Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An analysis of haemostatic variables was done in 31 prostate cancer patients treated with oestrogens (13 pts), estramustine phosphate (7 pts) or orchidectomy (11 pts) before, at about 7 weeks and 6 months of treatment. Six patients treated with either of the drugs developed venous thromboembolism or ischemic vascular disease. Already before treatment there were changes indicating some activation of blood coagulation, fibrinolysis and kallikrein systems. The drug treated group showed significant changes in several variables: i.e. increase in factor VII, plasminogen and prekallikrein but also a decrease in antithrombin and in inhibitors to the fibrinolytic and kallikrein system. Significant difference between the drug treated groups was found in circulating platelet aggregates and in kallikrein inhibiting activity. Tissue plasminogen activator capacity was significantly lower in the drug treated patients with complications than in those without. The study also showed that in addition to the assay of the tissue plasminogen activator capacity during the first weeks of therapy it might be helpful in predicting cardiovascular complications to investigate platelet aggregates, prothrombin complex, factor X, von Willebrand factor antigen, fibrinogen, antithrombin, fibrino-peptide A, and the inhibitors of fibrinolysis as well as C1-esterase inhibitor.
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PMID:Changes in blood coagulation and fibrinolysis in patients on different treatment regimens for prostatic cancer. Predictors for cardiovascular complications? 312 58

Both micro and macro-angiopathy involve interaction of blood vessel and plasma factors which may be altered in diabetes. Little is known concerning changes in contact and fibrinolysis factors as prekallikrein, plasminogen and fast antiplasmin in diabetes. We tested also the plasminogen/antiplasmin ratio in 151 diabetics and 64 normal subjects (18 to 74 years old). Our conclusion is:--the absence of correlation between the clinical characteristic of diabetes and prekallikrein level,--the decrease of plasminogen/antiplasmin ratio in complicated diabetes,--in complicated diabetes, correlation between antithrombin III, VIII factor and fibrinogen levels, perhaps, in relation with inflammation signs.
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PMID:[Contact (prekallikrein) and fibrinolytic (plasminogen/antiplasmin value) system in the physiopathology of vascular complications of diabetes]. 681 91

The effects of prostaglandins on the fibrinolytic activity of cultured human foreskin fibroblasts have been measured by a [125I]fibrin dish assay. Prostaglandin (PG) E1, added to fibroblasts in serum-containing medium, produced dose-dependent increases in the fibrinolytic activity of both cellular extracts and conditioned medium. PGE2 and PGI2, but not PGD2 or 6-keto-PGF1 alpha, also stimulated fibrinolytic activity. In each case, activity was due to the protease plasminogen activator because it was abolished by omitting plasminogen from the fibrinolytic assays. The effects of PGE1 were observed at 10 ng/ml and maximal stimulation occurred at 1 microgram/ml. Levels of both intra- and extracellular plasminogen activator increased, indicating that PGE1 stimulated the overall synthesis and release of the protease. The effects of PGE1 were slow in onset and persistent (greater than 48 hr) and were abolished by cycloheximide and actinomycin D. Cellular plasminogen activator was stimulated by 10 microM isoproterenol and 250 microM dibutyryl cyclic AMP; the effects of PGE1, isoproterenol and dibutyryl cyclic AMP were potentiated by the phosphodiesterase inhibitors 1-methyl-3-isobutylxanthine (100 microM) and dipyridamole (20 microM). The induction of plasminogen activator by PGE1 may therefore be initiated by stimulation of cellular adenylate cyclase. Increased fibrinolytic stimulation of cellular adenylate cyclase. Increased fibrinolytic activity could contribute to the prolonged beneficial effects which have been reported after the administration of PGE1 and PGI2 in the treatment of occlusive vascular disease.
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PMID:Stimulation of fibrinolytic activity in human skin fibroblasts by prostaglandins E1, E2 and I2. 705 Mar 42

We have studied the effects of amyloid beta-peptide analogues on the activity of tissue-type plasminogen activator (t-PA) in vitro. We have found that these peptides have a marked stimulatory effect upon plasminogen activation by t-PA, comparable to that of known stimulators of t-PA. This stimulatory activity appears to increase when beta-peptides form aggregated fibrillar structures similar to those found in amyloid deposits. This finding is significant in that it may provide insights into the pathogenesis of hereditary cerebral haemorrhage with amyloidosis-Dutch type (HCHWA-D) and cerebral amyloid angiopathy-related cerebral haemorrhage. It may also provide an explanation for the deaths resulting from intracerebral haemorrhage that have occurred in patients undergoing t-PA treatment for acute myocardial infarction.
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PMID:In vitro stimulation of tissue-type plasminogen activator by Alzheimer amyloid beta-peptide analogues. 758 10

The effect of a 17-kringle form of recombinant apo(a) [r-apo(a)] on in vitro fibrin clot lysis was studied. In these assays, fibrin clots were formed in the wells of microtiter plates, and lysis of the clots was monitored by measurement of the turbidity at 405 nm. The results indicate that r-apo(a) produces a dose-dependent antifibrinolytic effect in clots formed using either purified components or barium-adsorbed plasma. This effect was found to be independent of clot structure, since lysis of clots formed using both high and low concentrations of thrombin was prolonged by r-apo(a) to the same extent. The two components of the antifibrinolytic effect of r-apo(a) were determined to be (i) attenuation of tPA-mediated plasminogen activation (the major component) and (ii) inhibition of plasmin degradation of fibrin, although r-apo(a) did not directly attenuate plasmin activity, as measured by S-2251 hydrolysis. r-Apo(a) interfered most substantially with tPA-mediated activation of Glu-plasminogen and less substantially with tPA-mediated Lys-plasminogen activation and urokinase-mediated activation of plasminogen. In summary, we have demonstrated that apo(a) is able to attenuate fibrin clot lysis in vitro, primarily as a consequence of the interference by apo(a) with tPA-mediated Glu-plasminogen activation. These studies illuminate possible mechanisms by which Lp(a) may contribute to the development of vascular disease in vivo.
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PMID:Antifibrinolytic effect of recombinant apolipoprotein(a) in vitro is primarily due to attenuation of tPA-mediated Glu-plasminogen activation. 771 Oct 34

Plasminogen activator inhibitor-1 (PAI-1), specific inhibitor of plasminogen activators (PA), plays an important role in the regulation of fibrinolysis. Increased levels of PAI-1 have been associated with vascular disease such as thrombosis and atherosclerosis. In the present study the expression of PAI-1 mRNA in human healthy, atherosclerotic and thrombotic blood vessel walls was quantified by RNA-RNA hybridization in solution and localized by in situ hybridization. The mean expression of PAI-1 mRNA was significantly higher in healthy arteries (0.86 pg/microgram total RNA) than in healthy veins (0.29 pg/microgram total RNA), p < 0.01. The mean PAI-1 mRNA expression in thrombotic arteries (1.72 pg/micrograms total RNA) was significantly higher than that in healthy arteries, p < 0.05, and the mean PAI-1 mRNA expression in thrombotic veins (1.29 pg/micrograms total RNA) was significantly higher than that in healthy veins, p < 0.01. By in situ hybridization PAI-1 mRNA was detected in the intima, media and adventitia of healthy arteries and healthy veins. In atherosclerotic arteries PAI-1 mRNA was detected in the atherosclerotic plaque and in the medial and adventitial layers below the plaque. An increased expression of PAI-1 mRNA was found in the intimal layer of a thrombotic vein. The increased expression of PAI-1 mRNA in thrombotic arteries and veins indicates a role for PAI-1 in thrombogenesis.
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PMID:Expression of plasminogen activator inhibitor-1 mRNA in healthy, atherosclerotic and thrombotic human arteries and veins. 790 96

Lipoprotein Lp(a) is a pluri-molecular complex rich in cholesterol and composed of an LDL (low-density lipoprotein) particle to which is attached a large glycoprotein, apolipoprotein(a) (apo(a)). Numerous epidemiological studies have established a strong correlation between plasma levels of Lp(a) and the premature development of atheromatous vascular disease in man, an association which has subsequently been confirmed by the detection of Lp(a) in human atherosclerotic plaques. Furthermore, a marked structural resemblance has been demonstrated between apo(a) and plasminogen, a key protein of the fibrinolytic system and responsible for dissolution of blood clots. This discovery has provided evidence, for the first time, that Lp(a) might constitute an important link between atherosclerosis and thrombosis. Intense research effort is now underway to provide further understanding of (I) the structural organisation of the Lp(a) particle; (II) the molecular genetics of apo(a); (III) the processes involved in the synthesis, assembly intravascular metabolism and degradation of Lp(a) and apo(a); (IV) the nature of the interactions of Lp(a) and apo(a) with cellular and non-cellular components of the arterial wall; (V) the role of Lp(a) in fibrinolysis, and (VI) the relationship between Lp(a) and certain metabolic disorders such as familial hypercholesterolemia. These fascinating questions will be examined in the light of studies of different models of transgenic mce expressing human apo(a) alone, or both apo(a) and apo B100. In man, CETP assures the transfer of cholesteryl ester from high-density lipoproteins (HDL) to lipoproteins containing apo-B, and notably VLDL, IDL and LDL.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lipoprotein Lp(a) and CETP (cholesterol ester transfer protein): contribution of transgenic mice]. 807 82

Twenty obese subjects (Males = 8, Females = 12; average age = 39.5 +/- 2.5 years; B.M.I. = 36.2 +/- 2.5), 20 overweight subjects (Males = 8, Females = 12; average age = 38.5 +/- 2 years; B.M.I. = 28.8 +/- 0.4) and 20 non obese healthy subjects as controls, matched for sex and age (Males = 8, Females = 12; average age = 37.5 +/- 2 years; B.M.I. = 22.4 +/- 0.8) were selected. We determined: blood glucose, triglycerides, total cholesterol, HDL-cholesterol, Apolipoproteins A1 and B, Factor VII, fibrinogen and plasminogen. Before and after a venous occlusion test were also measured: t-PA Antigen, PAI activity and haematocrit. Metabolic, coagulative and fibrinolytic pathological changes were observed in overweight and obese subjects and the interaction of these risk factors may contribute to the pathogenesis of atherosclerosis vascular disease and to the high rate of thromboembolic events reported in obesity.
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PMID:Evaluation of cardiovascular risk factors in overweight and obese subjects. 807 94

Homocystinuria is a rare inherited metabolic disease. Arterial and venous thromboembolic events represent frequent and life-threatening complications in homocystinuric patients. It has been suggested that mild homocysteinemia could be a risk factor for vascular disease. We have therefore measured total plasma homocysteine (HCy) concentrations by radioisotopic assay in 50 subjects with venous or arterial thrombosis and studied the relationship between HCy, coagulation and fibrinolytic parameters. Values were considered abnormal if they were higher than 2.7 standard deviations (SD) above the mean, i.e., 14.1 mmol/l. Thus, eighteen of the 50 patients with thrombosis were classified in the hyperhomocysteinemia group. Nine of these subjects had only this isolated risk factor. No correlations were found between HCy and antithrombin III, protein C, protein S and plasminogen levels, or plasma plasminogen activator inhibitor activity. Nevertheless, the correlation between tissue-plasminogen activator antigen and total plasma HCy was significant (r = 0.61, p < 0.001). Increased homocysteinemia seems to be a risk factor for thrombotic events especially knowing that HCy presents a direct cytotoxic effect. Vitamin therapy, already used in homozygote homocystinuric patients, might be beneficial in the prevention of thromboembolic disease in heterozygous patients.
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PMID:Elevated total plasma homocysteine, a risk factor for thrombosis. Relation to coagulation and fibrinolytic parameters. 832 83

Diabetic patients have increased morbidity and mortality attributable to myocardial infarction, cerebrovascular disease and peripheral vascular disease, due to a high incidence of premature atherosclerosis. Abnormalities of hemostasis have been reported in many studies on diabetes over almost thirty years, but unfortunately the results have often appeared contradictory. The hemostatic alterations could lead to increased risk of vascular disease in diabetic patients. We have studied some coagulation factors (Fibrinogen, Factor II, Factor VII) and coagulation inhibitors (Protein C, Protein S), and plasminogen in fifty-four type 2 diabetic patients. The possible relationship between coagulation factors and coagulation inhibitors and parameters for glyco-metabolic control (glycosylated hemoglobin, fructosamine) and disturbed lipid metabolism (cholesterol, triglycerides) have ben analyzed. Our results show increase of fibrinogen, correlated with the metabolic control of the disease, positive correlation between plasminogen, factor II, protein S and hypertriglycerides, decreased levels of protein C correlated neither with metabolic control of disease neither with disturbed lipid metabolism.
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PMID:[Evaluation of the coagulation and fibrinolysis system in 54 patients with type 2 diabetes mellitus: correlations with lipid metabolism and blood glucose control]. 876 54


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