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PubMed1997

Inhaled nitric oxide inhibits platelet aggregation after pulmonary embolism in pigs.

BACKGROUND: Inhaled nitric oxide (NO) is reported to prolong bleeding time in animals and humans and to inhibit platelet aggregation in persons with acute respiratory distress syndrome. In pulmonary embolism (PE), inhibition of platelet aggregation appears useful because further thrombus formation may lead to right ventricular dysfunction that results in circulatory failure. In the present study, the effect of inhaled NO on platelet aggregation after acute massive PE was investigated. METHODS: After acute massive PE was induced in 25 anesthetized pigs by injecting microspheres, 5, 20, 40, and 80 parts per million inhaled NO were administered stepwise for 10 min each in 11 animals (NO group). In the control group (n = 14). NO was not administered. Adenosine diphosphate-induced initial and maximal platelet aggregation were measured before PE (10), immediately after induction of PE (PE), at the end of each 10-min NO inhalation interval (t10-t40), and 15 min after cessation of NO inhalation (t55) in the NO group, and at corresponding times in the control group, respectively. RESULTS: Two animals in the control group and one in the NO group died within 10 min after PE induction and were excluded from analysis. Peaking at t40 and t55, respectively, initial (-13 +/- 6%; P < 0.05) and maximal (+44 +/- 17%; P < 0.05) platelet aggregation increased significantly after PE in the control group. In contrast, NO administration after PE led to a significant decrease in initial (maximum decrease, -9 +/- 3% at t40; P < 0.05) and maximal (maximum decrease, -15 +/- 7% at t30; P < 0.05) platelet aggregation. In the NO group, platelet aggregation had returned to baseline levels again at t55. In addition, NO administration significantly decreased mean pulmonary artery pressure and significantly increased end-tidal carbon dioxide concentration and mean systemic blood pressure. CONCLUSIONS: Inhaled NO has a systemic and rapidly reversible inhibitory effect on platelet aggregation after acute massive PE in pigs. This may be beneficial in treating acute massive PE.

Administration, Inhalation↗
PubMed2006

The effects of estrone, estradiol and estriol on platelet aggregation induced by adrenaline and adenosine diphosphate.

The impact of estrogens on the cardiovascular system and their ability to regulate platelet functions remains controversial. Changes in platelet functions could contribute to thrombotic risk associated with estrogen treatments. Here, we investigated the effects of various forms of estrogen, including estrone (E1), estradiol (E2) and estriol (E3), on platelet aggregation induced by standard agonists (adrenaline and adenosine diphosphate). Platelet-rich plasma (PRP) was prepared from citrated blood donated by 25 normal volunteers. The study on platelet aggregation was carried out in 96-well flat-bottom microtitre plates and assessed using a microplate reader. For studying the effects of each estrogen, PRP was preincubated with 1, 10 and 100 nM of E1, E2 and E3 at 37 degrees C for 20 min, and then coincubated with normal saline (control untreated PRP), adrenaline (ADR) or adenosine diphosphate (ADP) in the microplate. Platelet aggregation was then measured every minute for 8 min. None of the estrogens (E1, E2 and E3) affected platelet aggregation in untreated PRP. Interestingly, only E1 and E3 can synergize the increased platelet aggregation by either ADR or ADP, while the effects of E2 on the increased platelet aggregation by either ADR or ADP depended on internal factors such as endogenous estradiol and platelet aggregated state. Thus, for the rational use of these internal factors for estrogen use, especially E2, in clinical applications, such as hormone replacement therapy, may need evaluation of thrombotic risk.

Adenosine Diphosphate↗
PubMed1989

Platelet aggregation inhibitory effects of the new positive inotropic agents pimobendan and UD CG 212 in whole blood.

A method is described for studying platelet function in human whole blood immediately after venepuncture in order to evaluate the antithrombotic potential of new pharmacological agents. In this method, platelet aggregation is quantified by measuring the fall in single platelet count, by using a whole blood platelet counter. We have investigated the platelet aggregation inhibitory effects of the new positive inotropic agents pimobendan and UD CG 212 (reported to be Ca++ sensitisers and phosphodiesterase inhibitors), alone and in combination with dipyridamole. Venous blood was drawn directly into prewarmed (37 degrees C) plastic syringes containing anticoagulants (3.2% trisodium citrate solution) plus a platelet aggregation inhibitor. Spontaneous platelet aggregation (SPA) was studied by roller mixing aliquots of blood in the collecting syringes for 6 min at 37 degrees C. Collagen induced platelet aggregation was studied by incubating aliquots of blood with 1 microgram/ml collagen on a shaking water bath for 3 min. In the absence of an inhibitor, there was a 50% fall in single platelet count due to SPA and a 65% fall was induced by collagen. Both SPA and collagen induced aggregation responses were inhibited by pimobendan (0.5-10 microM) and UD CG 212 (0.5-10 microM), in a dose dependent manner. A combination of 10 microM dipyridamole with 2 microM pimobendan or UD CG 212 was markedly a more effective inhibitor of platelet aggregation than a high dose of either inhibitor alone. It is suggested that the present method is simple and rapid, with minimal sample processing, and therefore the results may be protected from serious artifacts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Effects of dienogest (a synthetic steroid) on coagulation, fibrinolysis, and platelet aggregation in female monkeys.

We investigated the effects of dienogest (0.1-10 mg/kg per day, p.o.) on coagulation, fibrinolysis and platelet aggregation in female rhesus monkeys. Then, we also examined those of medroxyprogesterone acetate (MPA, 10 mg/kg per day, p.o.) or danazol (10-1000 mg/kg per day, p.o.) on these parameters in the same species. In addition, we assessed the effects of dienogest (1 and 3 mg/kg per day, p.o.) or MPA (10 mg/kg per day, p.o.) on platelet aggregation and platelet lipids in female cynomolgus monkeys. At doses of 0.3 mg/kg or greater, dienogest increased the levels of several coagulation and anticoagulation factors, but had no effect on the prothrombin time, activated partial thromboplastin time, fibrinolysis, or platelet aggregation. MPA (10 mg/kg) had no effect on coagulation or fibrinolysis, but significantly potentiated platelet aggregation in response to ADP and collagen and also increased the platelet cholesterol-to-phospholipid ratio. Danazol (10 mg/kg or more) increased the activities of coagulation factors V, VII, VIII, X, XI, and XII in comparison to dienogest and MPA. Consequently, dienogest caused less potentiation of platelet aggregation than MPA and less potentiation of coagulation than danazol.

Animals↗
PubMed1990

[Effect of cefaclor on guinea pig platelet aggregation in vitro].

Effects of cefaclor (3-chloro-7-D-(2-phenyl-glycinamido)-3-cephem-4-carboxylic acid) on PAF, ADP, collagen, endotoxin, and thrombin-induced platelet aggregation were examined in vitro with the use of guinea pig platelet-rich plasma and washed platelets. PAF, even at concentrations lower than its minimum effective concentration, enhanced ADP- or endotoxin-induced platelet aggregation and prolonged the time to attain the maximum aggregation. PAF also enhanced collagen-induced platelet aggregation and shortened the lag time. Cefaclor (CCL) inhibited the PAF, ADP or thrombin induced platelet aggregation and shortened their maximum aggregation times at higher concentrations such as 300 micrograms/ml or more. CCL also inhibited the collagen-induced platelet aggregation and prolonged the lag time, but showed no effect on endotoxin-induced platelet aggregation. The effect of CCL was almost the same as that of latamoxef (LMOX). CCL and LMOX, however, showed no effect on cellular Ca2+ increase produced by PAF, ADP, or thrombin, suggesting that the inhibitory effect of CCL and LMOX on platelet aggregation is caused by the inhibition of fibrinogen binding to the glycoprotein IIb/IIIa complex.

Adenosine Diphosphate↗
PubMed1985

Platelet aggregating factor in the epidemic form of hemolytic-uremic syndrome in childhood.

Plasma from six out of eleven children with the epidemic forms of hemolytic-uremic syndrome caused the aggregation of homologous platelets as has been described in thrombotic thrombocytopenic purpura. IgG purified from normal adults inhibited the platelet aggregation induced by plasma collected from three children during the acute phase of the disease. This inhibition by IgG may contribute to the reported successful management by infusions of plasma or plasma exchanges.

Blood Coagulation Factors↗
PubMed1996

Sevoflurane inhibits human platelet aggregation and thromboxane A2 formation, possibly by suppression of cyclooxygenase activity.

BACKGROUND: Halothane increases bleeding time and suppresses platelet aggregation in vivo and in vitro. A previous study by the authors suggests that halothane inhibits platelet aggregation by reducing thromboxane (TX) A2 receptor-binding affinity. However, no studies of the effects of sevoflurane on platelet aggregation have been published. METHODS: The effects of sevoflurane, halothane, and isoflurane were examined at doses of 0.13-1.4 mM. Human platelet aggregation was induced by adenosine diphosphate, epinephrine, arachidonic acid, prostaglandin G2, and a TXA2 agonist ([+]-9, 11-epithia-11, 12-methano-TXA2, STA2) and measured by aggregometry. Platelet TXB2 levels were measured by radioimmunoassay, and the ligand-binding characteristics of the TXA2 receptors were examined by Scatchard analysis using a [3H]-labeled TXA2 receptor antagonist (5Z-7-(3-endo-([ring-4-[3H] phenyl) sulphonylamino-[2.2.1.] bicyclohept-2-exo-yl) heptenoic acid, [3H]S145). RESULTS: Isoflurane (0.28-0.84 mM) did not significantly affect platelet aggregation induced by adenosine diphosphate and epinephrine. Sevoflurane (0.13-0.91 mM) and halothane (0.49-1.25 mM) inhibited secondary platelet aggregation induced by adenosine diphosphate (1-10 microM) and epinephrine (1-10 microM) without altering primary aggregation. Sevoflurane (0.13 mM) also inhibited arachidonic acid-induced aggregation, but not that induced by prostaglandin G2 or STA2, although halothane (0.49 mM) inhibited the latter. Sevoflurane (3 mM) did not affect the binding of [3H]S145 to platelets, whereas halothane (3.3 mM) suppressed it strongly. Sevoflurane (0.26 mM) and halothane (0.98 mM) strongly suppressed TXB2 formation by arachidonic acid-stimulated platelets. CONCLUSIONS: The findings that sevoflurane suppressed the effects of arachidonic acid, but not those of prostaglandin G2 and STA2, suggest strongly that sevoflurane inhibited TXA2 formation by suppressing cyclooxygenase activity. Halothane appeared to suppress both TXA2 formation and binding to its receptors. Sevoflurane has strong antiaggregatory effects at subanesthetic concentrations (greater than 0.13 mM; i.e., approximately 0.5 vol/%), whereas halothane has similar effects at somewhat greater anesthetic concentrations (0.49 mM; i.e., approximately 0.54 vol/%). Isoflurane at clinical concentration (0.84 mM; i.e., approximately 1.82 vol/%) does not affect platelet aggregation significantly.

Adenosine Diphosphate↗
PubMed2002

[Effects of Angelica polysaccharide on blood coagulation and platelet aggregation].

OBJECTIVE: To investigate the effects of angelica polysaccharide (AP) on blood coagulation and platelet aggregation. METHODS: Infrared turbidimetric method was used to estimate platelet aggregation, active partial thromboplastin time (APTT), prothrombin time (PT) and thrombin time (TT); bleeding time (BT) was measured by cutting the mouse's tail and coagulate time (CT) was measured by dropping the blood on carry sheet glass. RESULTS: AP prominently enhanced the platelet aggregation at 5 min, while showed less effects on the maximum platelet aggregation. It also markedly prolonged CT but shortened BT. AP significantly prolonged TT and APTT in dosage of 3 mg/kg and 10 mg/kg, while showed no obvious effect on PT. CONCLUSION: These results suggest that AP has potent anticoagulant and haemostasis effects. The haemostasis effect is related to promoting platelet aggregation.

Angelica sinensis↗
PubMed1986

Rat platelet aggregation: strain and stock variations.

Platelet aggregation induced by ADP, arachidonic acid, and collagen was monitored in rats from two stocks, WSU-SD and CD, and from three strains, Lewis, Holtzman, and NBR. ADP-induced aggregation did not vary between the WSU-SD, CD, Lewis, Holtzman, and NBR rats. In contrast, the response to AA and collagen depended upon the stock or strain of rat. Platelets from the Holtzman and especially the NBR were much more sensitive to AA than were those from the other strains. At 0.25 mM AA, 7 of 8 NBR rats and 5 of 8 Holtzman rats aggregated irreversibly, while only 1 in 8 WSU-SD, CD, and Lewis rats aggregated irreversibly at that concentration. Collagen-induced aggregation reflected that to AA. The possible relationship between the variation in platelet aggregation and sympathoadrenal activity is discussed.

Adenosine Diphosphate↗
PubMed2002

Effects of oxytocin and prostaglandin F(2alpha) (enzaprost) on platelet aggregation.

The effects of uterotonic agents (oxytocin and enzaprost) on platelet aggregation in pregnant and nonpregnant women were studied by low-angle light scattering. In nonpregnant women oxytocin produced different effects on ADP-induced platelet aggregation: potentiation at low (<200 nM) and inhibition at high (>400 nM) ADP concentrations. In pregnant women oxytocin did not modulate ADP-induced platelet aggregation or this effect was negligible. Enzaprost competitively inhibited ADP-induced platelet aggregation in all examined women (inhibition constant 84.8+/-25.7 nM).

Adenosine Diphosphate↗
PubMed1991

[The role of vitamin E during pregnancy--anti-platelet aggregation activity of alpha-tocopherol].

To clarify the role of vitamin E (alpha-tocopherol) during pregnancy, we mainly investigated the relation between platelet function and vitamin E and obtained the following results. 1. The concentration of vitamin E (alpha-tocopherol) in plasma and platelet increased gradually during pregnancy. The concentration of vitamin E in plasma was 6.65 micrograms/ml in non pregnant women and 15.5 micrograms/ml in full term pregnant women. And the concentration of vitamin E in platelet was 99 micrograms/g protein in non pregnant women and 244 micrograms/g protein in full term pregnant women. 2. Vitamin E (alpha-tocopherol) inhibited platelet aggregation induced by ADP (adenosine diphosphate) and PAF(platelet activating factor). At a concentration of 500 micrograms/ml vitamin E almost completely inhibited platelet aggregation induced by ADP and PAF. 3. There exists a strong platelet aggregation inhibiting activity in human placental brush border membrane vesicles. At a protein concentration of 20 micrograms/ml the brush border membrane vesicles almost completely inhibited platelet aggregation induced by ADP and PAF. 4. With the co-existence of the brush border membrane vesicles, the platelet aggregation inhibiting activity of vitamin E (alpha-tocopherol) increased prominently. These results indicate that vitamin E plays an important role in the regulation of platelet function and might contribute to the maintenance of placental microcirculation by inhibiting platelet aggregation.

Adenosine Diphosphate↗
PubMed1981

Effects of platelet inhibitors on the platelet aggregation induced by plasma from patients with thrombotic thrombocytopenic purpura.

Antiplatelet drugs have been used in the treatment of thrombotic thrombocytopenic purpura (TTP) but there in vivo efficacy remains controversial. It has been shown that, in vitro, the plasmas obtained from patients with TTP induced the aggregation of washed platelets from normal donors as well as patients in remission. The effects of platelet inhibitors on the TTP plasma-induced platelet aggregation were examined. It was found that aspirin, indomethacin, ibuprofen, sulfinpyrazone, 5, 8, 11, 14-eisacotetraynoic acid, prostaglandin E1, prostaglandin I2, dBcAMP, apyrase, creatine phosphate/creatine phosphokinase, antimycin, 2-deoxy-D-glucose, dipyridamole, clofibrate, dextran 40, dextran 70, dibucaine, xylocaine, methylmaleimide, and ethylenediamine tetraacetic acid had little or no effect at all. These data lead us to conclude that at least in certain cases, antiplatelet drugs probably play a limited role in the treatment of patients with TTP.

Adenosine Diphosphate↗
PubMed2005

No effect of taurine on platelet aggregation in men with a predisposition to type 2 diabetes mellitus.

Any diet therapy that potentially could affect platelet function would also influence the initiation of atherosclerotic plaque formation which is an important complication of diabetes mellitus eventually resulting in myocardial infarction and stroke. Blood platelets are rich in taurine, and it has been shown that taurine inhibits platelet aggregation in healthy subjects. The purpose was to examine the effect of taurine supplementation on platelet aggregation in high-risk subjects with a positive family history of T2DM. Twenty healthy men were included in a double-blinded, randomized, crossover study, receiving daily supplementation of 1.5 g taurine or placebo for two 8-week periods. Subjects were overweight and first-degree relatives of T2DM patients. At the end of each treatment, fasting blood samples for assessment of platelet aggregation was drawn. Platelet aggregation was induced by ADP. Plasma taurine concentration was significantly greater after taurine intervention compared to placebo (131.4+/-61.7 vs. 38.9+/-6.7 micromol/l, P<0.0001). There was no difference in the threshold level for complete platelet aggregation induced by ADP in vivo between placebo and taurine intervention (placebo 3.86+/-2.21 vs. taurine 3.86+/-3.25 micromol/l). Supplementation with 1.5 g of taurine for 8 weeks had no effect on platelet aggregation in overweight prediabetic men.

Adenosine Diphosphate↗
PubMed2006

PAR4, but not PAR1, signals human platelet aggregation via Ca2+ mobilization and synergistic P2Y12 receptor activation.

Regulation of platelet activation plays a central role in hemostasis and pathophysiological processes such as coronary artery disease. Thrombin is the most potent activator of platelets. Human platelets express two thrombin receptors, PAR1 and PAR4, both of which signal platelet activation. Evidence is lacking on the mechanism by which PAR1 and PAR4 may differentially signal platelet aggregation. Here we show that at the relatively high concentration of agonist most likely found at the site of a local thrombus, dual inhibition of the P2Y12 receptor and calcium mobilization result in a complete inhibition of PAR4-induced aggregation, while having no effect on either thrombin or PAR1-mediated platelet aggregation. Both PAR1- and PAR4mediated aggregation are independent of calcium mobilization. Furthermore, we show that P2Y12 receptor activation is not required for protease-activated receptor-mediated aggregation at higher agonist concentrations and is only partially required for Rap1 as well as GPIIbIIIa activation. P2Y12 receptor inhibitors clinically in use such as clopidogrel are postulated to decrease platelet aggregation through partial inhibition of PAR1 signaling. Our data, however, indicate that at high local concentrations of thrombin, it is the signaling through PAR4 rather than PAR1 that may be regulated through purinergic feedback. Thus, our data identify an intra-platelet mechanism that may function as a future site for therapeutic intervention.

Adenosine Diphosphate↗
PubMed1989

Relative effects of flurbiprofen on platelet 12-hydroxy-eicosatetraenoic acid and thromboxane A2 production: influence on collagen-induced platelet aggregation and adhesion.

Flurbiprofen has been shown to inhibit cyclo-oxygenase metabolism of arachidonic acid to thromboxane A2 (TxA2), resulting in the inhibition of platelet aggregation. Recently, our laboratory reported that the "irreversible" phase of platelet aggregation and adhesion were regulated, in part, by the lipoxygenase metabolism of arachidonic acid to 12-hydroxy-eicosatetraenoic acid (12-HETE) in platelets, and that selective inhibition of one enzyme i.e. either cyclo-oxygenase or lipoxygenase, resulted in paradoxical effects on the metabolism of arachidonic acid and platelet response related to the other pathway. Therefore, we performed experiments to assess the relative effects of flurbiprofen on TxA2 and 12-HETE synthesis, and on collagen-induced platelet aggregation and platelet adhesion to collagen-coated surfaces. "Irreversible" collagen-induced platelet aggregation was only partially inhibited by pre-incubation with 1 x 10(-6) M flurbiprofen, while TxA2 production was elevated and 12-HETE production was maximally inhibited in these platelets. At this concentration of flurbiprofen (1 x 10(-6)M), collagen-induced platelet adhesion was also reduced by 50%. At higher concentrations of flurbiprofen, both platelet aggregation and adhesion were further reduced, with a corresponding inhibition of TxA2 production. Thus it appears that the lipoxygenase pathway of arachidonic acid metabolism in platelets is not only inhibited by flurbiprofen, but is more sensitive to inhibition by flurbiprofen than the cyclo-oxygenase pathway. This differential effect of flurbiprofen on arachidonic acid metabolism in the platelet is related to differential effects on platelet function.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1981

Partial purification and studies of the plasma co-factor that potentiates platelet aggregation in diabetes mellitus.

A co-factor is present in the plasma of some diabetics that potentiates the degree of in vitro aggregation of normal platelets after ADP stimulus. This paper presents important changes in the analysis technique that utilize recently appreciated knowledge about platelet aggregation and that were needed to permit characterization of the co-factor. By this new technique, the plasma co-factor activity of 33 normal adults and 43 normal children was significantly lower (p less than 0.001) than that of the corresponding diabetic groups. Thirty-two percent of the adult and 23% of the child diabetics had an elevated plasma co-factor activity. None of the 71 diabetic children and only 12 of the 65 diabetic adults had severe retinopathy. These results correlate well with previous reports wherein the plasma co-factor activity was highest in patients who had severe retinopathy or nephropathy and was usually normal when microangiopathy was not evident. The co-factor was completely precipitated from the plasma of a diabetic with ammonium sulfate at the concentration of 34% of saturation. An aqueous solution of this precipitate retained co-factor activity during incubation at 56 degrees for 30 min but lost activity at neutral pH conditions. Co-factor activity eluted during gel filtration to indicate an estimated molecular weight of 21,000 daltons. The improved technique reported here should facilitate study of the platelet hyperaggregation co-factor and the pathophysiology of diabetic microangiopathy.

Adolescent↗
PubMed1981

Platelet aggregation in the cerebral and mesenteric microcirculation of mice with genetically determined diabetes.

Platelet aggregates were induced in pial arterioles of the following strains of mice with a genetic predisposition for diabetes: ob/ob and db+/db+. Aggregation was compared with that in 6J+/+ mice, the nondiabetic controls for ob/ob animals, and in +m/+m as well as db+/+m, the nondiabetic controls for db+/db+ mice. Aggregation was also induced within mesenteric arterioles of db+/db+ animals and compared with that in db+/+m mice. Aggregation was monitored microscopically, by measuring the time required for a noxious stimulus to initiate aggregation in an injured arteriole. Platelet aggregation was initiated with equal ease in the pial arterioles of ob/ob mice and their 6J+/+ controls. However, the onset of aggregation in the pial arterioles of the db+/db+ group was significantly delayed when compared with the onset in either of the nondiabetic control groups, +m/+m or db+/+m. A similar prolongation in the time required to produce aggregation was also observed in the mesenteric arterioles of the db+/db+ mice when compared with db+/+m controls. The basis for reduced platelet aggregation in the microcirculation of db+/db+ mice is not explained. The results differ from those showing enhanced aggregation in many in vitro studies of platelets from human diabetics and from those of in vivo studies of two other animal models described in the literature. However, not all published studies have reported enhanced aggregation. The delayed aggregation in the present study may provide a basis for analysis of factors that regulate platelet aggregation in diabetes.

Animals↗
PubMed1996

Platelet aggregation is inhibited by phycolectins.

Lectins from four marine algal species were examined for interaction with human platelets. The lectin designated hypnin A, from the red alga Hypnea japonica, inhibited adenosine diphosphate (ADP)- or collagen-induced human platelet aggregation in a dose-dependent manner. Complete inhibition was observed at concentrations of 100 and 5 micrograms/ml of the lectin with ADP (2 microM) and collagen (0.2 microgram/ml)-induced platelet aggregation, respectively. At the inhibitory concentration of 0.5 to 100 micrograms/ml, the lectin did not induce aggregation of resting platelets. Lectins from the other three algal species also inhibited ADP-induced human platelet aggregation. These results indicate that the algal lectins are a new group of inhibitors and may be useful to study glycoconjugates on platelet membranes and to design novel platelet aggregation inhibitors.

Adenosine Diphosphate↗