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PubMed1992

Dose-response aggregometry--contribution to the precise platelet function evaluation.

A method for the determination of blood platelet aggregability as the function of ADP concentration is described. Individual platelet aggregability was characterised by means of parameters of the sigmoidal relationship between the dose of the aggregating reagent and the aggregation curve amplitude. The method was applied to establish ADP-induced aggregability of various mammalian species. The aggregation curves of rabbit and rat platelets reached significantly lower maximum amplitudes than those of human and dog platelets. The eman concentration of ADP was significantly higher in dog platelets and the slope of the dose-response curve was significantly steeper in rat platelets compared to the other species studied. Some of the causes of individual intra-species ADP-induced aggregation variability revealed by means of dose-response aggregometry are discussed.

Animals↗
PubMed1992

A method for quantitative determination of flow induced human platelet adhesion and aggregation.

Adhesivity and aggregability of blood platelets may reflect normal and diseased states. A quantitative assessment of such reactivity should thus provide further insight into disease mechanism. The well defined conditions of stagnation point flow using platelet-rich-plasma (PRP) as fluid permit quantitative treatment of the formation of platelet microthrombi on the stagnation plate. By measuring the growth kinetics (photometry) and corresponding morphology (light- and electron microscopy) of the microthrombus, platelet adhesion as well as aggregation could be analyzed separately by means of a quantitative procedure. Parameters are evaluated for PRP samples obtained from patients exhibiting deep venous thrombosis, arterial angiopathy or myocardial infarction, respectively. The results obtained demonstrate the usefulness of the proposed method for quantifying platelet reactivity as reflected by type and degree of flow induced platelet deposition. This, in turn, provides a basis for correlating the in vitro findings with the disease state.

Humans↗
PubMed1993

Spectrophotometric evaluation of the adhesion of blood platelets to collagen and microfibrils.

We present an easy method in which the adhesion of platelets to collagen or to MFs was measured in a spectrophotometer, after an incubation of hypercitrated platelet rich plasma (PRP), or of a platelet suspension, with an inducer, followed by the filtration of non adhering platelets through translucent Isopore membrane filters (pore diameter = 5 microns). The adhering platelets, which are retained on the filter, were stained by Coomassie blue to quantify the adhesion by the simple reading of the O.D. 580 nm of the stained platelets which appear as a blue spot on the translucent membranes.

Blood Platelets↗
PubMed1996

Quantitative measurement of various 5-HT receptor antagonists on platelet activation induced by serotonin.

The effects of S2-serotonergic receptor antagonists, ketanserin, MCI-9042, and one of its major metabolite, M-1, were evaluated on human platelet activation induced by serotonin. A newly developed method for detecting particles in suspensions was used to assess serotonin-induced platelet aggregation. Serotonin added to platelets in plasma induced transient formation of small aggregates but not that of large ones. All the three antagonists in a dose-dependent manner suppressed serotonin-induced platelet aggregation. The ID50 values for ketanserin, MCI-9042, and M-1 are 10 nM, 0.6 microM, and 40 nM, respectively. The effects of these antagonists were also evaluated on [Ca+2]i elevation and shape change, the measurement of which does not require the presence of plasma proteins. These antagonists effectively inhibited [Ca+2]i elevation and shape change induced by serotonin. The ID50 value for MCI-9042 was approximately 1/10 for platelet aggregation. These findings suggest that MCI-9042 tightly binds to plasma proteins with resultant reduction in overall potency. The ID50 values obtained in this study are essentially equivalent to those reported for S2-serotonergic receptor binding in rabbit platelets, suggesting that these agents are also potent antagonists serotonin-induced activation of human platelets.

Blood Platelets↗
PubMed1996

Passive smoking and platelet thromboxane.

While active smoking is known to enhance platelet thromboxane production, no data on passive smoking is available yet. The influence of single and repeated exposure to passive smoke for 60 minutes in a 18 m3 room was assessed in non-smokers as compared to sex and age matched smokers. All the evaluated measures (malondialdehyde, plasma thromboxane B2, 11-dehydro-thromboxane B2, serum thromboxane B2, conversion of exogenous arachidonic acid to thromboxane B2 and to hydroxy-5, 8,10-heptadecatrienoic acid) were higher in smokers than non-smokers at baseline, immediately and 6 hours after passive exposure to cigarette smoke. Repeated exposure of non-smokers rendered their platelets more activated becoming close to the behaviour of smokers. These results indicate that passive smoking may activate thromboxane A2 release from the platelets, contributing to the development of hemostatic imbalance.

Adult↗
PubMedDate not supplied

Lowering of body temperature affects human platelet functions and norepinephrine release.

The effect of lowering body temperature on plasma epinephrine, norepinephrine, and platelet density distribution and volume was studied in a placebo-controlled double-blind study. Lowering of body core temperature was induced by either exposure to a cold environment at a temperature of 5 degrees C (CT) or by a single dose of the 5-HT1A agonist ipsapirone (IPS). A third group exposed to an ambient temperature of 28 degrees C was given placebo (PLAC). All of the three groups were investigated in a climate chamber. In the CT group the density distribution of blood platelet subpopulations was shifted to an increase in less dense platelets that were more sensitive towards aggregation-inducing agents. The mean platelet volume in this subpopulation was decreased. Epinephrine was not affected, whereas the increase of norepinephrine was correlated with an increase of platelets that were more sensitive to aggregation-inducing agents in the CT group but not in the PLAC and IPS groups.

Adult↗
PubMed1983

Turbidometric evaluations of platelet activation: relative contributions of measured shape change, volume, and early aggregation.

The relative contributions of ADP-induced changes in mean platelet axial ratio (R), mean volume (VT), pseudopod formation, refractive index, and early platelet aggregation to the changes in light transmission (%T) through stirred platelet suspensions (aggregometer) are determined. Measurement of the change in R within the first 10s of ADP addition indicates that the slope of the initial decrease in %T (5s) is in good agreement with that predicted from the theory of Latimer et al. (1977). However, when the changes in %T due to changes in VT are also considered, the observed rate of change of %T is shown to be 20-210% larger than predicted. These observations point to an additional process which produces a decrease in %T. It is shown that platelet aggregation occurring on this early time scale does not contribute to the initial changes in %T. Aggregation does lead to an increase in %T once there are greater than or equal to 30-40% singlet platelets aggregated which occurs at greater than or equal to 4-5s for 1-10 microM ADP. In the absence of aggregation, the extent of %T decrease at greater than 40s is greater than 25% smaller than predicted from the change in R and VT. It is suggested that at early times, changes in platelet refractive index produce significant decreases in %T which are on average offset by comparable increases due to the early volume increase, whereas at later times pseudopod formation has an important influence on %T.

Adenosine Diphosphate↗
PubMed1992

Paracentesis with Dextran 70 vs. paracentesis with albumin in cirrhosis with tense ascites. Results of a randomized study.

Forty-one patients with cirrhosis and tense ascites were randomized to receive daily paracentesis of 5 liters associated with Dextran 70 as volume expander (6 g for each 1000 ml of ascites removed) (group I = 20 patients) or paracentesis with albumin (6 g for each 1000 ml of ascites) (group II = 21 patients). The basal clinical features, laboratory data, and plasma renin activity were similar in both groups. The volume of ascites removed was 12.9 +/- 4.4 and 10.9 +/- 3.7 liters in group I and II, respectively (n.s.). No significant changes were observed in liver and renal function tests, KPTT, platelet count, factor VIII, serum electrolytes or plasma renin activity 24 and 96 h after the last paracentesis in both groups, except for a decrease in bilirubin in group I and a transient increase of serum albumin in group II. Four patients developed complications in each group, mainly hyponatremia, while one patient in each group developed renal impairment. One patient from group I died with hepatic encephalopathy. Moreover, the probability of survival and readmission to the hospital because of tense ascites were similar in both groups of patients during the follow-up. The treatment cost with Dextran 70 was 15.50 dollars vs. 364.30 dollars with albumin for each patient treated. These results indicate that repeated large volume paracentesis associated with Dextran 70 is as effective and safe as paracentesis associated with albumin in cirrhotic patients with tense ascites. However, due to its reduced cost, paracentesis with Dextran 70 may be considered the treatment of choice in cirrhotic patients with tense ascites without liver cancer and renal failure.

Ascites↗
PubMed1986

Platelet dysfunction in splenectomized patients with hairy cell leukemia.

Platelet function was assessed in 17 patients with hairy cell leukemia who had undergone splenectomy. Defective PAF-induced aggregation and selective reduction of beta-thromboglobulin were found in platelets from six and eight patients respectively. These defects were not necessarily associated with bleeding complications.

Adult↗
PubMed2005

The role of platelet glycoprotein IIIa polymorphism in the high prevalence of in vitro aspirin resistance in patients with intracoronary stent restenosis.

OBJECTIVES: The aim of our study was to determine the relation between platelet glycoprotein IIIa (Pl A ) polymorphism and aspirin resistance in patients with intracoronary stent restenosis. BACKGROUND: Clinically, aspirin resistance is defined as having thrombotic and embolic cardiovascular events despite regular aspirin therapy. Platelet glycoprotein IIIa polymorphism is said to be a possible mechanism of aspirin resistance. METHODS: We studied the prevalence of aspirin resistance in 204 previously intracoronary stent-implanted patients with stable coronary artery disease. In 102 of these patients, intracoronary stent restenosis was present. Platelet functions were analyzed in a platelet function analyzer (PFA-100, Dade Behring, Germany) with collagen and/or epinephrine (Col/Epi) and collagen and/or adenosine diphosphate cartridges. Closure time <186 seconds was defined as aspirin resistance with Col/Epi cartridges of PFA-100. The Pl A polymorphisms of 43 aspirin-resistant and 51 aspirin-sensitive subjects were determined with polymerase chain reaction and restriction fragments length polymorphism. RESULTS: A total of 31.3% (n = 32) of patients with intracoronary stent restenosis and 10.7% (n = 11) of patients with patent intracoronary stents were resistant to aspirin by PFA-100. The Pl A1,A1 allele of glycoprotein IIIa was present in 36 subjects (83.7.%) and the Pl A1,A2 allele was present in 7 subjects (16.2.%) in the aspirin-resistant patients group. The Pl A1,A1 allele of glycoprotein IIIa was present in 37 subjects (72.5%) and the Pl A1,A2 allele was present in 14 subjects (27.5%) in the aspirin-sensitive patients group ( P = .195). CONCLUSION: Our results suggest that platelets of patients with intracoronary stent restenosis with or without Pl A2 heterozygosity of glycoprotein IIIa are more likely to be resistant to low-dose aspirin therapy.

Aged↗
PubMed2004

Comparative effect of antiplatelet therapy in retinal vein occlusion evaluated by the particle-counting method using light scattering.

PURPOSE: To evaluate platelet aggregation in patients with retinal vein occlusion (RVO) by the light-scattering method and compare the effects of three antiplatelet drugs on aggregate formation. DESIGN: Prospective, nonrandomized, interventional clinical trial. METHODS: (1) Platelet aggregation was measured in 42 patients with untreated branch RVO (BRVO), 26 patients with central RVO (CRVO), and 30 healthy control subjects using a light-scattering platelet aggregometer. Platelet aggregates were classified as small, medium, and large according to light intensity. Total light intensities of each aggregate size were compared between BRVO, CRVO, and control subjects. (2) In 33 patients with RVO, platelet aggregation before and 2 weeks after the administration of ticlopidine, beraprost, or aspirin were compared. RESULTS: (1) There was a statistically significant difference (P = 0.0073) between the control subjects (8.3 x 10(6) a.u.) and CRVO patients (22.9 x 10(6) a.u.) with respect to small aggregates. There was no statistically significant difference with respect to medium and large aggregate formation between the control subjects and either patient group. (2) Compared with aggregates formed in the absence of antiplatelet drugs, ticlopidine significantly inhibited only the formation of small aggregates and beraprost that of all sizes; aspirin did not significantly inhibit the formation of any aggregate sizes. CONCLUSIONS: Increase in small platelet aggregates may be attributable to RVO pathogenesis. Beraprost and ticlopidine appear to inhibit small aggregate formation in RVO patients and may represent effective antiplatelet treatments. The light-scattering method is useful to investigate the pathogenesis of RVO and the effects of antiplatelet drugs.

Aged↗
PubMed2003

Incidence of aspirin nonresponsiveness using the Ultegra Rapid Platelet Function Assay-ASA.

We report the incidence of aspirin nonresponsiveness in a prospective, multicenter registry (n=422 patients) to be 23% using the Ultegra Rapid Platelet Function Assay-ASA, and determined a history of coronary artery disease to be associated with twice the odds of being an aspirin nonresponder (odds ratio 2.01, 95% confidence interval 1.189 to 3.411, p=0.009). Further prospective studies are needed to correlate aspirin nonresponsiveness to adverse clinical events.

Aspirin↗
PubMed2004

Frequency of nonresponse antiplatelet activity of clopidogrel during pretreatment for cardiac catheterization.

Platelet function was evaluated before and after clopidogrel therapy in 50 cardiology candidates scheduled for intervention; results were averaged from optical platelet aggregation with 2 significantly correlated point-of-care instruments, Thrombelastograph and Ichor PlateletWorks. Although this was a limited study with few complications, the failure of clopidogrel therapy (30% nonresponders with <10% average platelet inhibition) was not correlated with clinical pretreatment variables, including atorvastatin therapy, postintervention bleeding complications, or major adverse coronary events.

Adult↗