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PubMed1990

Platelet activation during preparation of platelet concentrates: a comparison of the platelet-rich plasma and the buffy coat methods.

The activation of platelets during the preparation of platelet concentrates (PCs) by two methods was compared. To eliminate interdonor differences, 2 units of whole blood were pooled and subsequently divided into two batches. From one batch, the platelets were harvested as pelleted platelets from platelet-rich plasma (PRP) and from the other as nonpelleted platelets from the buffy coat (BC). The activation of platelets in these PCs was studied immediately after preparation and during storage for up to 9 days at 22 degrees C with gentle agitation. The binding of monoclonal antibodies (MoAbs) against the GP IIb/IIIa complex and against activation-dependent antigens (GMP 140 from the alpha granules and a 53-kDa glycoprotein from the lysosomal granules) was measured. Beta-thromboglobulin (beta-TG) release was also determined. Disc-to-sphere transformation was quantitated by measuring on an aggregometer the difference in light transmission during stirring at different rates and also by light microscopy. Immediately after preparation, platelets derived from PRP had a more spheric morphology (p less than 0.01), had a higher beta-TG release (p less than 0.01), bound more MoAbs against GP IIb/IIIa (p less than 0.01), and expressed more GMP 140 and 53-kDa glycoprotein (p less than 0.01) than did BC-derived platelets. However, these differences had disappeared after 2 days of storage. It was concluded that, immediately after preparation, PRP-derived platelets are more activated than BC-derived platelets. This is most likely a result of the pelleting that follows the second high-speed centrifugation of the PRP.

Antibodies↗

PubMed1980

Platelet function studies in coronary heart disease. IX. Increased platelet prostaglandin generation and abnormal platelet sensitivity to prostacyclin and endoperoxide analog in angina pectoris.

Platelet prostaglandin generation (malondialdehyde production) and platelet sensitivity to prostacyclin (a vasodilator and platelet aggregation inhibitor) and to epoxymethanodienoic acid (EMA) (a vasoconstrictor and platelet aggregation stimulant endoperoxide analog) were studied in patients with angina pectoris and in control subjects. Platelet malondialdehyde production was higher in patients than in control subjects (mean +/- standard error of the mean 2.50 +/- 0.30 versus 1.70 +/- 0.13 nmol/10(9) platelets, p < 0.02). Platelets from patients were significantly less sensitive to prostacyclin's antiaggregatory effects than were those from control subjects (amount of prostacyclin required for 50 percent platelet aggregation inhibition 1.90 +/- 0.35 versus 0.68 +/- 0.05 ng, p < 0.02). Furthermore, less EMA was required to induce 50 percent platelet aggregation in patients with angina pectoris than in the normal subjects (133 +/- 8 versus 194 +/- 16 ng, p < 0.001). These observations suggest that increased platelet prostaglandin generation and abnormal platelet sensitivity to prostacyclin and endoperoxide analog in certain patients with coronary artery disease are important potential mechanisms in the pathogenesis of myocardial ischemia.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1992

DDAVP-induced enhancement of platelet retention: its dependence on platelet-von Willebrand factor and the platelet receptor GP IIb/IIIa.

Although DDAVP has been shown to be haemostatically efficacious in patients with various congenital or acquired platelet disorders, no reasonable explanation has been found for this effect. We have previously shown DDAVP to increase platelet adhesiveness as measured with a platelet retention test. The aim of the present study was to investigate the mechanism of action responsible for the increased platelet retention in response to DDAVP. Patients with vWD type III and type Ia, severe haemophilia and severe thrombasthenia, as well as healthy controls, were included in the study. The effect of different concentrations of vWF in plasma and platelets was explored, as was the effect on platelet function of apyrase and monoclonal antibodies against GP IIb/IIIa and GP Ib. We found the effect of DDAVP on platelet retention to be unaffected by changes in the plasma concentration of vWF. The enhanced platelet retention after DDAVP is apparently dependent on the presence of platelet-vWF and on a normal function of the GP IIb/IIIa. The effect is not mediated via ADP or thrombin. The platelet-stimulating effect of DDAVP may be one explanation for the positive haemostatic effect in patients with certain platelet disorders.

Adolescent↗

PubMed1975

Platelet antiheparin activity. The isolation and characterisation of platelet factor 4 released from thrombin-aggregated washed human platelets and its dissociation into subunits and the isolation of membrane-bound antiheparin activity.

Platelet factor 4 was isolated by gel filtration from the soluble release products of thrombin-aggregated washed human platelets as a proteoglycan-platelet factor 4 complex of molecular weight 358 000, Stokes radius (r-s) of 14.0 nm, sedimentation coefficient (s) of 7.1 S and frictional ratio (f/f-o) of 3.04. The complex was dissociated at high ionic strength (I equals 0.75) and the proteoglycan separated from platelet factor 4 by gel filtration. Platelet factor 4 had a molecular weight of 27 100, r-s of 2.52 nm, s of 2.4 S and f/f-o of 1.26, was insoluble under physiological conditions but readily soluble at pH 3. Under these conditions platelet factor 4 dissociated into four subunits with a molecular weight of 6900, r-s of 1.92 nm, s of 0.8 S, and f/f-o of 1.52. Qualitative N-terminal amino acid analysis showed the presence of glutamic acid or glutamine as the major end group. Platelet factor 4 was compared with protamine sulphate, which has similar biological properties, by electrophoresis at pH 2.2, in which both migrated as single bands but with differing mobility, and by amino acid analysis which showed a more normal distribution of residues than occurred in protamine sulphate. Of the basic amino acids platelet factor 4 (molecular weight 27 100) contained 5.97% arginine, 3.18% histidine, and 12.31% lysine compared to protamine sulphate with 64.2% arginine, 0.6% lysine and no histidine. A partial specific volume (v) of 0.747 was calculated for platelet factor 4 from its amino acid analysis. A membrane fraction with antiheparin activity, an isopycnic density of 1.090-1.110 and r-s of 15-35 nm, was also isolated by sucrose density gradient centrifugation from the ultrasonicated insoluble platelet residue remaining after thrombin-induced aggregation of washed human platelets. Trypsin treatment of the membrane fraction neither solubilised nor destroyed the activity.

Amino Acid Sequence↗

PubMed1992

Defective platelet aggregation in response to platelet-activating factor in uremia associated with low platelet thromboxane A2 generation.

The bleeding tendency associated with uremia is likely due to a qualitative platelet dysfunction. So far the data available on platelet aggregation are conflicting. Since platelet-activating factor (PAF) plays a role in primary hemostasis, we studied platelet aggregation in response to PAF in 40 patients with chronic uremia on regular hemodialysis and 12 control subjects. Our results showed that in 28 of 40 uremics, platelet aggregation response to PAF was normal, whereas in the remaining 12 it was defective in that no second wave of aggregation was elicited even if the PAF concentrations were increased by a factor of 10,000. This abnormal response was peculiar to PAF and only partially related to factor(s) of plasma origin. The number of platelet PAF receptors and their affinity for the agonist were comparable in controls and "PAF-unresponsive" patients. The defective platelet aggregation in response to PAF was associated with a statistically significant reduction (P less than 0.01) in thromboxane A2 (TxA2) generation in platelet-rich plasma (PRP) challenged with PAF (10 and 100 nmol/L). When PRPs from PAF-unresponsive patients were preincubated with a stable analogue of prostaglandin endoperoxides/TxA2 U-46619, an irreversible platelet aggregation in response to PAF was obtained. Thus in a subpopulation of uremics, platelet aggregation in response to PAF is selectively abnormal as a consequence of a reduced TxA2 generation.

Adult↗

PubMedDate not supplied

Platelet factor 4 release from the platelets stored in platelet concentrates.

Many consider that granular components of platelets should remain intact during storage of platelet concentrates (PCs) in order to participate in hemostasis when infused. The present investigations were done to determine factors affecting the release of an alpha-granular component, platelet factor 4 (PF-4), from platelets stored as PCs. Sedimentation of the pelleted platelet button and stronger flat-bed agitation induced a significant PF-4 release. After 1 day of storage at 22 degrees C, the percent PF-4 release correlated roughly with a pH fall in PCs (r = 0.520, y = 0.014 + 7.204). Rates of pH fall were roughly proportional to the platelet count. In addition, there was a positive relationship between PF-4 release and the platelet count per unit volume (r = 0.615, y = 0.045 + 1.327). The results indicated that one of the critical factors which determines the amount of PF-4 release during storage is concentrated pH. Lowering the platelet count per unit volume in PCs is better for the maintenance of granular components in platelets during storage because of the intact platelet metabolism.

Adolescent↗

PubMed1978

Impairment of platelet thromboxane A2 generation and of the platelet release reaction in two patients with congenital deficiency of platelet cyclo-oxygenase.

Two cases of thrombocytopathia with congenital deficiency of platelet cyclo-oxygenase were investigated. The platelet release reaction was impaired. There was a marked decrease of aggregation with collagen and with adrenalin and a total absence of aggregation with sodium arachidonate. The platelet response to labile aggregation stimulating substance (LASS, mostly thromboxane A2) was normal. There was no biosynthesis of prostaglandin cyclic endoperoxides or of thromboxane A2 from arachidonic acid. Basal levels of platelet PGE1 were lowered although plasma levels were normal. Thrombin decreased the cyclic AMP content of patients' platelets and also that of control platelets pretreated with aspirin. The patients platelets showed no ultrastructural difference when compared with control platelets, except for a slight decrease of granule volume, but, in contrast to control platelets, thrombin (0.02 U/ml) did not provoke contraction of the patients' platelets.

Adult↗

PubMed1989

Collagen-platelet interactions: evidence for a direct interaction of collagen with platelet GPIa/IIa and an indirect interaction with platelet GPIIb/IIIa mediated by adhesive proteins.

Using intact human platelets as the immunogen and a functional, collagen-coated bead agglutination assay, we have produced a murine monoclonal antibody (6F1) that blocks the interaction between platelets and collagen in the presence of Mg++. 6F1 affinity-purified the platelet glycoprotein Ia/IIa complex, and approximately 800 molecules of 6F1 bound per platelet at saturation. 6F1 nearly completely inhibited collagen-induced platelet aggregation and inhibited platelet adhesion to collagen by greater than 95% when plasma proteins were absent. Antibody 10E5, which blocks the binding of adhesive glycoproteins to GPIIb/IIIa, produced only minor inhibition (approximately 25%) of adhesion under the same circumstances. In contrast, when tested in platelet-rich plasma (PRP), 6F1 had only a minor effect on collagen-induced platelet aggregation, prolonging the lag phase but not the slope or maximum aggregation. Similarly, when collagen was precoated with plasma, 6F1 caused less inhibition of platelet adhesion (53%) than without the precoating (greater than 95%). Antibody 10E5 inhibited this adhesion by 32%, and the combination of 6F1 and 10E5 was more effective than either alone, inhibiting it by 90%. Time course studies of platelet agglutination of collagen-coated beads using PRP containing physiologic concentrations of divalent cations showed early inhibition by 6F1, indicating that the GPIa/IIa receptor operates in this environment. With more prolonged incubation, however, 6F1 was less effective; this later agglutination could be partially prevented by adding 10E5 or PGE1 to the 6F1. These data support a model wherein collagen can directly interact with GPIa/IIa and can indirectly interact with GPIIb/IIIa via intermediary adhesive proteins. The physiological significance of these interactions, and potential interactions with other receptors, remains to be established.

Antibodies, Monoclonal↗

PubMed1984

Platelet coagulant activities in diabetes mellitus. Evidence for relationship between platelet coagulant hyperactivity and platelet volume.

Platelets have been shown to be capable of initiating and promoting some of the reactions in intrinsic coagulation and have been implicated in the pathogenesis of vascular lesions in diabetes mellitus. We have examined the contribution of platelets to the coagulation reactions in 39 patients having diabetes mellitus with and without retinopathy [background retinopathy (BR) or proliferative retinopathy (PR)], 18 patients with nonvascular eye diseases (patient controls), and 38 normal subjects. As compared to control patients, significant elevations were noted in four of the five assays for platelet coagulant activities in diabetic patients with PR and in three of five assays in patients with BR. Thus platelet coagulant hyperactivity is present in diabetics with retinopathy. Significant elevations were noted in two of the assays in patients without retinopathy (NR), suggesting that platelet coagulant hyperactivity may not necessarily be secondary to the vasculopathy. The predominant abnormalities noted were in assays reflecting the contribution of platelets to the early stages of intrinsic coagulation rather than to later stages of prothrombin activation. In addition, the mean platelet volume was found to be significantly greater in patients with PR and BR but not NR than in normal controls. A positive linear correlation (r = 0.81) was noted between the mean of the coagulant activities and platelet volume in diabetic subjects, suggesting a hitherto undescribed relationship between platelet coagulant activities and platelet volume.

Adult↗

PubMed1985

The effect of dialyser membrane material on intradialytic changes in platelet count, platelet aggregation, circulating platelet aggregates and antithrombin III.

Blood surface interaction during hemodialysis leads to impairment of platelet function and decrease in platelet number, which besides heparinization, may cause or exacerbate bleeding in risk patients. Furthermore, antithrombin III has been shown to increase during dialysis, probably due to vascular endothelial injury caused by infusion of activated platelets into the patient. 23 patients were examined during two successive dialyses, using membranes based on regenerated cellulose (RC) and cellulose acetate (CA). In 12 of the patients, platelet aggregation induced by ADP, circulating platelet aggregates and immunological AT III and AT III activity were determined. Irrespective of the membrane used, hemodialysis was associated with deterioration of platelet function, reflected by a decrease in platelet aggregation with return to predialysis values at the end of dialysis. However, the decline in platelet count and the increase in circulating platelet aggregates were membrane dependent, with RC causing greater changes than CA. No changes in threshold concentration of ADP inducing secondary platelet aggregation or in either immunological AT III or AT III activity were seen during dialysis.

Adolescent↗

PubMed1991

Leukocyte removal filtration of platelet concentrates. A study of platelet loss using 111In-labelled platelets and dynamic gamma camera scintigraphy.

111In labelled platelets and gamma camera scintigraphy were used for the study of the platelet loss during leukocyte removal filtration of stored platelets. Two different filters were examined, Imugard IG500 and Pall PL100, and platelet pools containing varying number of platelet concentrates were filtered. It was found that a sizeable amount of the platelets was trapped within the filter. Some of the trapped platelets could be recovered by rinsing the filters with normal saline. The most appropriate rinsing volume to recover lost platelets seemed to match with the "dead space" volume within the filter. It is concluded that radiolabelled platelets and gamma camera scintigraphy appears to be an excellent method to investigate the dynamic events of platelet loss during leukocyte removal filtration. This technique should be well applicable for the study of technological advances in filter construction.

Blood Platelets↗

PubMed1975

Detection of platelet isoantibodies by (3H)serotonin platelet release and its clinical application to the problem of platelet matching.

The detection of platelet isoantibodies by the release of (3H)serotonin from platelets has been evaluated. The conditions for optimal release of (3H)serotonin with platelet isoantibodies using a microtechnique have been defined. A group of cardiac surgery patients were followed pre- and post-transfusions, with 48percent developing a positive serotonin release assay. Of these patients, 16percent also had a platelet complement-fixing and/or lymphocytotoxic isoantibody. There was variation in the degree of correlation between (3H)serotonin release and lymphocytotoxicity using individual National Institutes of Health typing serum. The matching obtained between family members by both techniques showed a close correlation when each technique was evaluated separately using the same NIH typing serum. The detection of iso-antibodies in patients with hematological malignancies correlated with the unresponsiveness to unmatched platelet transfusions in 15 out of 17 cases. The use of the patient's isoantibody to matched platelets of family members by (3H)serotonin release correlated well with the clinical response to transfusion with these platelets. The data suggest that (a) platelet isoantibodies can be detected with increased frequency by (3H)serotonin release; (b) (3H)serotonin release is a specific reaction depending on the surface antigen of the platelet; and (c) the method can be used to match compatible family members for platelet transfusions.

Blood Donors↗

PubMed1986

Platelet turnover and kinetics in immune thrombocytopenic purpura: results with autologous 111In-labeled platelets and homologous 51Cr-labeled platelets differ.

Mean platelet survival and turnover were simultaneously determined with autologous 111In-labeled platelets (111In-AP) and homologous 51Cr-labeled platelets (51Cr-HP) in ten patients with chronic immune thrombocytopenic purpura (ITP). In vivo redistribution of the 111In-AP was quantitated with a scintillation camera and computer-assisted image analysis. The patients were divided into two groups: those with splenic platelet sequestration (spleen-liver 111In activity ratio greater than 1.4), and those with diffuse sequestration in the reticuloendothelial system. The latter patients had more severe ITP reflected by pronounced thrombocytopenia, decreased platelet turnover, and prominent early hepatic platelet sequestration. Mean platelet life span estimated with 51Cr-HP was consistently shorter than that of 111In-AP. Platelet turnover determined with 51Cr-HP was thus over-estimated. The difference in results with the two isotope labels was apparently due to greater in vivo elution of 51Cr. Although the limitations of the techniques should be taken into account, these findings indicate that platelet turnover is not always normal or increased in ITP, but is low in severe disease. We suggest that this may be ascribed to damage to megakaryocytes by antiplatelet antibody. The physical characteristics in 111In clearly make this radionuclide superior to 51Cr for the study of platelet kinetics in ITP.

Adolescent↗

PubMedDate not supplied

VIP elevates platelet cyclic AMP (cAMP) levels and inhibits in vitro platelet activation induced by platelet-activating factor (PAF).

Platelet-activating factor (PAF), a potent endogenous phospholipid released by a variety of mammalian cells, induces platelet activation in vivo and in vitro. Little is known, however, about the physiological modulation of its actions. We have examined the ability of two naturally occurring compounds which stimulate cAMP production, vasoactive intestinal peptide (VIP) and prostacyclin (PGI2), to inhibit PAF-induced platelet aggregation and secretion in vitro. Washed, [3H]serotonin-labeled, rabbit platelets were incubated 60 sec in the presence of VIP, PGI2 or 3-isobutyl-1-methylxanthine (IBMX) and subsequently stimulated with PAF. In separate studies, cAMP levels were determined in similar aliquots of platelets incubated for 30 sec with VIP, PGI2 or IBMX. VIP, PGI2 and IBMX inhibited platelet aggregation and secretion in a dose-dependent manner. Fifty percent inhibition was achieved at final concentrations of 1.7 X 10(6) M VIP, 3.6 X 10(6) M PGI2 and 6.5 X 10(5) M IBMX. IBMX potentiated the inhibitory effects of VIP and PGI2 on PAF-induced platelet activation. VIP and PGI2 elevated platelet cAMP levels four-fold and 50-fold, respectively, in the presence of 10(3) M IBMX. These findings demonstrate that VIP inhibits PAF-induced platelet activation, with a potency comparable to that of PGI2.

1-Methyl-3-isobutylxanthine↗

PubMed1989

The relationship of insulin antibodies, platelet-fixing immune complexes and platelet-associated IgG to in vitro platelet aggregation and thromboxane B2 synthesis in childhood type 1 (insulin-dependent) diabetes mellitus.

The relationship of insulin antibodies, platelet-fixing soluble immune complexes and platelet associated IgG to in vitro platelet aggregation and thromboxane B2 synthesis was studied in a group of children with type 1 (insulin-dependent) diabetes mellitus. Insulin antibodies, through the formation of insulin anti-insulin platelet-fixing immune complexes, seem to increase the levels of platelet associated IgG and both insulin immunity and increased platelet associated IgG are associated with the highest degree of platelet aggregation and thromboxane synthesis. These data suggest a possible role of immune factors in the platelet disfunction of diabetic subjects. Both platelet abnormalities and immune factors have been thought to play a role in the pathogenesis of the late diabetic complications. In this paper data concerning a possible interaction between these two factors are presented.

Adenosine Diphosphate↗

PubMed1985

Expression of coagulant activity in human platelets: release of membranous vesicles providing platelet factor 1 and platelet factor 3.

The relationship between the appearance of membrane-associated factor V-like activity (platelet factor 1, PF1) and phospholipid-like catalytic activity (platelet factor 3, PF3) has been examined, in vitro, in collagen-stimulated, human platelets. Both activities increased 7 fold upon collagen treatment relative to stirred controls. After sedimentation of stimulated platelets, 31% of total PF1 and 41% of PF3 remained in the supernatant fraction. PF1 eluted from a Sepharose CL-4B column in the same void volume fractions as PF3, phospholipid, and vesicular particles. These fractions had roughly 100 fold (lipid basis) or 1000 fold (protein basis) enhanced specific activity when compared to the stimulated platelet suspension. Freeze-fracture electron microscopy demonstrated that these void volume fractions contain two populations of membranous vesicles (80-200 nm and 400-600 nm in diameter). Upon centrifugation of the void volume fractions, PF1 and PF3 activities, phosphate-containing material, and ultraviolet-absorbing material all sedimented at the same rate, indicating that PF1 and PF3 are activities associated with one or both of the platelet-derived vesicle populations. Finally, we examined the effects of inhibitors on the appearance of PF1, PF3, platelet factor 4, total intrinsic factor V activity, and serotonin as well as on platelet aggregation. These studies suggest that the collagen-stimulated release of PF1 and PF3 is not coupled to either platelet aggregation or PF4 release but is probably a separate phase of the release reaction.

Blood Coagulation Factors↗

PubMed1988

In-vitro platelet sensitivity to collagen-induced aggregation and in-vitro platelet deterioration rate during storage, are both inversely proportional to the in-vivo blood platelet concentration in normal individuals: preliminary documentation of these theoretically predictable relationships.

This preliminary study documents two new functional relationships for platelets obtained from normal subjects, whose individual blood platelet concentrations (IBPCs) are in the normal range. Firstly, platelets from subjects (or donors) with high-normal IBPCs are the least sensitive to collagen-induced aggregation (a significant inverse correlation). This may be of importance in determining the likely efficacy of fresh platelet transfusions obtained from donors with different IBPCs within the normal range. Secondly, platelets from subjects/donors with high-normal IBPCs deteriorate less rapidly during storage (a significant inverse correlation), perhaps due to differences in platelet biochemical activity between individuals. Such measurements of platelet deterioration rate were based upon the development of a new experimental technique, in which sterile test-PRP was incubated at 37 degrees C with continuous (quarter-hourly) indirect measurements of changes in platelet morphology. This tube-based method is described in detail. The functional relationships observed do have a theoretical basis within the work of others, which is appopriately outlined. Particular discussion pivots around the possibility of using the deterioration rate relationship to predict how therapeutic platelet concentrates prepared from a given donor of know IBPC, may retain their morphological integrity during routine blood bank storage.

Adolescent↗

PubMed1992

[Efficacy of leukocyte-depleted platelet concentrates for prevention of HLA-alloimmunization in patients with frequent platelet transfusions: a prospective multi-institutional study using a polyester platelet filter].

A prospective multi-institutional study was conducted to assess the efficacy of leukocyte-depleted platelet concentrates, prepared by a method using a newly developed polyester filter, in the prevention of HLA-alloimmunization in patients with hematological disorders. Patients who were expected frequent platelet transfusions, were assigned into two groups, receiving either standard platelet concentrates (control group) or leukocyte-depleted platelet concentrates prepared through a polyester platelet filter, Sepacell-PL (filtered group). All patients received leukocyte-depleted red cell products. Of III patients enrolled, 72 were evaluable, 23 in the control and 49 in the filtered group. Both groups were comparable according to age, sex ratio, underlying disorders, previous exposure to alloantigens by transfusion and/or pregnancy. There was no statistically significant difference in the number and duration of transfusion in the two groups. There were significant differences in HLA-alloimmunization rate (9 cases out of 23, 39% in the control group versus 4 cases out of 49, 8% in the filtered group; p less than 0.01) and refractoriness to platelet transfusion from random donors (6 cases out of 23, 26% in the control group versus 2 cases out of 49, 4% in the filtered group; p less than 0.05). These results indicated that leukocyte-depleted platelet concentrates prepared through the polyester platelet filter are beneficial to reduce HLA-alloimmunization in patients with frequent platelet transfusions.

Adolescent↗