protects endothelial cells from activated PMN, but only if added simultaneously. The hydrophobic iron chelator and antioxidant, U74500A, abrogates heme-augmented hydrogen peroxide and PMN-mediated endothelial damage. Such compounds, therefore, may have therapeutic potential in one or more of the listed clinical syndromes. We speculate that exposure of endothelium to free heme may potentiate vascular damage in various clinical syndromes, including acute renal failure after massive intravascular hemolysis, crush injuries, reperfusion after myocardial infarction (perhaps secondary to cardiac myoglobin release), retrolental fibroplasia associated with neonatal hemopexin deficiency, and, perhaps, atherosclerosis involving sites of turbulence that may trigger minor red blood cell lysis.
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PMID:Heme uptake by endothelium synergizes polymorphonuclear granulocyte-mediated damage. 213 29

The pattern of immunocytochemical staining with antibodies to caeruloplasmin, myosin, myoglobin and C-reactive protein seen in myocardium taken from deaths with macroscopic evidence of myocardial infarction and/or significant coronary artery atherosclerosis and from deaths with neither of these lesions has been correlated with H&E, PTAH and HBFP staining of myocardium and circumstances of each death indicative of antemortem hypoxia and/or ischaemia. Loss of staining with these antibodies correlated well with fuchsinorrhagia and both techniques are more sensitive than H&E and PTAH staining in the detection of early ischaemic/hypoxic damage to myocardium. However, their sensitivity is such that they appear to detect agonal changes and, therefore, cannot be used for specific diagnosis of early myocardial infarction.
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PMID:Further evaluation of immunocytochemical staining in the diagnosis of early myocardial ischaemic/hypoxic damage. 233 27

The sensitive and reliable dinitrophenyl (DNP) hapten sandwich staining (DHSS) procedure (B. Jasani et al., Virchows Arch (Pathol. Anat.), 406 (1985) 441-448) was used to study the distribution of immunoperoxidase staining seen with antibodies to seven protein markers in post-mortem heart tissue. This was obtained from 12 cases with macroscopic myocardial infarction and 17 cases without myocardial infarction (10 with and 7 without significant coronary artery atherosclerosis). The immunostaining patterns were compared with the appearances seen in adjacent sections stained by the routine haematoxylin and eosin (H & E) and phosphotungstic acid haematoxylin (PTAH) methods and a method previously recommended for the detection of early myocardial infarction, the haematoxylin basic fuchsin picric acid (HBFP) stain. Loss of immunostaining with an antibody to myoglobin was found to be a reliable and more objective marker of both early and established myocardial infarction compared with the histological stains. Antibodies to myosin, caeruloplasmin, C-reactive protein and pre-albumin gave similar but less reliable results, whilst those to complement factor C3b and alpha-1 anti-trypsin gave the least reliable results for early myocardial ischaemic/hypoxic damage. The immunocytochemical results are considered sufficiently encouraging to extend the work to a large number of sudden death cases in order to establish a new, more reliable approach to the detection of histologically latent ischaemic/hypoxic damage in the myocardium.
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PMID:Immunocytochemical diagnosis of early myocardial ischaemic/hypoxic damage. 264 26

Serum myoglobin (MG) concentration was measured in 25 patients with obliterating atherosclerosis of the aorta and main arteries of the lower extremities and in 30 normal subjects. Serum MG levels were also measured repeatedly following aortofemoral bifurcation shunting. An original one-step enzyme (immunoassay technique was used to determine serum MG concentration. Serum MG was increased in patients with obliterating diseases of the lower extremities. There was marked myoglobinemia, reaching its peak within 8 to 10 hours after the reconstructive operations on the aorto-iliac segments.
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PMID:[Myoglobin level in patients with occlusive diseases of the lower extremities]. 275 19

Bezafibrate is a lipid-lowering drug, chemically related to clofibrate. At its recommended dosage of 200 mg 3 times daily, or alternatively 400 mg once daily as a sustained-release preparation, it produces substantial reductions in plasma triglyceride and cholesterol concentrations in patients with hypertriglyceridaemia and hypercholesterolaemia, respectively. Preliminary investigations indicate that a single daily dose of 400 mg in a sustained-release preparation is as effective as 200 mg 3 times daily. In patients with any type of hyperlipoproteinaemia bezafibrate also increases the plasma HDL-cholesterol concentration. These effects are equivalent in patients with primary hyperlipoproteinaemia or hyperlipoproteinaemia secondary to diabetes or renal disease, although dosage adjustment is important in the latter group. During long term therapy (2 to 4 years) the influence of bezafibrate on the lipid profile is sustained. The lipid-lowering effects of bezafibrate are at least equivalent to those of clofibrate, fenofibrate, colestipol, probucol or sustained release etofibrate. In addition, the increase in HDL-cholesterol tends to be at least as great as with all alternative treatments studied. Bezafibrate is rapidly eliminated, and thus does not accumulate during prolonged administration in patients with normal renal function. Experimental studies have shown bezafibrate to have a complex range of effects on lipoproteins and on the enzymes and receptors involved in lipid metabolism. However, its exact mechanism of lipid-lowering action is unclear. Bezafibrate enhances anticoagulation in hyperlipoproteinaemic patients requiring anticoagulant therapy, and preliminary investigations indicate that it reduces the plasma fibrinogen concentration, especially in patients with hyperfibrinogenaemia. These properties of bezafibrate could contribute to an antiatherogenic effect of the drug, but further investigation is required to establish the drug's potential as chronic therapy in patients with hyperfibrinogenaemic atherosclerosis. Adverse reactions to bezafibrate have largely been restricted to gastrointestinal disturbances, with some cutaneous reactions and central nervous system effects. The incidence of side effects has been no greater than with comparative lipid-lowering drugs. In patients with renal disease, a few cases of marked elevation of serum creatine phosphokinase and myoglobin, and associated muscle cramps, have been reported (diagnosed as rhabdomyolysis). Hepatic enzyme induction by bezafibrate in rats results in hepatomegaly, but there has been no case of significant hepatotoxicity in man.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Bezafibrate. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic use in hyperlipidaemia. 330 1

Adult, male, Sprague-Dawley rats were subjected to an acute and massive myocardial infarct with isoproterenol. Some of the animals were treated with the anti-hyperuricemic agent, allopurinol, either before or during the induction of myocardial infarction. Autopsy of animals at hourly and daily intervals demonstrated that treatment with allopurinol provided protection against the untoward pathophysiologic changes which attend this kind of experimental infarct. Allopurinol was anti-arrhythmic and caused improved myocardial repair accompanied by reduced fluctuations in circulating CPK, SGOT, SGPT, LDH, and myoglobin. Changes in blood lipids, glucose, and BUN suggests that allopurinol exerts some of its myocardial protective effects through its positive influence on protein metabolism. Allopurinol appears to alter adrenal steroidogenesis which may also play a role in the myocardial salutary effects of this drug.
Atherosclerosis 1981 Apr
PMID:Allopurinol amelioration of the pathophysiology of acute myocardial infarction in rats. 724 92

Endogenous alpha-tocopherol of low density lipoprotein (LDL) particles exposed to ferrylmyoglobin (iron in the form of FeIV = O) vanishes as a function of myoglobin concentration. After alpha-tocopherol depletion, subsequent heavy lipid peroxidation is prevented by caffeic and p-coumaric acids, i.e., phenolic acids present in foods and beverages, by a mechanism involving the one-electron transfer reaction between the phenols and the ferrylmyoglobin, with formation of metmyoglobin and the corresponding phenoxyl radicals from caffeic and p-coumaric acids, as previously discussed. Caffeic acid delays alpha-tocopherol consumption when present before oxidation challenging and restores alpha-tocopherol when added halfway during the reaction. Conversely, p-coumaric acid accelerates the rate of alpha-tocopherol consumption when added either before or during the oxidation reaction. In LDL enriched with alpha-tocopherol, caffeic acid induces an inhibition period of oxidation longer than that expected from the sum of discrete periods characteristic of the phenolic acid and alpha-tocopherol. Surprisingly, p-coumaric acid decreases the peroxidation chain rate. Similar effects of these phenolic acids on alpha-tocopherol consumption were observed in a Triton X-100 micellar system, i.e., in the absence of a peroxidation chain reaction. Results suggest that caffeic acid acts synergistically with alpha-tocopherol, extending the antioxidant capacity of LDL by recycling alpha-tocopherol from the alpha-tocopherol radical (i.e., alpha-tocopheroxyl radical). By contrast, the phenoxyl radical from p-coumaric acid (produced by electron-transfer reaction between phenolic acid and ferrylmyoglobin) oxidizes alpha-tocopherol. However, in spite of alpha-tocopherol consumption, the exchange reaction recycling p-coumaric acid can still afford an antioxidant protection to LDL on basis of the chain-breaking activity of p-coumaric acid. These results emphasize the biological relevance of small structural modifications of phenols on the interaction with alpha-tocopherol in LDL. The significance of these results in the context of atherosclerosis is discussed.
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PMID:Two related phenolic antioxidants with opposite effects on vitamin E content in low density lipoproteins oxidized by ferrylmyoglobin: consumption vs regeneration. 748 1

The authors used the immunohistochemical reaction with antibodies against myoglobin of the heart muscle in three groups of suddenly deceased subjects with a macroscopically apparent myocardial infarction and revealed focal disappearance of myoglobin in 90%. In the second group of sudden deaths with advanced atherosclerosis without a macroscopically apparent infarction, without a macroenzymatic reaction and without any positive histological finding a disseminated reduction up to complete disappearance of myoglobin from cardiac muscle fibres was observed in 70%. In the third control group of subjects who died from a violent death without advanced coronary atherosclerosis a disseminated reduction or disappearance of myoglobin was recorded only in 26%, and this was the case where death was preceded by massive suffocation. The immunochemical method for detection of myoglobin is very sensitive. Disappearance or reduction of myoglobin in myocardial muscle fibres occurs not only in ischaemic but also in hypoxic conditions.
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PMID:[Personal experience with detection of myoglobin in the myocardium using the immunoperoxidase method]. 786 80

Histochemical (= HIS) methods (haematoxylin-eosin, luxol fast blue, chromotrope aniline blue) and various immunohistochemical (= IH) markers (myoglobin, desmin, fibrinogen, complement C5b-9) were applied in parallel to test the efficiency, specificity and sensitivity for the recognition of early ischemic myocardial damage. The whole series was subgrouped into cardiac deaths (N = 35) and controls (N = 13). Cardiac deaths were sub-divided into 3 groups: 1. infarction visible in gross examination (N = 15), 2. coronary thrombosis without infarction (N = 11), 3. stenosing coronary atherosclerosis without infarction (N = 9). The control group (group 4) consisted of unnatural deaths with presumed short agonal periods (N = 13). Group 1 cases usually exhibited extended coagulation necrosis of the diffuse type and the contraction type in combination (1 exception). Group 2 showed mainly a patchy type of coagulation necrosis and contained 1 cases where all methods failed to react and 3 more cases where only the HIS methods failed to react. Group 3 and 4 were associated with a disseminated type of single and/or grouped fibre necrosis. In addition, the average reaction strengths showed a decrease from group 1 to group 4 which was more pronounced in the HIS reactions compared with the IH reactions. One case in group 1 showing negative IH reactions cannot be explained. Positive IH reactions observed in a few cases in group 2 contrasting with negative HIS reactions would indicate a greater sensitivity of this methodology and this interpretation also applies to groups 3 and 4. From pathophysiological considerations, the positive cases in groups 3 and 4 can be well explained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The application of selected histochemical and immunohistochemical markers and procedures to the diagnosis of early myocardial damage. 811 91


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