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PubMedDate not supplied

Studies on placental inhibition of platelet aggregation: a comparison of human syncytiotrophoblast brush border and basal plasma membranes.

We compared the platelet aggregation inhibiting activity of human placental syncytiotrophoblast brush border membrane vesicles (BBMV) and basal plasma membrane vesicles (BpMV), and obtained the following results. Strong platelet aggregation inhibiting activity is found in placental BBMV. BBMV inhibited platelet aggregation induced by ADP (adenosine diphosphate) and arachidonic acid in a way which depended on the protein concentration of BBMV added. In contrast, BpMV showed no detectable platelet aggregation inhibiting activity. Quite high ADP degrading activity (ADPase activity) was present in the placental BBMV. ADP was quickly degraded by BBMV. In contrast, BpMV did not degrade ADP so quickly. Platelet TXB2 production was almost completely abolished at the protein concentration of 40 micrograms/ml of BBMV. In contrast, BpMV did not significantly inhibit platelet TXA2 (TXB2) production. These results show that syncytiotrophoblast brush border and basal plasma membranes of the human placenta have markedly different properties with respect to platelet aggregation inhibiting activity.

Adenosine Diphosphate↗
PubMed1995

Factors that contribute to spontaneous platelet aggregation and streptokinase-induced aggregation in whole blood.

When whole blood is stirred there is a "spontaneous" platelet aggregation (SPA) which is presumed to be caused by proaggregatory factors released from platelets and other blood cells. Adding streptokinase (SK) to stirred whole blood frequently increases the rate and extent of the platelet aggregation that occurs; this is likely to be via immune complex formation between SK and natural anti-SK antibodies leading to increased release of pro-aggregatory factors. In this investigation we have examined the effects of several inhibitors and antagonists in an attempt to identify the proaggregatory factors that contribute to both SPA and SK-induced aggregation (SKA) and to evaluate different means of inhibiting both processes. The effects of the inhibitors/antagonists were determined in vitro after adding them to citrated whole blood obtained from healthy volunteers. Platelet aggregation was measured using a platelet counting technique. Inhibition of both SPA and SKA by apyrase and by FPL 66096 (a P2T receptor antagonist) demonstrated the involvement of ADP in both processes. Inhibition by chlorpromazine indicated that the most likely source of the ADP is red cells. The effects of sulotroban (a TXA2 antagonist) indicated involvement of TXA2 in SKA but not in SPA. The lack of effect of specific antagonists at S2, alpha 2 and PAF receptors suggested lack of involvement of serotonin, catecholamines and platelet-activating factor in either SPA or SKA. Both SPA and SKA were potently inhibited by low concentrations of iloprost (a PGI2 analogue), but a high concentration of SIN-1 (a NO donor) was much less effective.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMedDate not supplied

Platelet aggregability and the occurrence of anastomotic leakage after esophageal reconstruction.

In 21 patients who had undergone resection and reconstruction for esophageal carcinoma, the postoperative platelet aggregability was measured and the correlation between the occurrence of anastomotic leakage and platelet aggregability was investigated. There was no statistical difference in the clinical features of the patients between those with (n = 5) and without (n = 16) anastomotic leakage. Platelet aggregability was measured by the turbidimetric method from blood samples taken preoperatively, and at 1, 3, and 7 postoperative days (POD). The average values of platelet aggregability in patients without anastomotic leakage were 81.2, 70.4, 80.1, and 81.8%, while those with leakage were 81.3, 47.6, 52.3, 70.6% preoperatively, and 1, 3, and 7 POD, respectively. Thus, platelet aggregability significantly decreased in patients with anastomotic leakage on the first postoperative day (p < .05), and then gradually recovered postoperatively as time passed. Therefore, the measurement of platelet aggregability is considered to be one of the parameters predicting the occurrence of anastomotic leakage, and a prevention in the decrease of platelet aggregability as well as its activation could become a treatment for preventing anastomotic leakage.

Aged↗
PubMed1990

Long-range interactions in mammalian platelet aggregation. II. The role of platelet pseudopod number and length.

In part 1, we reported that human (H) platelets, activated with high concentrations (10 microM) of adenosine diphosphate, aggregate under Brownian diffusion (nonstirred, platelet-rich plasma) with an apparent efficiency of collision (alpha B) approximately 4 times and 8 times larger than observed, respectively, for canine (C) and rabbit (R) platelets. Further evaluations of parallel inhibition of alpha B and shape change suggested a central role for platelet pseudopods in mediating the long-range interactions associated with the elevated alpha B values. We found that greater than 90% of all platelet contacts in the doublets and triplets formed were via at least one pseudopod. We therefore compared pseudopod number and length per platelet generated by approximately 30 s post ADP activation in nonstirred PRP from human, canine, and rabbit donors, using phase-contrast, video-enhanced microscopy of fixed platelets. Theoretical calculations assessing the effects of pseudopod length and number on the collision frequency enhanced by an increased radius of a collision sphere supported the experimental observations that approximately 3 or 4 pseudopods per human or canine platelet, and approximately 5 or 6 pseudopods per rabbit platelet yield optimal alpha B values, with the average pseudopod length: approximately 3:2:1 for H/C/R, paralleling the alpha B differences. After correcting for effects of pseudopods and platelet size on platelet diffusion and sedimentation, it still appeared that the small number of long pseudopods formed on human platelets could largely explain the unusually large alpha B values. The quantitative discrepancies between theory and experiment do not appear related to time-dependent refractoriness within the less than 60 s of observation, but may be related to biochemical differences in dynamics and surface density of adhesive (sticky sites) present on the pseudopod surface.

Adenosine Diphosphate↗
PubMed1995

Sulphonylurea agents inhibit platelet aggregation and [Ca2+]i elevation induced by arachidonic acid.

The effects of three hypoglycaemic agents--glimepiride, glibenclamide and gliclazide--were evaluated on platelet aggregation and intracellular Ca2+ elevation induced by arachidonic acid. Platelet aggregation was assessed both by the conventional method using changes in light transmission and by a newly-developed procedure using light scattering which allows the detection of small as well as large aggregates. Glimepiride and glibenclamide inhibited the formation of small and large aggregates induced by optimal concentrations of arachidonic acid in a dose-dependent manner. The ID50 values for the inhibition of platelet aggregation were approximately one third of those for arachidonic acid metabolism, suggesting that both agents have certain direct inhibitory effects on platelet aggregation unrelated to arachidonic acid metabolism. Gliclazide inhibited the formation of small aggregates induced by low concentrations of arachidonic acid to a limited extent. However, it inhibited the formation of large aggregates but not small aggregates when higher concentrations of arachidonic acid were used. Glimepiride and glibenclamide inhibited [Ca2+]i elevation induced by arachidonic acid in a dose-dependent manner, whereas gliclazide had no inhibitory effect. Taken together, these suggest that gliclazide does not inhibit arachidonic acid metabolism but does have certain direct inhibitory effects on platelet aggregation.

Arachidonic Acid↗
PubMed1993

Platelet aggregation induced by the endoperoxide analogue U46619 is inhibited by polymorphonuclear leukocyte ADPase activity.

Platelet activation by the stable endoperoxide analogue U46619 is mediated largely by ADP released from platelet-dense granules. Polymorphonuclear leukocytes (PMNs) endowed with ecto-ADPase activity may operate as antiaggregatory cells in platelet aggregation induced by U46619. Unstimulated PMNs were effective in reducing aggregation when platelets were stimulated by threshold concentrations of U46619, whereas at higher concentrations of the stimulus, PMN activation is required. Evidence that the inhibition was mediated by PMN ecto-ADPase activity was obtained by high-performance liquid chromatography analysis, indicating that PMNs were able to efficiently metabolize platelet-active ADP into AMP. Moreover, PMN-derived supernatants were able to inhibit platelet aggregation, suggesting that under this circumstance the inhibition was exerted by an uncharacterized, releasable ADPase activity. This study supports the hypothesis that, besides nitric oxide and hydrogen peroxide, ADPase activity may represent another PMN-mediated pathway capable of regulating platelet activity in areas of reduced blood flow, such as those found in conditions of myocardial ischemia.

Adenosine Diphosphate↗
PubMed2000

Effect of iron therapy on the whole blood platelet aggregation in infants with iron deficiency anemia.

This study was performed to investigate the platelet aggregation alterations in whole blood samples of infants with iron deficiency anemia. Platelet aggregation induced by various concentrations of adenosine diphosphate (ADP) and collagen was studied with impedance aggregometry in 25 patients before and after oral iron therapy and in 12 children of the control group. The posttreatment mean maximum aggregation values were significantly higher (p<0.01) and the posttreatment mean aggregation times were significantly lower (p<0.01) in the study group at all concentrations of ADP and collagen. The aggregation time and maximum aggregation values revealed no significant difference except for the maximum aggregation value at 5 microM ADP (p<0.05) between the study group after therapy and the control group. The differences between the pretreatment and posttreatment mean platelet counts and mean platelet volume values in the study group were statistically significant (p<0.01), whereas those values in the study group after therapy and in the control group were not significantly different. We conclude that iron deficiency anemia in infants, even without clinically meaningful platelet abnormality, may cause dysfunction of the ex vivo whole blood platelet aggregation, and can be reversed by iron therapy. Further studies should be carried out at the enzymatic level to determine whether this platelet aggregation dysfunction in iron deficiency anemia is due to a deficiency in the activation of iron-containing enzymes.

Adenosine Diphosphate↗
PubMed2005

Inhibition and reversal of platelet aggregation by alphaIIbbeta3 antagonists depends on the anticoagulant and flow conditions: differential effects of Abciximab and Lamifiban.

Shear influences platelet aggregate formation and stability, as well as the inhibitory capacities of antithrombotic drugs. We compared the inhibitory and disaggregating properties of two distinct alphaIIbbeta3 antagonists, Abciximab and Lamifiban, on platelet aggregation induced by adenosine diphosphate (ADP) (5 micromol/l) in platelet-rich plasma (PRP), in an aggregometer (poorly defined low shear, <100/s) and in a microcouette at arterial shear rate (1,000/s). Platelet aggregation was detected by changes in light transmission in the aggregometer (TA), and by particle counting with a flow cytometer (PA). Lamifiban (1 mumol/l) completely inhibited TA or PA induced by ADP in citrated PRP in the aggregometer or microcouette. In contrast, Abciximab (2 micromol/l) only partially inhibited PA in the microcouette while blocking both TA and PA in the aggregometer. Moreover, Abciximab did not reverse platelet aggregates formed either in the microcouette or in the aggregometer, whereas Lamifiban caused complete reversal. On the contrary, Abciximab completely inhibited platelet aggregation induced by ADP in hirudin/d-Phe-Pro-Arg-chloromethylketone PRP in the microcouette. Our results demonstrate a marked dependence of inhibitory capacity of Abciximab on shear conditions, with citrate anticoagulant responsible for the residual aggregation, in contrast to Lamifiban, another alphaIIbbeta3 antagonist interacting with a distinct site on beta3.

Abciximab↗
PubMed1982

In vivo platelet aggregation and plasma catecholamines in acute myocardial infarction.

In vivo platelet aggregation assessed with the Filtragometer and potential correlates were compared among (1) patients with acute myocardial infarction (AMI), (2) normal controls, (3) patients with acute chest pain in whom AMI was eventually ruled out (ROMI), and (4) chronic outpatients (Cardiac Clinic group) with a history of myocardial infarction and/or angina pectoris. The measure was independent of sex, age, platelet count, immediate food intake, serum cholesterol, and triglyceride levels. The AMI group showed higher in vivo platelet aggregation than any of the other three groups (p less than 0.01). Least in vivo aggregation was seen in the normal group. Despite lack of correlation with the platelet aggregation measure, plasma epinephrine and norepinephrine showed statistically significant differences between the AMI and each of the other three groups. Our data support an association between platelet function and AMI, although not necessarily a cause and effect relationship.

Cholesterol↗
PubMed2004

The effect of dietary and plasma fatty acids on platelet aggregation in senior generation of Japanese women.

Dietary factors that influence platelet aggregation have not been fully clarified in humans. 63 Japanese women, aged 40-70 years old, completed one-day weighted dietary records, and received physical and laboratory examinations. Platelet aggregation was measured by 1.0 and 3.0 microM ADP induction. The results were analyzed with special reference to fatty acids. The short and medium chain fatty acid intake showed negative correlation with maximum percent of platelet aggregation induced by 1.0 microM ADP. Short and medium chain fatty acids in this study were mostly derived from milk and dairy products. Importance of short and medium chain fatty acid intake on platelet aggregation requires further study for prevention of cardiovascular diseases.

Adipose Tissue↗
PubMed1990

[Effects of the combination of aspirin and nifedipine on platelet aggregation and thrombogenesis].

The effects of nifedipine (Nif), aspirin (ASA) and ASA + Nif on platelet aggregation and generation of thrombosis were studied. Both ASA and Nif inhibited rabbit platelet aggregation in vitro and rat platelet aggregation in vivo induced by ADP, also prolonged the occlusion time of thrombosis induced electrically in the carotid artery of the rat and reduced the death rate resulting from pulmonary thrombosis induced by i.v collagen and epinephrine in mice. The above effects were markedly increased when Nif and ASA were used in combination. All the above effects were dose-dependent.

Animals↗
PubMed1996

Inverse relationships between haemoglobin and ristocetin-induced platelet aggregation in haemodialysis patients under erythropoietin therapy.

BACKGROUND: Amelioration of the anaemia of chronic renal failure and subsequent improved haemorheology result in correction of bleeding diathesis as evidenced by shortening of the skin bleeding time (BT). However, the relationship between the haematocrit and platelet-vessel wall interactions in haemodialysis (HD) patients under recombinant human erythropoietin (rHuEpo) therapy, assessed by platelet aggregation in response to ristocetin is more complex and somewhat inconsistent. METHODS: We investigated the relationship between haemoglobin (Hb) levels and whole blood ristocetin-induced platelet aggregation (electric impedance method) in 28 HD patients treated with rHuEpo, and with normal BT. The measurements were repeated in 16 subjects after having reduced platelet aggregability with orally administered ketanserin. RESULTS: Ristocetin-induced platelet aggregation in the whole group was comparable to those found in 21 age-matched healthy subjects (normals) and in 25 HD patients not treated with rHuEpo (uraemics). Interestingly, a significant inverse correlation between this aggregation and Hb concentration was found (r = -0.392, P < 0.05). In the group of 16 patients, the pre-ketanserin aggregation was more intensive than in the normals and uraemics (P < 0.05). Ketanserin produced a fall in ristocetin-induced platelet aggregation (P < 0.02), prolongation of the BT (P < 0.02) and, unexpectedly, a decrease in serum Epo concentration (P < 0.0002) and the Hb level (P < 0.001). Again, an inverse correlation between depressed ristocetin-induced platelet aggregation and lowered Hb concentration was found (r = -0.590, P < 0.02). Moreover, a strong positive correlation between the extent of preketanserin platelet aggregation and the decrease in the intensity of this process that followed the trial was observed (r = 0.919, P < 0.000005). There were no changes in other haematological parameters or arterial blood pressure. CONCLUSIONS: Considering the role of von Willebrand factor and fibrinogen in mediating ristocetin-induced platelet aggregation, and enhanced synthesis and/or release of these macromolecules in response to uraemia or inflammation, we suggest that exaggerated whole-blood platelet aggregability to ristocetin points to blunted erythropoiesis in HD patients on rHuEpo therapy.

Adult↗
PubMed1999

Different platelet aggregability during mental stress in two stages of essential hypertension.

To determine whether platelet response to mental stress is altered in essential hypertension, platelet aggregability and plasma beta-thromboglobulin were determined in 24 patients with essential hypertension (11 patients with World Health Organization (WHO) stage I and 13 patients with stage II) and 14 normotensive controls before and after a 10-min arithmetic stress (serial subtraction of 7 from 1000). In normotensive subjects, arithmetic stress did not affect primary aggregations to 1.0 micromol/L adenosine diphosphate (ADP) and to 2.5 micromol/L 5-hydroxytryptamine (5-HT), ADP threshold for biphasic aggregation and plasma beta-thromboglobulin level. In hypertensive patients with WHO stage I, these parameters were similar to those in normotensives before arithmetic stress, but the arithmetic stress test significantly increased primary aggregation to reagents and beta-thromboglobulin level, and decreased threshold of ADP for biphasic aggregation. In WHO stage II patients, platelet aggregability to reagents and beta-thromboglobulin level were already enhanced as compared with WHO stage I patients and normotensive subjects before arithmetic stress. However, the stress-induced changes in platelet function were less pronounced in WHO stage II patients compared with stage I patients. In conclusion, platelet aggregability and proaggregatory effect of mental stress differed depending on the severity of hypertension in patients with essential hypertension; the transient activation of platelet function during stress with no enhancement under the resting condition in the early phase of hypertension and the continuous activation of platelet function in the advanced phase with hypertensive organ damage.

Adenosine Diphosphate↗
PubMed1984

Effects of prostacyclin on tumor cell-induced platelet aggregation.

Prostacyclin has been evaluated for its ability to inhibit tumor cell-induced platelet aggregation (TCIPA) induced by several rodent tumor lines: B16a (melanoma); 3LL (carcinoma); 15091A (adenocarcinoma); and W256 (carcinosarcoma). Aggregation of human platelets by all four lines was inhibited by prostaglandin I2 (PGI2) in a dose-dependent manner, with complete inhibition observed at 10 ng/ml. However, higher PGI2 concentrations were required to inhibit aggregation of homologous rat platelets induced by W256 cells. Prostacyclin was compared to other icosanoids known to inhibit platelet aggregation and was found to be 100-fold more potent than either prostaglandin E1 or prostaglandin D2 and 1000-fold more potent than its stable nonenzymatic metabolite (6-ketoprostaglandin F1 alpha). Prostaglandin E2 in contrast to prostaglandin E1 and prostaglandin D2, did not inhibit TCIPA; however, both prostaglandin E2 and its enzymatic metabolite (13,14-dihydro-15-ketoprostaglandin E2) prevented PGI2 inhibition of TCIPA. The addition of prostaglandin I2 (100 ng/ml) after initiation of TCIPA (50% of maximum response) resulted in immediate arrest of TCIPA followed by reversal of platelet aggregation. Prostacyclin partially reversed platelet aggregation when added at 100% of maximum response. Platelets enhanced the adhesion of [125I]uridine-labeled W256 cells to plastic culture dishes under both aggregatory and nonaggregatory conditions. Prostacyclin in vitro inhibited platelet-facilitated tumor cell adhesion. These in vitro results demonstrated that PGI2 is a potent inhibitor of TCIPA and of tumor cell adhesion; we suggest that these are possible mechanisms to explain the antimetastatic effects of PGI2 in vivo [Honn, K. V., Cicone, B., and Skoff, A. Science (Wash. D.C.), 212: 1270-1272, 1981].

Animals↗
PubMed1983

In vitro effects of mercury on platelet aggregation, thromboxane and vascular prostacyclin production.

Mercuric chloride [25-50 micrograms/ml platelet-rich plasma (PRP)] lowers the threshold concentration of arachidonic acid (AA) required for triggering rabbit platelet aggregation and causes a marked increase of thromboxane production. The metal, added as HgCl2, does not modify (50 micrograms/ml PRP) or block (100 micrograms/ml PRP) the platelet aggregation wave induced by a normal aggregating dose of AA. Whether or not AA-induced platelet aggregation takes place, a large increase in thromboxane production is observed. Methyl mercury, assayed as reference drug, induces platelet aggregation and a significant increase of thromboxane levels. Finally, HgCl2 and methyl mercury, in a concentration range of 0.125-0.5 micrograms/microliters in the incubation liquid, induce an increased prostacyclin release from rat aortic tissue.

Animals↗
PubMed1994

Inhibitory effect of tetrahydroberberine on platelet aggregation and thrombosis.

Tetrahydroberberine (THB), an alkaloid extracted from Corydalis ambigua, inhibited the rabbit platelet aggregation triggered by arachidonic acid (AA), ADP, and collagen with IC50 of 0.86, 1.31, and 1.10 mmol.L-1, respectively. THB reduced the thromboxane B2 (TXB2) generation in rabbit platelet-rich plasma triggered by AA. THB 30 mg.kg-1.d-1 ip for 3 or 5 d restrained the ADP-induced platelet aggregation in rats. THB 30 mg.kg-1.d-1 ip for 1, 3, or 5 d inhibited the AA-induced platelet aggregation in rats. THB 15-30 mg.kg-1 iv showed an inhibition of venous thrombosis in rats. The results show that THB is a potent inhibitor of platelet aggregation in vitro and in vivo and is a promising antithrombotic drug.

Adenosine Diphosphate↗
PubMed1990

The role of fibronectin in platelet aggregation.

A monoclonal antibody (anti-Fn2) was prepared which was reactive with both plasma fibronectin and fibronectin located within the platelet alpha granule. Immunoblotting analysis, on thermolysin digestion fragments of fibronectin, identified two immunoreactive fragments of Mr 145 kDa and 155 kDa which are known to contain a cell and DNA binding region. Anti-Fn2 was found to inhibit binding of fibronectin to platelets and DNA. Functional platelet studies, measuring platelet aggregation and 14C-serotonin release in washed platelet systems, demonstrated the ability of anti-Fn2 to totally inhibit low dose thrombin and low-dose collagen induced platelet aggregation and serotonin release. Anti-Fn2 partially inhibited platelet aggregation induced by ADP (10 microM) and arachidonic acid, but had no effect on platelet aggregation induced by high-dose thrombin or by the calcium ionophore A23187. These studies indicate that fibronectin participates in platelet aggregation and release induced by a range of agonists and suggest that it has a more important involvement in platelet function than previously described.

Antibodies, Monoclonal↗
PubMed2000

[Platelet aggregation in patients with hypertrophic cardiomyopathy].

AIM: To examine correlation between platelet aggregation and the degree of left ventricular hypertrophy (LVH) in patients with hypertrophic cardiomyopathy (HC). MATERIAL AND METHODS: Routine clinical examination, ECG, echo-CG, measurement of platelet aggregation, routine biochemical blood tests were made in 45 HC males and 15 healthy controls. RESULTS: HC patients were characterized with high induced and spontaneous platelet aggregation which increased with left ventricular myocardial mass. In LVH, platelets were especially sensitive to the aggregation inductor U-46619, thromboxane A2 analogue. CONCLUSION: It is demonstrated that there is a positive correlation between platelet aggregation and the degree of LVH in HC patients.

Cardiomyopathy, Hypertrophic↗