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)

Mice were implanted subcutaneously with a pellet containing 0.5 mg estradiol or with a placebo. Eight to 12 days later platelet aggregation was produced in pial arterioles by injuring their endothelium in vivo with a noxious light/dye stimulus. The time between the onset of the noxious stimulus and the appearance of platelet aggregates was significantly shortened (p less than .02) by estradiol treatment in young (2 month old) mice. The same treatment had the opposite effect in 4-6 month old mice and significantly delayed the onset of aggregation (p = .01). When platelet rich plasma (PRP) was prepared, aggregation by sodium arachidonate was always inhibited in PRP from estradiol treated mice, irrespective of age. Estradiol treatment had no effect on aggregation induced ex vivo by ADP. Thus the enhanced aggregation observed in pial arterioles of young estradiol treated mice may not reflect direct effects of estradiol on the platelet itself. The data are discussed in light of the literature suggesting enhancement of ischemic vascular disease, including strokes, in patients receiving estrogens, and especially high doses of estrogens.
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PMID:Effects of estradiol on platelet aggregation in cerebral microvessels of mice. 393 2

A study of platelet function and whole-blood viscosity in 11 patients with the confirmed diagnosis of psoriasis revealed a significant elevation in whole-blood viscosity (3.33 +/- 0.37 cP) as compared with that found in a control group (2.80 +/- 0.1 cP). The platelet count and platelet aggregation with ADP, epinephrine and collagen as well as platelet malonyldialdehyde were all within the normal range in all the patients. It is suggested that the increased blood viscosity may contribute to the higher incidence of occlusive vascular disease occurring in patients with psoriasis.
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PMID:Blood hyperviscosity in psoriasis. 616 94

A chemically stable carboprostacyclin analogue, ZK 36374 has been compared with two other prostacyclin derivatives with respect to ADP-induced in vitro aggregation of baboon and human platelets and ex vivo platelet aggregation in the baboon. ZK 36374 was also tested on the systemic arterial blood pressure of the baboon and against vasopressin-induced ECG changes in primates. Compared to the other two compounds, ZK 36374 displayed enhanced anti-platelet aggregating activity; there was dissociation between this property and its hypotensive potency. ZK 36374 antagonized the vasopressin-induced ECG changes. These results indicate that ZK 36374 possesses therapeutic potential in vascular disease including that affecting the coronary vessels.
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PMID:Inhibition of platelet aggregation and antagonism of vasopressin-induced ECG changes in primates by a carboprostacyclin analogue, ZK 36374. 620 Sep 48

To determine the effect of improved, short-term glycemic control on various functions of hemostasis in insulin-dependent diabetes, we measured changes in plasma fibrinogen, fibrinopeptide A (FPA), functional antithrombin III (AT-III), factor VIII:ristocetin cofactor ( VIIIRCoF ), beta-thromboglobulin (BTG), platelet factor 4 (PF4), and platelet aggregation responses to ADP and collagen in 12 patients with low or undetectable stimulated (postprandial) serum C-peptide levels during 4-8 wk (median, 6 wk) of treatment with constant subcutaneous insulin infusion. Mean plasma fibrinogen, FPA, AT-III, VIIIRCoF , and BTG at baseline were elevated compared with normal. Three patients had heightened platelet responses to ADP that did not correlate to other indicators of a hypercoagulable state; the affected patients, in fact, had significantly lower plasma BTG (25.5 +/- 5.3 [SEM] versus 44.6 +/- 4.6 ng/ml, P less than 0.05) and FPA (1.1 +/- 0.1 versus 2.5 +/- 0.5 ng/ml, P less than 0.05) than the remaining patients. Patients with clinically evident vascular disease had higher baseline plasma BTG and FPA than those without vascular disease (44.6 +/- 5.4 versus 30.2 +/- 4.6, and 2.6 +/- 0.6 versus 1.3 +/- 0.2 ng/ml, P less than 0.05, respectively). During treatment, all patients had declining blood glucose (200 +/- 18 to 102 +/- 5 mg/dl, P less than 0.001) and HbA1 (11.8 +/- 0.6 to 10.2 +/- 0.4%, P less than 0.005). No statistically significant changes in hemostatic functions were noted. During treatment, one patient had an acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma beta-thromboglobulin, platelet factor 4, fibrinopeptide A, and other hemostatic functions during improved, short-term glycemic control in diabetes mellitus. 620 89

Platelet aggregation was studied in 14 diabetic children with no signs of angiopathy and in 14 healthy matched control children. The magnitude of the platelet shape change after ADP stimulation was decreased in diabetic patients while the maximal aggregation after ADP and low dose collagen was significantly higher than in healthy control children. In 28 diabetic children the platelet shape change after ADP stimulation was positively correlated with the serum concentration of apolipoprotein A-I and negatively correlated with serum triglyceride concentration. The ratio between the fatty acids 20:3/20:4 in cholesterol esters was strongly correlated with the relative incidence of irreversible aggregation (p less than 0.001) and with the magnitude of the maximal aggregation (p less than 0.01) after ADP stimulation (3.3 mumol/l). The ratio between the polyunsaturated and saturated fatty acids in the triglyceride fraction was negatively correlated to the maximal aggregation after collagen stimulation (10 mg/l). This study shows tha platelet aggregation is increased early in the course of diabetes in childhood. It suggests that the abnormalities in platelet aggregation pattern in diabetic patients are related to several of the lipid factors associated with an increased risk of atherosclerosis.
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PMID:Increased platelet aggregability in diabetic children: relation to serum lipid and fatty acid composition. 665 42

The platelets of many patients with diabetes mellitus are abnormally sensitive to the effects of aggregatory agents in vitro. It has been proposed that this abnormal platelet function may play a role in the pathogenesis of vascular disease in diabetic subjects. We have investigated the effects of six weeks of treatment with the sulfonylurea agents gliclazide and glyburide on platelet aggregation in 10 noninsulin-dependent diabetic subjects. During treatment with diet alone, the platelets of these patients were abnormally sensitive to aggregation in response to 1 microM of adenosine diphosphate, as compared with those in normal controls. Treatment with both drugs normalized ADP-induced aggregation in these patients. Treatment with glyburide significantly reduced aggregation in response to 10 microM of epinephrine and collagen at 750 microgram/ml. The alteration in platelet function did not correlate with the improvement in plasma glucose concentration, thus suggesting that this may be an effect of the drug. Although one must be cautious in extrapolating these in vitro findings to the clinical situation, this alteration in platelet aggregatory function may be of importance in the prevention of vascular disease in diabetic subjects.
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PMID:Sulfonylureas and platelet function. 678 75

Platelet factor 4-like activity, circulating platelet-aggregate ratios, ristocetin cofactor, Willebrand antigen, ADP-induced platelet aggregation-enhancing factor, and quantitative platelet aggregation response to ADP, epinephrine, and collagen in platelet-rich plasma were measured in four groups of subjects with similar age and sex distribution. Neither platelet factor 4-like activity nor circulating platelet-aggregate ratios differentiated these four groups. Platelet aggregation studies with ADP a subthreshold concentration support the concept of hypersensitivity of diabetic platelets in males. Male and female subjects differ significantly in their quantitative response to aggregating agents when such studies are done under similar conditions. Willebrand factor activity and Willebrand antigen normally increase with age. Elevation in these activities above that accounted for by age characterizes the presence of vascular disease but not diabetes mellitus in the absence of vascular disease. A plasma factor enhancing platelet aggregation could not be demonstrated in most diabetic patients in this study.
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PMID:A prospective study of peripheral occlusive arterial disease in diabetes. IV. Platelet and plasma functions. 697 78

Plasma fron some diabetic patients, particularly those with advanced retinopathy and nephropathy, will potentiate ADP-induced platelet aggregation. Partial purification of plasma from a diabetic patient with nephropathy has yielded a fraction with this activity. A linea dose response curve relating plasma factor (6.25-50 ng protein) and platelet aggregation or ATP release at 4 minutes after adding ADP has been found. The effect is blocked by exposure of platelets to aspirin, prostaglandin or eicosapentaenoic acid. Soluble immune complexes are found in many diabetics and are known to be platelet-active. We have isolated immune complexes from sera of six diabetics and have shown enhancement of the second phase of platelet aggregation and of ATP release by these immune complexes from platelets sensitized to ADP. We conclude that plasma proteins from diabetics may accentuate ADP-induced platelet aggregation and ATP release, possibly by acting through prostaglandin pathways. Immune complexes appear to be one group of plasma proteins with such platelet active behavior. Further studies are indicated to characterize these plasma factors and to assess their in vivo significance regarding platelet function and vascular disease in diabetes mellitus.
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PMID:Plasma factors and platelet aggregation in diabetes mellitus. 697

The possibility of occurrence of daily variations in blood fibrinogen levels, platelets aggregation. Howell's time values and values for PTT, TT and antithrombin III was explored in 10 healthy subjects and in 10 patients with vascular disease. In normal subjects blood fibrinogen, platelets aggregation in ADP, PTT, Howell's time and TT values showed statistically significant daily variations, while the AT III values showed no significant variations over the 24-h cycle. In patients with vascular disease, on the other hand, the daily variations of the fibrinogen blood levels, of the maximum amplitude of platelets aggregation and of the Howell's values were not detected. In fact, the first two parameters remained consistently high and the third parameter remained consistently low throughout the 24-h cycle. In contrast, the PTT as well as the TT values in these patients showed statistically significant daily variations but with time patterns different than those found in normal subjects. Also, unlike to what obtained in healthy subjects, the AT III values in patients with vascular disease showed highly significant variations over the period of 24-h.
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PMID:Daily modifications of plasma fibrinogen platelets aggregation, Howell's time, PTT, TT, and antithrombin II in normal subjects and in patients with vascular disease. 711 42

The rarity of atherosclerotic vascular disease and a mild bruising tendency in Greenland Eskimos has been linked to their ingestion of omega 3 fatty acids contained in foods obtained from the sea. Previous studies have shown that feeding salmon oil to normal volunteers resulted in reductions of plasma cholesterol and triglycerides. We wished to learn whether salmon oil feeding would result in the incorporation of omega 3 fatty acids into platelets and whether platelet function or platelet-vessel interaction would be altered. Diets containing salmon oils led to the incorporation of eicosapentaenoic acid (C20:5 omega 3) into platelets (6.1%) with a reduction in arachidonic acid (C20:4 omega 6). The ratio of C20:5/C20:4 increased from 0.0045 on the control diet to 0.3 on the salmon diet. Bleeding times were prolonged (from 6.75 to 10 min, p less than 0.005), platelet retention on glass beads was mildly reduced (from 89% to 78%, p less than 0.0005), and platelet aggregation in response to dilute concentrations of ADP was inhibited in the subjects ingesting the salmon oil. We conclude that in normal subjects dietary omega 2 fatty acids derived from salmon oil are incorporated into platelet phospholipids and that these changes are accompanied by alterations in bleeding time and platelet function.
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PMID:The effects of dietary omega 3 fatty acids on platelet composition and function in man: a prospective, controlled study. 729 99


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