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PubMed1982

111In-oxine platelet imaging in hemodialysis patients: detection of platelet deposition at vascular access sites.

The value of 111In-oxine platelet imaging to assess abnormal platelet deposition at different vascular access sites was studied in 19 hemodialysis patients. Platelets were labelled immediately following dialysis and imaging was performed 2 and 48 h later; abnormal platelet deposition was defined as a localized increase in activity over time when compared to the opposite, control extremity. 10 patients had bovine grafts, 4 had arteriovenous fistulae, and 5 had Gore-Tex grafts. 111In-oxine platelet imaging demonstrated abnormal platelet deposition in 13 out of 19 patients. Positive images were obtained in some patients with each type of vascular access. Preliminary evaluation showed no clear relationship between image positivity and the history of prior graft occlusion. The imaging method provided in vivo evidence of the efficacy of treatment with the antiplatelet agent sulfinpyrazone in half of the treated patients. Following 1 week of sulfinpyrazone, 200 mg t.i.d., in 6 patients, 3 showed a definite decrease in platelet deposition, 2 showed a probable decrease, and 1 showed no change following therapy. We conclude that platelet imaging may provide organ-specific, in vivo evidence for abnormal platelet deposition in several types of vascular access sites, and may be useful in assessing the thrombogenicity of prosthetic materials and the efficacy of antithrombotic drugs.

Adult↗
PubMed2001

Anti-human platelet tetraspanin (CD9) monoclonal antibodies induce platelet integrin alpha IIb beta 3 activation in a Fc receptor-independent fashion.

OBJECTIVES: To characterize the activation of platelet integrin alpha IIb beta 3 induced by two anti-human platelet tetraspanin monoclonal antibodies (mAbs), HI117 and SJ9A4, and investigate their potential mechanism of action. METHODS: Using 125I-labeled human fibrinogen (Fg), specific Fg binding to human platelets induced by HI117 and SJ9A4 was measured. RESULTS: HI117 and SJ9A4 (10 micrograms/ml and 20 micrograms/ml) induced specific Fg binding to human platelets, suggesting that the two mAbs evoked activation of platelet integrin alpha IIb beta 3. Further study indicated that HI117 and SJ9A4 induced integrin alpha IIb beta 3 activation independent of platelet Fc-receptors, and that HI117 and SJ9A4-induced integrin alpha IIb beta 3 activation was inhibited by pretreatment of platelets with sphingosine, aspirin, apyrase, and/or PGI2. CONCLUSIONS: Anti-platelet tetraspanin (CD9) mAbs, HI117 and SJ9A4, can induce platelet integrin alpha IIb beta 3 activation independent of Fc-receptors. Three signaling pathways, namely thromboxane, secreted ADP, and cAMP pathways, may be involved in the process, with protein kinase C activation presumably being the common step of the three pathways.

Antibodies, Monoclonal↗
PubMed1976

Effects of phototherapy on platelet counts in low-birthweight infants and on platelet production and life span in rabbits.

The effects of conventional phototherapy on platelets in vivo were studied in rabbits and in low-birthweight infants. Rabbits were divided into three groups and individually treated continuously for 96 hours, with blue light, daylight, or no phototherapy. Incorporation of selenomethionine Se75 was used to evaluate platelet production and life span. Platelet turnover was significantly increased in the blue-light phototherapy group, and was also increased in the daylight group but to a lesser degree. Daily platelet counts and hematocrits were performed in infants weighing less than 2,000 gm at birth randomized at 24 +/- 12 hours of life to receive daylight phototherapy continuously for 96 hours (31 infants) or no phototherapy (26 infants). In 12 treated infants (38.7%) platelet counts fell below 150,000/cu mm whereas this occurred in only 3 (11.5%) of the controls. These two lower platelet count subgroups differed significantly in mean gestational age and birthweight with the phototherapy group being the more mature. Pre-phototherapy, the mean platelet count of these 12 infants was lower than the mean of the entire control group, suggesting that these infants had borderline marrow reserve before phototherapy was given. These results suggest that phototherapy increases the rate of platelet turnover. When bone marrow compensation is inadequate, the platelet count may fall.

Animals↗
PubMedDate not supplied

[Risk of underestimating platelet count because of the increase of mean platelet volume at the end of pregnancy].

We report the case of a pregnant woman for whom the platelet count (77 x 10(9)/L) was underestimated by Coulter STKS analyzer during the third trimester because of large platelets. The microscopic counting of platelets revealed an isolated thrombocytopenia (120 x 10(9)/L). When not pregnant, the patient has low but normal platelet count (155 x 10(9)/L) with high mean platelet volume (MPV > 12 fL). This case report recalls that concomitantly to the decrease in platelet count, the MPV significantly increases at the end of pregnancy. This poorly known phenomenon does not impair platelet count by blood cell analyzers in as much as the platelet volume is in the range of measurement but may be responsible for underestimation of the platelet count if the MPV is already high before pregnancy. We describe how to detect this anomaly and propose simple guidelines for thrombocytopenia in normal pregnancy.

Adult↗
PubMed1991

Platelet 5-hydroxytryptamine increases with platelet age in dogs.

Thrombocytopenia was induced in mongrel dogs by two mechanisms: immunologically, by intravenous injection of heterologous antiplatelet antibody, and non-immunologically, by circulating the blood through glass beads in anesthetized animals. The platelet content of 5-HT was monitored before and during the recovery of the blood platelet counts. This period is associated with the normalization of the mean platelet survival time and with a progressive increase in the mean age of the circulating platelet population. A continuous increment in platelet 5-HT closely followed the increase in platelet counts in both models of thrombocytopenia, and a strong correlation was found between the platelet age and 5-HT content. These findings support the concept that platelets accumulate 5-HT during their physiological aging process, contradicting the notion that a negative balance in 5-HT content results at the end of their physiological lifespan in circulation. These results are not in conflict with the concept that circulating platelets release and re-uptake 5-HT.

Animals↗
PubMed1990

A rapid embedding procedure for the study of platelet interactions with extracellular matrices in a flowing system. Effect of aspirin on platelet activity.

The cultured endothelial cell (EC) is currently used as a model for the study of the interaction of platelets with the vascular wall. Described is a method for rapid quantitative and qualitative evaluation of platelet interactions with extracellular matrices (ECM) produced by human cultured ECs growing on plastic coverslips. Morphometric calculations can be performed on the same perfused coverslips. A very good correlation (r = 0.96) was found between results of a morphometric method en face and those obtained from analysis of cross sections of the perfused coverslips. A shear rate-dependent increase on platelet deposition onto ECMs was observed with both morphometric procedures. The method is sensitive enough to detect drug-related changes of platelet function. An impairment of the interaction of platelets with the ECM was observed when blood obtained from healthy volunteers who took 500 mg aspirin/day for five days was perfused. Aspirin showed a marked effect, decreasing platelet spreading onto the subendothelium (p less than 0.05). The embedding method described benefits from the use of plastic coverslips that are easily detected from the glycol methacrylate compound used for the embedding procedure. Quantitative analysis en face (covered surface) and qualitative evaluation of platelet interactions (contact, adhesive and aggregated platelets) in cross sections are performed on the same coverslip. This embedding procedure provides a useful tool for the study not only of platelet interactions with ECMs but also for the investigation of interactions of blood elements with other cultured cells.

Aspirin↗
PubMed1987

High-dose intravenous gamma globulin improves responses to single-donor platelets in patients refractory to platelet transfusion.

Ten patients, with bone marrow failure or malignant disorders, became refractory to platelet transfusions using random, as well as partial or fully HLA-matched, single-donor platelets. To determine its effect on platelet refractoriness, intravenous gamma globulin (IV IgG) was administered at 400 or 800 mg/kg/d for five days, and postinfusion platelet responses were monitored. Platelet transfusion responses following intravenous gamma globulin (IV IgG) were graded as follows: Excellent, 48-hour posttransfusion count greater than 50,000/microL; good, 48-hour count greater than 20,000 but less than 50,000/microL; Fair, increased increment, 48-hour count less than 20,000; and failed, no increased increment. Six of ten patients (60%) had improved responses to selected single-donor platelets (two were excellent, three were good, and one was fair). The time to achieve a platelet transfusion count greater than 25,000/microL ranged from one to nine days of IgG therapy. One individual had sustained benefit (greater than 1 year); the remaining responses persisted for 6 to 8 weeks. These results suggest that IV IgG may be useful in the management of platelet refractoriness, especially in patients receiving single-donor platelets.

Adult↗
PubMed1987

[Quantitative study of platelet deposition on expanded polytetrafluoroethylene grafts using 111indium-labeled platelets].

The count of platelets deposited on expanded polytetrafluoroethylene grafts (2 cm long, 3 mm internal diameter, implanted into thoracic aortae of 59 rabbits) was measured using 111Indium-labeled autologous platelets. The changes due to the time courses after implantation, the effect of aspirin and the differences of the platelet deposition on the thrombus and thrombus free surface were studied. In non-treated grafts, platelet deposition on the thrombus free surface was significantly and repeatedly decreased on the 3rd (42.3 +/- 16.6 X 10(4)/mm2, mean +/- S.D.), 9th (17.7 +/- 5.3 X 10(4)/mm2), and 30th (6.8 +/- 3.2 X 10(4) mm2) days after the implantation (p less than 0.05). In treated grafts, platelet deposition on the thrombus free surface was significantly inhibited by aspirin on the 3rd day (20.5 +/- 8.4 X 10(4)/mm2) after implantation (p less than 0.03), while significant inhibition of platelet deposition by aspirin was not noted on the 9th (13.4 +/- 3.8 X 10(4)/mm2) and 30th (13.1 +/- 4.5 X 10(4)/mm2) days after the implantation. Platelet deposition on the thrombus was not inhibited by aspirin. (3600 +/- 2400 X 10(4)/mm2, non-treated grafts. 3500 +/- 520 X 10(4)/mm2, treated grafts). It is concluded that administration of aspirin is necessary immediately after implantation, and its effect is not noted at the time when the deposition of the platelet decreased, and the effect of aspirin cannot be expected in tissues where easy platelet aggregation occurs.

Animals↗
PubMed1979

A solid-phase radioimmunoassay for bound anti-platelet antibody: studies on 45 patients with autoimmune platelet disorders.

A highly sensitive, solid-phase radioimmunoassay has been developed for detecting platelet-bound immunoglobulin, which employs 125I-staphylococcal protein A. The assay detects platelet IgG at the picogram level, which is 10- to 50-fold more sensitive than currently available procedures. It is relatively simple and can be performed on frozen extracts from as little as 2 X 10(5) platelets. Washed platelets are frozen, thawed, sonicated, and centrifuged at 20,000 X g. The supernatant, which contains 7S IgG, is applied in serial dilution to the wells of a plastic microliter plate capable of adsorbing protein. Commercial rabbit anti-human IgG is added and then "sandwiched" to 125I-staphylococcal protein A. The wells are removed from the plate and assayed for radioactivity. Thirty-two of 35 thrombocytopenic patients (92%) with ATP had platelet IgG values greater than those of controls by 2 S.D. and averaged 150 +/- 145 (S.D.) ng/10(6) platelets; 11 healthy controls, 11.4 +/- 7.4 ng; five "thrombocytopenic" controls, 9.7 +/- 13 ng. The platelet count (X) correlated inversely with IgG/platelet (Y) according to the equation: Log Y = -0.66 log X + 4.8; r = -0.71, p less than 0.001. Elevated platelet IgG levels were also found in 5 ATP patients in "apparent remission"; two of four had evidence for compensated thrombocytolysis (increased megathrombocytes). Elevated platelet IgG levels were also found in six patients with thrombocytopenia secondary to lymphoproliferative disorders.

Autoantibodies↗
PubMed1984

The effect of dietary cholesterol on platelet survival in the rabbit--a study using 14C-serotonin and 51chromium double-labelled platelets.

Hypercholesterolemic men and monkeys have shortened platelet survival but attempts to demonstrate this in rabbits have been unsuccessful. The present study examines platelet survival in cholesterol-fed rabbits. Platelets were double-labelled in vitro with 51Cr and 14C-serotonin or in vivo by intravenous injection of 14C-serotonin. In the double-label experiments 51Cr survival was always shorter than 14C survival but changes in survival of one label were accompanied by similar changes in the other label. Survival was shortened after 4 and 7 weeks of cholesterol feeding. This was demonstrated when the donor platelets were from normal rabbits for both cholesterol and control recipients but no shortening was demonstrated when cholesterol-rich platelets were injected into cholesterol-fed recipients and normal platelets were injected into the control rabbits. When 14C-serotonin was injected intravenously 14C survival was the same as when platelets were labelled ex vivo prior to injection and 14C survival was shortened in rabbits fed cholesterol for 1, 2, and 6 weeks. These results indicate that cholesterol-feeding shortens platelet survival. This effect may be masked if the test platelets are not identical in both test and control groups.

Animals↗
PubMed1993

The Streptococcus sanguis platelet aggregation-associated protein. Identification and characterization of the minimal platelet-interactive domain.

Streptococcus sanguis expresses a cell wall-bound protein that induces the activation and aggregation of platelets. This platelet aggregation-associated protein (PAAP) contains a collagen-like, platelet-interactive domain within a 23-kDa protein fragment. To isolate the minimal platelet-interactive domain, p23 PAAP was digested with collagenase, and the digest chromatographed to isolate fractions with activity inhibitory to S. sanguis-induced platelet aggregation. The active fraction was then digested with cyanogen bromide, the product chromatographed, and a smaller inhibitory peptide isolated. Finally, this fraction was digested with endoproteinase Lys-C, and the digest fractionated. After each step, inhibitory activity resolved into single chromatographic peaks of 13 kDa (p13 PAAP), 2.7 kDa (p2.7 PAAP), and a minimal 7-mer peptide, respectively. These PAAP fragments showed similar ID50 (19-28 nM), suggesting that each contained a single copy of the platelet-interactive domain. The minimal 7-mer peptide was purified by immunoaffinity chromatography and reverse phase high pressure liquid chromatography. The primary structure was determined to be Pro-Gly-Glu-Gln-Gly-Pro-Lys. This sequence conforms to the predicted structural motif of the platelet-interactive domains of types I and III collagen. This 7-mer peptide is therefore the platelet-interactive domain of the PAAP from S. sanguis. Its structure explains the molecular basis for immunological cross-reactivity and functional similarity to the platelet-interactive domains of collagens.

Amino Acid Sequence↗
PubMed1997

Effect of cold exposure on platelet concentrates: changes in platelet indices and aggregation states.

Samples from platelet concentrates (filtered/non-filtrated, at the beginning/the end of shelf life) were exposed to 4 degrees C overnight, subsequent to dilution in platelet storage media (PSM) and/or exposure to EDTA to induce shape changes. Paired sampling protocol (+/- EDTA) was used and changes in cellular indices and induced-aggregation states were measured by Technicon H*1. Cold induced changes in platelets as identified by increase in MPV (0.5-0.8 fL for EDTA; 1.5-2.0 fL for citrated samples) with concomitant reverse changes in PDW ranging from 2-13 per cent was observed. Processing, storage and cold exposure also induced disparity between leucocyte peroxidase/basophil counts. This in conjunction with changes in platelet counts and cellular indices upon exposure to EDTA provide a unique new tool for assessing the aggregation states of platelets during processing and storage. Both filtration and dilution in PSM affect platelet storage stability. Platelets which have already undergone shape changes (i.e. exposure to EDTA) responded to a lesser degree to cold exposure. Our findings indicate that platelets's response to cold exposure can be used as a simple, reliable and accurate test for assessment of platelet morphological and function integrities.

Blood Preservation↗
PubMed1978

Heterogeneity of human whole blood platelet subpopulations. II. Use of a subhuman primate model to analyze the relationship between density and platelet age.

A subhuman primate model was developed to ascertain whether or not platelet heterogeneity could be explained by aging in the peripheral circulation. Density-dependent platelet cohorts, postulated to represent cells of different ages, were isolated on isosmolar arabinogalactan gradients and labeled with radiochromium. Mean platelet lifespan was measured for the different density cohorts, and simultaneous sequential density distribution analysis was performed to follow changes in cell density during aging. The average mean lifespan of light platelets was 74.6 hr, compared to 313.6 hr for heavy platelets. After injection, labeled light platelets were recovered only in the gradient light region, in contrast to labeled heavy platelets, which were initially restricted to the dense region and progressively migrated to the light region during their lifespan. This study supports the hypothesis that platelet age in unstressed primates correlates with cell density and provides a rationale for the use of "age-dependent" markers to estimate platelet turnover rates.

Animals↗
PubMed1990

Enhanced botrocetin-induced type IIB von Willebrand factor binding to platelet glycoprotein Ib initiates hyperagglutination of normal platelets.

Botrocetin, a protein isolated from the venom of the snake Bothrops jararaca, induces platelet aggregation/agglutination by von Willebrand factor (vWF) binding to the membrane glycoprotein (GP) Ib, an action resembling that of ristocetin. However, some differences in the interaction between vWF and platelet GPIb induced by these two substances have been reported. We have recently shown that the GPIb binding domain on the vWF molecule, in both instances, resides in the tryptic 52/48 kDa fragment extending from amino acid residue 449 to 728 of the constituent subunit. In the present report, we demonstrate that botrocetin does not induce agglutination of formalin-fixed platelets from a patient with Bernard-Soulier syndrome congenitally lacking GPIb and GPIX as well as GPV, a finding similar to that shown with ristocetin. A monoclonal antibody against GPIb (AP-1) inhibits either ristocetin- or botrocetin-dependent vWF binding to formalin-fixed platelets from normal individuals. Therefore, botrocetin-induced vWF binding to formalin-fixed platelets may reflect the interaction between vWF and platelet GPIb. To strengthen this concept, we have now found that heightened botrocetin-induced type IIB vWF binding to platelet GPIb causes hyperagglutination of normal platelets.

Antibodies, Monoclonal↗
PubMed1996

Flow cytometric analysis of the platelet surface area and surface density of glycoprotein IIb-IIIa of unactivated human platelets of various sizes.

Large (L) activated platelets exhibit greater aggregability and express more activated glycoprotein IIb-IIIa (GPIIb-IIIa) per cell and per unit surface area than small (S) activated platelets. We studied the binding of CD61 monoclonal antibody to GPIIb-IIIa on resting platelets and developed a new method for determining platelet surface area by flow cytometry. Using this method, we found that resting L platelets contain two times more GPIIb-IIIa per cell than S platelets but the same amount of GPIIb-IIIa per unit surface area. The data suggest that the greater aggregability of L platelets is likely to be due to increased activation and/ or expression of GPIIb-IIIa rather than to elevated density of unactivated GPIIb-IIIa on resting L platelets.

Blood Platelets↗
PubMed1997

The release mechanism of platelet-activating factor during shear-stress induced platelet aggregation.

We previously reported that 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (platelet-activating factor, PAF), released from activated platelets stimulated with thrombin plus collagen, is associated with platelet microparticles. In the present study, we found that PAF is concentrated and associated with microparticles released from high shear stress-induced activated platelets. The total amount of PAF released from 3 x 10(8) platelets under high shear stress (108 dyne/cm2) was 3.2 +/- 0.6 x 10(-15)mol (n = 5, mean +/- S.D.). Eighty percent of the PAF released from the platelets was recovered in the microparticle fraction after ultracentrifugation in the presence of albumin. Under high shear stress, PAF was not released from platelets within 3 minutes, although microparticles were released. In conclusion, microparticles released from activated platelets in the rheological condition of high shear stress are major carriers of PAF.

Animals↗
PubMed1993

The actions of lovastatin on platelet function and platelet eicosanoid receptors in type II hypercholesterolaemia. A double-blind, placebo-controlled, prospective study.

We have studied the effects of 12 weeks of lovastatin (20 mg per day) on platelet function and thromboxane formation in 18 patients with type II hypercholesterolaemia in a double-blind, placebo-controlled, prospective study. Lovastatin significantly reduced total serum and LDL-cholesterol by 20% and 25% respectively. Washed platelets of lovastatin-treated patients had significantly reduced collagen-induced aggregation and thromboxane formation ex vivo. There was no change in ADP-induced platelet aggregation, but a significant increase in prostacyclin (iloprost)-stimulated platelet cyclic AMP concentrations in lovastatin-treated patients. This was associated with a significant increase in the number of prostacyclin receptors in platelet membranes prepared from lovastatin-treated patients. There was also an increase in platelet thromboxane receptors. There were no such changes in the placebo group. These data confirm our original observation of normalization of platelet function in hypercholesterolaemia by HMGCoA reductase inhibitors and suggest changes in platelet membrane composition at the megakaryocyte level as a possible site of action.

Adolescent↗
PubMed1983

Aggregation of equine platelets by PAF (platelet-activating factor).

Platelet-activating factor (PAF), a lipid released as a result of immediate allergic reactions from basophils and mast cells as well as by a variety of other cell types and stimuli, is one of the most potent platelet agonists and hypotensive agents known. Equine platelets stimulated over a wide range of PAF concentrations aggregated in a time- and dose-dependent manner. Maximum aggregation was observed at concentrations of PAF as low as 3.58 x 10(-14) M with platelet-rich plasma (PRP) and 3.58 x 10(-16) M with washed platelets. Furthermore, the aggregation observed did not appear to be breed-dependent. Finally, the platelet arachidonate pathway appeared to play no role in PAF-induced aggregation as exogenous arachidonate did not enhance the reaction, nor were equine platelets pretreated with 38 microM aspirin inhibited in their response to PAF. This level of aspirin totally inhibited the equine platelet aggregation response to arachidonate.

Animals↗