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PubMed2002

The effect of type II diabetes mellitus on platelet aggregation in patients who underwent percutaneous transluminal coronary angioplasty.

BACKGROUND: In noninsulin-dependent type II diabetic (tIIDM) patients it was reported that ADP-induced platelet aggregation response was increased with decreased level of platelet guanylate cyclase. This study was therefore designed to examine the effects of tIIDM on collagen-induced, in-vitro platelet aggregation in percutaneous transluminal coronary angioplasty (PTCA) patients. METHODS: Twenty patients with tIIDM and 30 nondiabetic patients who had successful PTCA were included in the study. Platelet-rich plasma samples from the patients before and after PTCA were treated with in-vitro collagen and platelet aggregation waves were calculated via the turbidometric method of Born. The maximum amplitude (%) and the ratio of changes after PTCA in the study participants were measured by these waves and data were compared by student's t tests and nonparametric methods. The maximum amplitude of collagen-induced platelet aggregation before and after the procedure was also compared using variant analysis. RESULTS: The change in collagen-induced maximum amplitude of platelet aggregation in both wave 1 and wave 2 was significantly more (P < 0.001- P < 0.001) in the tIIDM group. The ratio of restenosis seen in the control coronary angiography made 6 months after intervention was found to be significantly more in the tIIDM group (P < 0.05). CONCLUSIONS: Collagen-induced platelet aggregation response was greater in patients with tIIDM than in nondiabetic patients. This makes us think that tIIDM patients could need more potent antiplatelet therapy before PTCA after the blood glucose levels have been regulated.

Adult↗
PubMed1990

Histamine release by platelet aggregation.

Coincubation of rat serosal mast cells with human platelets leads to a significant release of histamine. which dose-dependently increases when platelet aggregation is induced by various concentrations of arachidonic acid. In turn, histamine enhances platelet aggregation induced by different agonists, this effect being mimicked by pyridyl-ethyl-amine (PEA), blocked by mepyramine and amplified by ranitidine. The data suggest the existence of a platelet-derived histamine releasing factor (PDHRF) and indicate the presence of platelet H1 and H2 receptors, capable of modulating platelet aggregation.

Animals↗
PubMed1984

Platelet aggregation, beta-thromboglobulin and platelet factor 4 in diabetes mellitus and in patients with vasculopathy.

We have studied 155 subjects, 48 normals, 36 diabetics without complications, 44 with complications and 27 patients with macroangiopathy. beta-Thromboglobulin (beta-TG) and platelet factor 4 (PF4) are elevated in the patients groups. There is no correlation between the plasma levels of beta-TG and the stages of either retinopathy or macroangiopathy or nephropathy. The difference is more marked between normals and diabetics with neuropathy (p = 0.026). The aggregation response to ADP and platelet activating factor (PAF) is enhanced at lower stimulator concentration. Using the beta-TG, PF4 and aggregation values the discriminant analysis allows a distinction of several subgroups especially with nephropathy and neuropathy (Table 6).

Blood Platelets↗
PubMed2003

Effect of glycoprotein IIb/IIIa antagonist abciximab on monocyte-platelet aggregates and tissue factor expression.

OBJECTIVE: Activated platelets rapidly adhere to monocytes and upregulate the expression of tissue factor (TF), the major trigger of the coagulation cascade. In this study, we examined the effect of abciximab, a nonselective glycoprotein IIb/IIIa-receptor antagonist, on monocyte TF expression in thrombin receptor activator-stimulated whole blood in vitro. METHODS AND RESULTS: Abciximab (50 microg/mL) reduced the mass of platelets attached to monocytes, measured by the mean fluorescence intensity (MFI) of CD42b on CD14+ cells, 1 (CD42b, 471+/-197 versus 1073+/-217 MFI, mean+/-SD, P<0.05), 5, and 10 minutes after thrombin receptor activator stimulation of whole blood to the same extent as anti-P-selectin (50 microg/mL; 288+/-177 MFI, P<0.05) when determined by flow cytometry. In parallel, the expression of the platelet activation marker P-selectin colocalized with CD14+ monocytes was reduced up to 25% by abciximab at the same time points. Expression of monocyte TF antigen (CD14+/TF+, 39.9+/-8.7% versus 66.3+/-19.9%, P<0.05), chromogenic TF-activity (TF, 8.4+/-1.9 versus 13.2+/-2.8 U, arbitrary units, P<0.05), and TF mRNA was suppressed in the presence of abciximab as a consequence of reduced platelet mass attached to monocytes. CONCLUSIONS: Our data suggest that heterotypic monocyte-platelet aggregates are a target for abciximab, which suppresses monocyte TF because of a reduction of monocyte-platelet cross talk.

Abciximab↗
PubMed1987

Effect of vitamin E and ticlopidine on platelet aggregation in Fabry's disease.

Thromboembolism, increased platelet aggregation and high plasma concentration of beta-thromboglobulin were observed frequently in hemizygotes and heterozygotes of Fabry's disease. The administration of vitamin E and ticlopidine could improve the increased platelet aggregation in this disease. The platelet activation, probably induced by vascular endothelial damages, would accelerate atherosclerotic and thromboembolic vascular changes. Antiplatelet therapy will be effective for the prevention of these vascular complications in this disease.

Adolescent↗
PubMed1989

Differential effects of low-dose tissue plasminogen activator and streptokinase on platelet aggregation.

Despite increasing success with low-dose intra-arterial thrombolysis, early rethrombosis still occurs. Platelet aggregation is thought to play a major part in this process. We have therefore investigated the effects of recombinant tissue plasminogen activator (rt-PA) and streptokinase on platelet function at doses currently used for peripheral arterial thrombolysis. Platelet-rich plasma was stirred at 37 degrees C, with either streptokinase (100, 300 or 1000 units ml-1) or rt-PA (10 (T10), 30 (T30) and 100 (T100) mg l-1), with immediate addition of an agonist for platelet aggregation (thrombin, collagen, adenosine diphosphate (ADP) or adrenaline) at a predetermined threshold dose. Significant inhibition of collagen-induced and adrenaline-induced platelet aggregation was produced with rt-PA at all doses used (P less than 0.05). With adrenaline as the agonist, T100 produced disaggregation to a mean (s.d.) level of 26 per cent. Thrombin-stimulated platelet aggregation was significantly reduced by T100 (P less than 0.001) and T30 (P less than 0.01) only, disaggregation being dose-dependent and complete with T100. Using ADP as the agonist, T100 produced a significant reduction in maximum platelet aggregation (P less than 0.01), and disaggregation was achieved to a mean (s.d.) level of 48(13) per cent. Streptokinase did not produce any significant changes in any parameter of aggregation.

Adenosine Diphosphate↗
PubMed1994

Daily variations of platelet aggregation in relation to blood and plasma serotonin in diabetes.

The circadian rhythms of platelet aggregation in the whole blood and platelet rich plasma-PRP and plasma serotonin were studied in healthy volunteers (n = 10) and diabetic patients (type II diabetes mellitus n = 12). Platelet aggregation in the whole blood induced by collagen (2 micrograms/ml), ADP (10 microM), arachidonic acid (0.5 mM) and epinephrine (10 microM), and in PRP induced by collagen (2 micrograms/ml), ADP (5 microM), arachidonic acid (250 microM), epinephrine (10 microM) and serotonin-5-HT (1 microM) was measured at 7:30, 11:30, 17:00, 23:00, 4:00 and 7:00. In healthy subjects collagen- and ADP-induced platelet aggregation in the whole blood was significantly lower at 23:00 and 4:00 when compared to values at 7:30. In PRP normal and diabetic platelet response was the lowest during the night. Diabetic platelets exhibited an enhanced response to 5-HT starting from 17:00 until 4:00 when compared to 7:30. 5-HT-induced platelet aggregation was found to be significantly higher throughout the study in DM patients over controls in parallel to plasma 5-HT. In healthy volunteers plasma 5-HT was higher at 17:00 when compared to baseline values, whereas in DM patients plasma 5-HT was elevated starting from 17:00 until 4:00. An enhanced response of diabetic platelets to 5-HT together with elevated plasma 5-HT levels may contribute, at least partly, to the pathogenesis of diabetic vasculopathy and 5HT2 receptor blockers may be of value in DM patients.

Adenosine Diphosphate↗
PubMed1989

The existence of a platelet-activating factor (Paf-acether)-like substance in blister fluid derived from patients with bullous pemphigoid as demonstrated by human platelet aggregation techniques.

We investigated the presence of a platelet-activating factor-like substance in blister fluid obtained from patients with bullous pemphigoid. Human platelet aggregation activity was present in blister fluids obtained from 4 out of 6 patients with bullous pemphigoid and in blister fluids obtained from 3 cases with contact dermatitis. Platelet aggregation activity of pemphigoid blister fluids was inhibited by pretreatment with lyso-PAF, which is a precursor metabolite of platelet activating factor. The activity of blister fluids obtained from patients suffering from contact dermatitis was not inhibited by precursor. Blister fluid obtained from burn lesions and blisters of normal skin induced in the suction revealed no platelet aggregation activity. These results suggest that platelet-activating factor or a similar substance is present in the blister fluid obtained from suffered bullous pemphigoid.

Adult↗
PubMed2003

Plasma thioredoxin levels and platelet aggregability in patients with acute myocardial infarction.

BACKGROUND: Oxidative stress is thought to play an important role in atherosclerotic vascular disease. Recently, it has become possible to quantitatively measure thioredoxin, a marker of oxidative stress in human plasma. A platelet aggregometer that uses laser-light scattering enables minimal changes in platelet aggregability to be monitored; however, the relationship between oxidative stress and platelet aggregability in vivo is not well understood. METHODS: We investigated plasma thioredoxin levels and platelet aggregability, in particular small platelet aggregates, in 45 patients with acute myocardial infarction (AMI); we compared the results with 33 patients with stable exertional angina (SEA) and 30 patients with chest pain syndrome (CPS). RESULTS: The plasma thioredoxin levels and the degree of small platelet aggregates were higher in the AMI group than in the SEA and the CPS groups: in the AMI group, at 4 weeks after admission, both of those parameters were significantly decreased (P <.01), but they were still higher (P <.05) than in the SEA or the CPS group. There was a significant positive correlation between small platelet aggregates and plasma thioredoxin levels (rho = 0.354, P =.0002). We divided the AMI patients into 2 groups according to the 75 percentile of plasma thioredoxin levels on admission. At the chronic phase, the left ventricular ejection fraction was significantly higher in the lower thioredoxin group than in the higher thioredoxin group. CONCLUSIONS: We showed that plasma thioredoxin levels and platelet aggregability increased concomitantly in patients with AMI. In these patients, increased plasma thioredoxin was associated with platelet hyperaggregability and lower left ventricular ejection fraction.

Adult↗
PubMed1997

Platelet aggregation and neutrophil sequestration in the mesenteric circulation in inflammatory bowel disease.

BACKGROUND AND OBJECTIVES: Mesenteric microvascular thrombosis may be an early pathogenic event in Crohn's disease (CD), and intravascular platelet aggregates have been identified in mucosal biopsies in ulcerative colitis (UC). Activated platelets are involved in thrombogenesis and exhibit inflammatory properties. In active inflammatory bowel disease (IBD) increased numbers of platelet aggregates are detectable in the peripheral circulation. The aim of this study was to test the hypothesis that in IBD, platelet aggregation is triggered in the mesenteric vasculature. PATIENTS AND METHODS: Platelet numbers, platelet aggregate ratios and differential leucocyte counts were compared in mesenteric arterial and venous blood obtained from paired vessels at the time of intestinal resection from 13 patients with inflammatory bowel disease and, as controls, 6 patients with colonic carcinoma or diverticular disease. RESULTS: In UC and CD, but not in controls, fewer neutrophils were found in blood draining the intestine compared with that supplying it (arteriovenous gradient median 1.0 x 10(9)/l (interquartile range 0.2-1.3) for UC, P < 0.05; 0.8 (0.2-1.5) for CD, P < 0.02; 0.4 (-0.3-1.1) for controls, P = NS). In CD, increased numbers of circulating platelet aggregates were identified in venous samples (platelet aggregate ratio 0.83 (0.71-0.93)) than in paired arterial samples (0.99 (0.95-1.01), P < 0.02) and control venous samples (0.99 (0.93-0.97), P < 0.05). The mesenteric arteriovenous gradient for neutrophils in IBD reflects their migration into the extravascular tissue and lumen of the inflamed intestine. Increased circulating platelet aggregates in the mesenteric venous circulation support the hypothesis that platelet activity is stimulated in the mesenteric microcirculation in CD.

Adult↗
PubMed2001

Pathogenetic analysis of three cases with a bleeding disorder characterized by defective platelet aggregation induced by Ca2+ ionophores.

We report three cases of platelet dysfunction characterized by defective Ca2+ ionophore-induced platelet aggregation without impaired production of thromboxane A2 (TXA2). The patients had mild to moderate bleeding tendencies, and their platelet aggregation and secretion induced by ADP, collagen, arachidonic acid, stable TXA2 (STA2) and Ca2+ ionophore A23187 was defective or much reduced. However, ristocetin- or thrombin-induced platelet aggregation was normal. The analysis of second messenger formation showed that inositol 1,4,5-triphosphate formation or Ca2+ mobilization induced by thrombin, STA2 or A23187 was normal. Furthermore, the phosphorylation of 47 kDa protein (pleckstrin) and 20 kDa protein (myosin light chain, MLC) in response to those agonists was normal. These findings suggest that the defective site in the patients' platelets lies in the process distal to or independent of protein kinase C activation, Ca2+ mobilization and MLC phosphorylation.

Adenosine Diphosphate↗
PubMed2002

Modulation of platelet aggregation by areca nut and betel leaf ingredients: roles of reactive oxygen species and cyclooxygenase.

There are 2 to 6 billion betel quid (BQ) chewers in the world. Areca nut (AN), a BQ component, modulates arachidonic acid (AA) metabolism, which is crucial for platelet function. AN extract (1 and 2 mg/ml) stimulated rabbit platelet aggregation, with induction of thromboxane B2 (TXB2) production. Contrastingly, Piper betle leaf (PBL) extract inhibited AA-, collagen-, and U46619-induced platelet aggregation, and TXB2 and prostaglandin-D2 (PGD2) production. PBL extract also inhibited platelet TXB2 and PGD2 production triggered by thrombin, platelet activating factor (PAF), and adenosine diphosphate (ADP), whereas little effect on platelet aggregation was noted. Moreover, PBL is a scavenger of O2(*-) and *OH, and inhibits xanthine oxidase activity and the (*)OH-induced PUC18 DNA breaks. Deferoxamine, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) and neomycin prevented AN-induced platelet aggregation and TXB2 production. Indomethacin, genistein, and PBL extract inhibited only TXB2 production, but not platelet aggregation. Catalase, superoxide dismutase, and dimethylthiourea (DMT) showed little effect on AN-induced platelet aggregation, whereas catalase and DMT inhibited the AN-induced TXB2 production. These results suggest that AN-induced platelet aggregation is associated with iron-mediated reactive oxygen species production, calcium mobilization, phospholipase C activation, and TXB2 production. PBL inhibited platelet aggregation via both its antioxidative effects and effects on TXB2 and PGD2 production. Effects of AN and PBL on platelet aggregation and AA metabolism is crucial for platelet activation in the oral mucosa and cardiovascular system in BQ chewers.

Animals↗
PubMed1993

Platelet aggregation inhibiting and anticoagulant effects of oligoamines, XXII: Bisoxazol-, bisimidazol-, bisthiazol- and oligo-1,2,4-thiadiazolimines.

One mesoionic 4,4'-propylene-bis-oxazol-5-imine (5), two 2,2'-m-phenylene-bis-imidazol-4-imines (9a,b), five 4,4'-benzene-bis-(and tris)-thiazol-2-amines (13a,b, 14a-c) and 14 3,3'-benzene-bis-(and tris)-1,2,4-thiadiazolimines (18a-o) were synthesized and assayed for their antiplatelet and anticoagulant activities. The most potent compound was the tris-thiadiazole derivative 18m which inhibited the aggregation of platelets induced by collagen at a concentration of 10 mumol/L by 50 percent (Born-test). No anticoagulant effects (Quick-test) were observed up to 400 mumol/L. In the thiazolamine series combined antiplatelet and anticoagulant activities were seen.

Anticoagulants↗
PubMed1985

The platelet reactivity of the alpha 2(I)-chain of type I collagen: platelet aggregation induced by polymers of the molecule [alpha 2(I)]3.

Polymers of the collagenous species alpha 2(I) trimer, a molecule of which contains three alpha 2(I) chains derived from type I collagen, have been shown to induce the aggregation of platelets when tested at a temperature low enough to avoid loss of the tertiary structure of the molecule. Under these conditions, the alpha 2(I) chain appears to possess greater platelet reactivity than the corresponding type I collagen-derived alpha 1(I) chain. In contrast to previous reports of its lack of reactivity, our results indicate that the alpha 2(I) chain must contribute importantly to the overall platelet reactivity of collagen type I in vivo. Our findings furthermore support the concept that any collagen-like structure may be expected to interact with platelets provided due regard is given to tertiary and quaternary structural requirements.

Animals↗