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PubMed1985

Inhibition of platelet aggregation by ketamine hydrochloride.

Ketamine hydrochloride, 10 mg/kg by intramuscular injection, inhibited aggregation of platelets from three out of three baboons. Aggregation to ADP, arachidonic acid, epinephrine, and collagen was inhibited but aggregation to ristocetin was normal. Two baboons anaesthetised with the related drug phencyclidine, 1.0 mg/kg intramuscularly, had delayed aggregation. Ketamine inhibition of human platelets was irreversible in that aggregation could not be restored by either gel filtration of inhibited platelets and the re-addition of normal plasma, or by increasing the concentrations of agonists. Mixtures of human ketamine inhibited and aspirinised platelets failed to aggregated. Thromboxane B2 production was reduced to 3% of the amount produced by non inhibited platelets but the oxygen burst was not inhibited.

Adenosine Diphosphate↗
PubMed1987

Tumor-cell-induced platelet aggregation is a glycoprotein-dependent and lipoxygenase-associated process.

To characterize the platelet receptor sites and the platelet metabolic pathways involved in tumor-cell-induced platelet aggregation, we have used a homologous system consisting of human platelets and 2 tumor cell lines of human origin, which activate platelets through different mechanisms. Preincubation of platelets with an MAb against platelet glycoprotein Ib partially blocked tumor-cell-induced platelet aggregation, and preincubation of platelets with an MAb against the glycoprotein complex GPIIb/IIIa totally blocked the aggregation induced by the 2 tumor-cell lines. No inhibitory effect was found when platelets were treated with PAF-receptor antagonists or with specific peptides which block the platelet sites involved in bacterially induced platelet aggregation. Compounds which raised intra-platelet cAMP levels inhibited tumor-cell-induced platelet aggregation in a dose-related manner. Inhibition of cyclo-oxygenase by aspirin which blocked TxB2 formation by platelets did not inhibit platelet aggregation induced by tumor cells whereas the BW755 compound which inhibits cyclo- and lipoxygenase blocked platelet aggregation. These results demonstrate that tumor-cell-induced platelet aggregation is a glycoprotein-dependent and a lipoxygenase-associated phenomenon.

Aspirin↗
PubMed1991

The effect of agonists and antagonists of platelet aggregation on von Willebrand factor-mediated platelet agglutination.

Ristocetin-induced platelet agglutination (RIPA) in EDTA-treated citrated platelet-rich plasma was reduced to 49 +/- 11% by 1.25 microM ADP, 41 +/- 14% by 1 microM A23187, and 26 +/- 7% by 0.1 microgram/ml platelet activating factor (PAF). The effect of 5-110 microM epinephrine was not dose-dependent, but varied between donors, with RIPA from 56-100% of the control. The inhibitory effects of these agonists were not altered by prior treatment of platelets with aspirin. Prior addition of 200 microM ATP (an ADP receptor antagonist acting at both high and low affinity ADP receptors) prevented the inhibitory action of ADP but not that of A23187 or PAF, suggesting that the inhibitory actions of the latter are not mediated by released ADP. As 700 microM 8-bromoadenosine 5-diphosphate (an ADP receptor antagonist acting mainly at the high affinity receptor) did not prevent ADP-induced inhibition of RIPA, interaction of ADP with the low affinity receptor is presumably responsible for its inhibitory action. As A23187, but not phorbol myristate acetate (0.1 microM) inhibited RIPA, an increase in intracellular calcium ions rather than direct stimulation of protein kinase C appears to mediate agonist-induced inhibition. Cytochalasin B (10.5-21 microM), dibucaine (0.5-1 mM), and prostaglandin E1 (25 nM), added before or after the agonist, prevented or reversed ADP-, A23187-, and PAF-induced inhibition of RIPA, suggesting that the state of the platelet cytoskeleton affects inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed2005

Use of native or platelet count adjusted platelet rich plasma for platelet aggregation measurements.

BACKGROUND: It is still not clear whether native or platelet count adjusted platelet rich plasma (PRP) should be used for platelet aggregation measurements. AIM: To evaluate the necessity of using adjusted PRP in platelet function testing. METHODS: Platelet aggregation with native PRP and adjusted PRP (platelet count: 250/nl, obtained by diluting native PRP with platelet poor plasma) was performed on the Behring Coagulation Timer (BCT(R)) using ADP, collagen, and arachidonic acid as agonists. Healthy subjects, patients on antiplatelet treatment, and patients with thrombocytosis (platelet counts in PRP > 1250/nl) were investigated. RESULTS: No significant differences in the maximum aggregation response were seen when using either native or adjusted PRP from healthy subjects and patients on antiplatelet treatment. Nevertheless, some patients taking aspirin or clopidogrel showed reduced inhibition of ADP and arachidonic acid induced aggregation in adjusted PRP but not in native PRP. The maximum velocity of healthy subjects and patients on antiplatelet treatment varied significantly as a result of the degree of dilution of the adjusted PRP. Surprisingly, the BCT provided good results when measuring platelet aggregation of native PRP from patients with thrombocytosis, whereas commonly used aggregometers could not analyse platelet aggregation of native PRP in these patients. CONCLUSION: The time consuming process of PRP adjustment may not be necessary for platelet aggregation measurements. Moreover, using adjusted PRP for monitoring aspirin or clopidogrel treatment may falsify results. Therefore, it may be better to use native PRP for platelet aggregation measurements, even in patients with thrombocytosis.

Adult↗
PubMed1995

The influence of time of storage, temperature of storage, platelet number in platelet-rich plasma, packed cell, mean platelet volume, hemoglobin concentration, age, and sex on platelet aggregation test.

The influences of time of storage of platelet-rich plasma (PRP), temperature of storage of PRP, platelet number in PRP, mean platelet volume in whole blood, sex, age, hemoglobin concentration, and different forms of PRP storage on platelet aggregation (PAG) tests, performed with epinephrine, collagen, arachidonate, and ristocetin by a four-channel aggregation profiler (Platelet Aggregation Profiler, Model PAP-4, Bio/Data Corporation, Hatboro, PA 19040, U.S.A.), were evaluated in four groups of subjects (52 men, 22 women, age range 20-85 years, hemoglobin concentration range 8.4-16.8 g/dl). The PRP was stored with or without packed cells, at room temperature or at 4 degrees C, for 0-6 h. The ideal platelet number of PRP for performing the PAG test fell between 150 and 500 x 10(9)/l. If the number was less than 150 x 10(9)/l, the result of PAG should be meaningless. No significant change was noted for up to 6 h when the PRP was stored either at room temperature or at 4 degrees C. Hemoglobin concentration and mean platelet volume did not affect the PAG. However, there was significant but weak correlation (p = 0.0125, r = 0.3696) between age and PAG when using arachidonic acid as the agonist. Men had significantly increased PAG when collagen and ristocetin were used as the agonists. The PRP was stored best at room temperature, without packed cells. In conclusion, to obtain the best result from a PAG test, the PRP should be kept without packed cells at room temperature for no longer than 6 h, and the platelet number should fall between 150 and 500 x 10(9)/l.

Adolescent↗
PubMedDate not supplied

Serotonin induced platelet aggregation in systemic sclerosis.

We studied in vitro platelet aggregation response to serotonin in 19 patients with systemic sclerosis and 18 matched controls. Individuals with early systemic sclerosis had increased % platelet aggregation at 3 minutes over a wide range of serotonin concentrations when compared to individuals with late systemic sclerosis. Patients with generalized disease did not differ from those with limited disease. No significant differences in initial slope of platelet aggregation were detected in any patient subgroup. These data support previous studies suggesting platelet activation in systemic sclerosis and further suggest that future studies of platelet abnormalities in systemic sclerosis should consider the effects of disease duration.

Adult↗
PubMed1984

The effect of pyridoxal-5-phosphate on the inhibition of platelet aggregation and adenosine-3'-5'-cyclic monophosphate accumulation in human platelets.

Platelet adenosine-3'-5'-cyclic monophosphate (c-AMP) was determined in platelet rich plasma and washed platelets by a modification of the c-AMP protein binding assay. Studies were performed in the presence and absence of platelet aggregation inducers (adenosine diphosphate and thrombin) and inhibitors (pyridoxal-5-phosphate (PALP), prostaglandin E1 (PGE1), theophylline and papaverine). At 70% inhibitory concentration of platelet aggregation (PA) induced by papaverine or theophylline, a small but significant increase in platelet c-AMP level was found. With PALP however the inhibition of PA was not associated with a significant increase in the c-AMP level. PALP or theophylline potentiated greatly both the inhibition of PA and c-AMP accumulation induced by PGE1. Yet PALP potentiated the inhibition of PA induced by theophylline without increasing platelet c-AMP level. Our results indicate that the inhibition of PA by PALP is not mediated by c-AMP accumulation. However in the presence of PGE1, the increment in PA inhibition, is mediated by further indirect activation of the adenyl-cyclase.

Alprostadil↗
PubMed2003

Follow-up of hemorheological parameters and platelet aggregation in patients with acute coronary syndromes.

Pathologic hemorheological parameters and increased platelet aggregation in association with other risk factors significantly increase the possibility of the development of myocardial ischemia. Hemorheological parameters and platelet aggregation were investigated in 157 patients (mean age: 65+/-12 years) with acute coronary syndromes and in 68 healthy subjects (mean age: 36+/-6 years). Plasma fibrinogen, plasma and whole blood viscosity, red blood cell aggregation and filterability and platelet aggregation were measured in the hospital phase (after admission, on 2nd and 6th days) and monitored after discharge (at 1, 6 and 12 months). After admission all these parameters were significantly higher in patients than in control subjects (p<0.01) and almost all of them remained in the pathologic range at discharge. Some of the rheologic parameters showed a slight improvement after 1 month, but hematocrit and whole blood viscosity were higher than those after admission and of control subjects (p<0.05). After 6 and 12 months these parameters showed a small, but significant increase. Pathologically altered hemorheological parameters could be observed in patients with classical cardiovascular risk factors and significant improvement was found after elimination of them. Antiplatelet therapy was efficient in about half of the treated patients after admission; and despite a significant improvement, the proportion of ineffectively treated patients was still considerable during the follow-up. Our results support the role of abnormal hemorheological parameters in the development of myocardial ischemia and draw attention to the rheologic risk of these patients. The results of platelet aggregation measurements show the insufficiency of antiplatelet therapy at some cases and confirm the importance of guided secondary prevention.

Acute Disease↗
PubMed1966

Effect of normal and atheromatous aortic tissue on platelet aggregation in vitro.

An investigation was made into the platelet-aggregating ability of human aortic tissue. It was found that potent aggregating substances are present in the vascular wall but that the degree and character of platelet aggregation produced was dependent on the method employed in the preparation of the tissue for study. The supernatants of aortic tissue homogenates were found to produce potent irreversible platelet aggregation that occurred after a latent period of one to two minutes. The activity was heat labile, destroyed by collagenase, sedimented by ultracentrifugation, and was considered to be identical or similar to collagen. An extract obtained by boiling aortic tissue with saline was found to cause less powerful reversible platelet aggregation that occurred within 15 to 30 seconds' contact with platelets; the activity was not affected by heating, incubation with collagenase, or ultracentrifugation, and was considered to be due to adenosine diphosphate. Atheromatous aortic tissue when extracted by either method was found to contain less than one half of the potency of normal tissue in causing platelet aggregation.

Aorta↗
PubMed1991

Comparison of in vitro platelet aggregation and its inhibition by three antithrombotic drugs between human and guinea pig.

Platelets of guinea pigs are frequently used to evaluate the effect of new antiplatelet agents. Although several studies have compared the platelet aggregation between humans and guinea pigs, but so far the information is still limited. In this study, we compare the inhibitory effect of aspirin, dipyridamole and pentoxifylline on the platelet aggregation induced by adenosine diphosphate (ADP), collagen, arachidonic acid and thrombin between humans and guinea pigs. The results for humans and guinea pigs were compared and analysed by two-way analysis of variance (ANOVA). Our results showed: 1. The trends wherein these three drugs suppressed collagen-induced platelet aggregation was very similar in humans and guinea pigs. 2. In ADP-induced aggregation, the trend of inhibition caused by the three drugs was also similar in humans and guinea pigs except that a difference in platelet disaggregation at a late phase of platelet aggregation was noted. 3. In arachidonic acid- and thrombin-induced aggregations, the trend of inhibition caused by the three drugs was somewhat different in humans and guinea pigs. 4. Considering all activators as a whole, it was found that the status of platelet disaggregation at the late phase of platelet aggregation was different in humans and guinea pigs. Therefore, we concluded that: 1. Collagen was the most appropriate platelet activator when we used platelets of guinea pigs to study the effect of new antiplatelet agents. 2. When platelets of guinea pigs were used to study platelet aggregation, no matter which activator was used, we should avoid using the late phase of aggregation as the control index for comparison, because the results thus obtained might not be applicable to human platelets.

Adenosine Diphosphate↗
PubMed1975

Increased platelet aggregation in early diabetus mellitus.

In view of the tendency toward vascular disease in diabetes mellitus, we studied platelet aggregation in 15 normal, 7 prediabetic, 12 latent, and 20 frankly diabetic subjects. Platelets from latent and frank diabetics showed increased platelet aggregation 4 minutes after adding adenosine 5'-diphosphate (60% verus 29% at 1.0 mu-M), epinephrine (46% versus 14% at 0.25 mu-M), and collagen (72% versus 17% at 0.25 mu-g/ml). Three prediabetics had increased platelet aggregation. Platelet sensitivity to aggregating agents was most marked in frank diabetics, intermediate in latent diabetics, and least in prediabetics. Second-phase platelet aggregation was reversed with acetylsalicylic acid, intravenous tolbutamide, and oral glucose administration. We conclude that platelet aggregation may be increased early in diabetes mellitus and may be involved in the genesis of diabetic microangiopathy. Prospective studies on the effect of therapeutic agents such as acetylsalicylic acid on the natural course of diabetic vascular disease are indicated.

Adenosine Diphosphate↗
PubMed1978

Prostaglandin E1 inhibitis platelet aggregation by a pathway independent of adenosine 3',5'-monophosphate.

Aggregation of human blood platelets induced by adenosine diphosphate or 1-epinephrine was inhibited when the platelets were suspended in plasma which had been previously exposed to an insolubilized omega-aminohexylagarose derivative of prostaglandin E1. This decrease of platelet aggregation was not accompanied by a change in the concentration of adenosine 3',5'-monophosphate (cyclic AMP) in platelets. The results demonstrate the existence of an alternative pathway independent of cyclic AMP for the inhibition of platelet aggregation by plasma.

Adenosine Diphosphate↗
PubMed1999

Diminished platelet aggregation in patients with iron deficiency anemia.

To evaluate platelet function in iron deficiency anemia, using impedance (in whole blood) and optic (in platelet-rich plasma methods, platelet aggregation analyses were performed in 42 children with iron deficiency anemia at the time of diagnosis and after iron therapy. Collagen-induced platelet aggregation was decreased in patients before therapy compared to after therapy and control levels as indicated by the two methods while adenosine diphosphate (ADP)-induced platelet aggregation was decreased only by the whole blood method. Platelet aggregation with epinephrine, performed only by the optic method, was not altered in patients with iron deficiency anemia. Platelet counts were found to be increased in patients with iron deficiency anemia, and decreased with therapy. These results indicate that some platelet functions are decreased in patients with iron deficiency anemia. These decreased functions may be compensated by increased platelet numbers.

Adenosine Diphosphate↗
PubMed1990

Effects of protopine on blood platelet aggregation. II. Effect on metabolic system of adenosine 3',5'-cyclic monophosphate in platelets.

The mode of action of protopine on rabbit platelet aggregation was investigated in the metabolic system of adenosine 3',5'-cyclic monophosphate (cyclic AMP) in vitro experimental models. The inhibitory activity of protopine on adenosine 5'-diphosphate induced platelet aggregation was increased in the presence of prostaglandin I2 or papaverine in platelets. Protopine elevated content of the basal cyclic AMP accumulation in platelets and enhanced activity of crude adenylate cyclase prepared from platelets, but was ineffective on cyclic AMP phosphodiesterase. It is concluded that protopine has an inhibitory activity on platelet aggregation, activates adenylate cyclase and increases cyclic AMP content in platelets, in addition to other inhibitory actions in the metabolic system of cyclic AMP.

Alkaloids↗
PubMed2000

Sevoflurane does not inhibit human platelet aggregation induced by thrombin.

BACKGROUND: Sevoflurane reportedly inhibits adenosine diphosphate-induced platelet aggregation by suppressing thromboxane A2 formation. The increase in intracellular calcium concentration that fosters platelet aggregation, however, is also induced by other cell signaling pathways, such as activation of the production of inositol 1,4,5-triphosphate by thrombin. The current study aimed to clarify the net influence of sevoflurane on thrombin-induced platelet aggregation. METHODS: Washed platelets were stimulated by thrombin after incubation with 0.5, 1.0, or 1.5 mM sevoflurane, halothane, or isoflurane. Aggregation curves were measured by an aggregometer. Intracellular calcium concentration was measured fluorometrically using fura-2. Calcium mobilization via plasma membrane calcium channels and the dense tubular system was assessed differentially. Intracellular inositol 1,4,5-triphosphate was measured by radioimmunoassay. RESULTS: Halothane significantly suppressed aggregation ratios at 5 min compared with those in controls (89 +/- 7%) to 71 +/- 10% (1.0 mM) and 60 +/- 11% (1.5 mM) and the increase in intracellular calcium concentration (controls, 821 +/- 95 nM vs. 440 +/- 124 nM [1.0 mM] or 410 +/- 74 nM [1.5 mM]). Halothane also significantly inhibited release of calcium from the dense tubular system (controls, 220 +/- 48 nM vs. 142 +/- 31 nM [1.0 mM]). Neither sevoflurane nor isoflurane produced a net change in aggregation ratios, intracellular calcium concentration, or calcium mobilization. Halothane (1 mM) significantly suppressed inositol 1,4,5-triphosphate concentrations, whereas neither 1 mM isoflurane nor 1 mM sevoflurane had any effect. CONCLUSIONS: Although sevoflurane has been reported to inhibit human platelet aggregation induced by weak agonists such as adenosine diphosphate, it does not inhibit human platelet aggregation induced by strong agonists such as thrombin.

Anesthetics, Inhalation↗
PubMed1994

Relationship of platelet aggregation to bleeding after cardiopulmonary bypass.

Excessive bleeding after cardiopulmonary bypass operations is a persistent problem. This study assessed the influence of platelet function on blood loss for 134 patients undergoing cardiopulmonary bypass. Platelet function was measured by platelet aggregation in platelet-rich plasma and whole blood using collagen as the agonist. Adenosine triphosphate release was assessed concurrently. Measurements were made 1 day before operation and 1 hour after the cessation of cardiopulmonary bypass. Three important findings were made. First, statistically significant correlations were shown between preoperative and postoperative platelet aggregation and blood drainage for the first 3 hours postoperatively. Second, correlations were greatest when preoperative measurement was performed on whole blood and postoperative measurement was performed on platelet-rich plasma. Third, patients with reduced postoperative platelet aggregation in platelet-rich plasma had significantly greater transfusion requirements in the first 24 hours postoperatively. In defining the 16 patients who bled excessively among the 134 patients studied, the preoperative aggregation in whole blood had a sensitivity of 62%, specificity of 75%, positive predictive value of 26%, and negative predictive value of 94%. The postoperative aggregation in platelet-rich plasma had a sensitivity of 86%, specificity of 69%, positive predictive value of 28%, and negative predictive value of 97%. These results indicate that preoperative and postoperative measurement of platelet aggregation may provide a rationale for the prophylaxis or treatment of patients to reduce blood loss after cardiopulmonary bypass.

Adenosine Triphosphate↗
PubMed1991

Reproducibility and temporal stability of ADP-induced platelet aggregation: comparison of the anticoagulants sodium citrate and D-phenylalanyl-L-prolyl-L-arginyl-chloromethyl ketone.

We compared the reproducibility and temporal stability of ADP-induced aggregation of platelet-rich plasma anticoagulated with citrate or with D-phenylalanyl-L-prolyl-L-arginyl-chloromethyl ketone (PPACK), a thrombin inhibitor. Citrate- or PPACK-platelet-rich plasma (PRP) was stored at room temperature in capped plastic tubes or in plastic syringes from which all air was expelled. At intervals over 1-5 hr after venipuncture, platelet aggregation was induced by 1-1.5 microM ADP. Initially, the aggregation of PPACK-PRP was nearly twice that of citrate-PRP. The response of PPACK-PRP stored in the syringe remained essentially constant over the interval of study, in contrast to the responses of the other samples which declined with time. The improved stability of the response obtained from samples anticoagulated with PPACK was due to the absence of citrate, since PRP containing both citrate and PPACK became less responsive over time in a manner similar to PRP which contained only citrate. Anticoagulation with PPACK rather than citrate results in a more reproducible and stable aggregation response and more closely reproduces the in vivo environment of the platelet.

Adenosine Diphosphate↗
PubMed1987

Characterization of a genetic difference in the platelet aggregation response of two inbred mouse strains, C57BL/6 and C3H/He.

An in vitro platelet aggregation assay has been used to characterize the platelet response of two inbred mouse strains, C57BL/6J and C3H/J. Arachidonic acid, ADP, ristocetin, and collagen, but not epinephrine, were effective inducers of platelet aggregation in C57BL/6 mice. In C3H mice, however, platelets responded differently to some, but not all, inducers of platelet aggregation. The difference between the two strains was particularly striking for arachidonic acid; at 0.375 microM arachidonic acid, platelets from C57BL/6 mice aggregated well, but platelets from C3H mice failed to aggregate. The two strains also differed in serotonin release from platelets. When the pool of platelet serotonin was labeled by incubating platelets with [14C]serotonin, the amount of label subsequently released from platelets in response to 0.375 microM arachidonic acid was 20.5% +/- 2.5 SE for C57BL/6 mice and 1.5% +/- 1.5 SE for C3H mice. The platelets from F1 progeny of a cross between C57BL/6 and C3H mice were indistinguishable in aggregation response from the C57BL/6 parent. The defect in aggregation response found in C3H mice appears to reside in the platelets rather than in the plasma. Experiments which involved adding the plasma of one strain to the washed platelets of the other strain indicated that C57BL/6 platelets aggregated well whether they were resuspended in plasma from C57BL/6 or C3H mice, while C3H platelets failed to aggregate regardless of the origin of the plasma. Strain C57BL/6 is susceptible to diet-induced formation of atherosclerotic lesions, but strain C3H is resistant to lesion formation. This genetic difference in atherosclerosis susceptibility is not related to the genetic difference in platelet aggregation since a recombinant inbred strain, BXH-9, is susceptible to atherosclerosis like the C57BL/6 parent but has the reduced platelet aggregation response of the C3H parent.

Animals↗