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PubMedDate not supplied

Effect of heparin reversal and fresh platelet transfusion on platelet emboli post-cardiopulmonary bypass in a pig model.

Heparin reversal by protamine and fresh platelet transfusion may decrease bleeding complications post-cardiopulmonary bypass (CPB) and may increase the level of organ trapped platelet emboli. Platelet emboli were quantified in two groups of 12 Yorkshire pigs (30-35 kg), where 111indium labeled autologous platelets (INPLT: 850-1,200 microCi) were injected intravenously before and after CPB (BCPB, ACPB), and the platelet emboli level in intact organs and their samples (brain, heart, kidneys, lung, liver, and spleen) was quantified with an ion chamber and a gamma counter, respectively. All pigs were systemically heparinized (ACT > 400 sec). CPB was carried out at 2.5-3.5 L/min at 28 degrees C using a centrifugal pump, an oxygenator (OX:Bentley Univox 1.8 m2), an arterial filter (AF:0.25 m2), and a cardiotomy reservoir (CR: BMR 250) for 90 min. Heparin was reversed with an equivalent dose of protamine. The percent of INPLT dose (ID%, mean +/- SD) in organs of BCPB and ACPB pigs was calculated. The sequence of platelet emboli on a unit weight basis (ID%/g) had the following order: Spleen > Liver > Lung > Kidneys > Heart > Brain. The presence of significantly higher levels of emboli in brain, heart, and kidneys in the ACPB than the BCPB group suggest that platelet transfusion after heparin reversal with protamine may increase the risk of platelet emboli. However, it is an acceptable risk for patients having bleeding complications post-CPB.

Animals↗
PubMed1994

Platelet-derived adenosine contributes to the cardioprotective effects of platelets against ischemia-reperfusion injury in isolated rat heart.

Platelets have been shown to protect isolated perfused rat hearts from injury and dysfunction after ischemia and reperfusion. We examined the role of platelet-derived adenosine in the cardioprotective effects of platelets against reperfusion injury. Isolated perfused rat hearts were subjected to 40-min global ischemia followed by 30-min reperfusion. The buffer-perfused hearts developed dysfunction, as indicated by 40 +/- 4% decrease in force of cardiac contraction (FCC) and 24 +/- 3% increase in coronary perfusion pressure (CPP). Creatine kinase (CK) was released in coronary effluent during reperfusion, indicating myocardial injury. At the end of reperfusion, myocardial CK content and superoxide dismutase (SOD) activity were lower than in sham ischemia-reperfused hearts. Perfusion of hearts with washed platelets resulted in protection against myocardial dysfunction and injury after ischemia and reperfusion, indicated by preservation of FCC (-2 +/- 5%) and CPP (-3 +/- 2%) (both p < 0.01 vs. buffer-perfused hearts). Myocardial CK and SOD activity were also preserved, and release of CK in the coronary effluent was minimal (all p < 0.05 vs. buffer-perfused hearts). The cardioprotective effects of platelets were attenuated by preincubation of platelets with adenosine deaminase. Perfusion with adenosine or the adenosine2 receptor agonist N6-[2-(3,5-dimethoxyphenyl)-2-(2- methylphenyl)-ethyl]adenosine (DPMA) also protected heart from myocardial dysfunction and injury after ischemia and reperfusion. Both adenosine and DPMA had salutary effects on indexes of cardiac injury. Platelet-derived adenosine contributes at least in part to the cardioprotective effects of platelets against ischemia and reperfusion in isolated rat heart.

Adenosine↗
PubMed1992

Initial platelet deposition at the human microvascular anastomosis: effect on downstream platelet deposition to intact and injured vessels.

Initial platelet deposition (PD) in and around the region of a small-vessel anastomosis may set the stage for thrombosis and tissue loss. To study this problem, a human vessel model (human placental artery, HPA) has been designed to mimic the vascular injuries attendant on clinical microsurgery. To perform these studies, dissected lengths of human placental artery were treated to provide the following four types of injury: group I: control, dissected but otherwise uninjured (N = 5); group II: distal portion of vessel endothelium removed (N = 5); group III: central anastomosis, distal endothelium intact (N = 7); and group IV: central anastomosis, distal endothelium removed (N = 4). Vessels were perfused with 25 ml human whole blood for 17 +/- 5 s at an average shear rate of 536 s-1. Vessels in groups I to IV were segmented at 2-cm intervals, and the number of 111In-labeled platelets was measured. Data from the following groups of exposure zones were pooled and analyzed: endothelium intact, endothelium absent, anastomosis present, postanastomosis with endothelium intact, and postanastomosis with endothelium absent. Significant numbers of platelets were found to attach to intact endothelium, indicating that ischemia and microsurgical handling may augment platelet deposition to otherwise uninjured vessels. A similar degree of platelet deposition was measured after exposure of the subendothelium and perfusion, indicating that superficial subendothelial exposure in the absence of an additional prothrombotic stimulus may lead to no greater platelet deposition than occurs on slightly injured endothelium alone. Platelet deposition at anastomoses was strikingly elevated, although the anastomosis had no additive effect on platelet deposition to downstream endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)

Anastomosis, Surgical↗
PubMed1981

Two platelet aggregation inhibitors in tsetse (Glossina) saliva with studies of roles of thrombin and citrate in in vitro platelet aggregation.

Two inhibitors of platelet aggregation have been identified in saline extracts of Glossina morsitans (tsetse) salivary glands. A protein fraction (MW greater than 30 000) inhibited primary and secondary aggregation to ADP, secondary aggregation to adrenalin, and aggregation to collagen. It also caused disaggregation of platelets stimulated by ADP and adrenalin. These properties could be explained by ADP hydrolytic activity. A previously identified antithrombin fraction (MW 11 000-13 000) abolished thrombin-induced aggregation. It did not affect platelet aggregation to ADP, adrenalin or collagen, as compared to aggregation in citrate, when used as sole anticoagulant for platelet rich plasma or when added to citrated platelet rich plasma. These results fail to support hypotheses (i) that thrombin plays an important role in platelet aggregation by other agonists and (ii) that secondary platelet aggregation is an artefact induced by citrate. It is proposed that these inhibitors may be important in maintaining mouthpart and crop patency during feeding. Their discovery suggests that other arthropods may also have antiplatelet agents in their saliva which might be entomologically important, provide useful tools for platelet studies, and be of potential therapeutic interest.

Animals↗
PubMed1975

Immunofluorescence microphotometry for the detection of platelet antibodies. III. Demonstration of autoantibodies against platelets.

After a survey of the literature dealing with the demonstration of platelet autoantibodies by immunofluorescence techniques, the results are given of a study in which immunofluorescence microphotometry was used for this purpose. The serum of 58, the platelets of 34, and the megakaryocytes of 2 patients with thrombocytopenia were investigated. In 21 of 52 sera (40%) in which the presence of platelet autoantibodies could be expected, positive results were obtained that could not be due to isoantibodies, either because the patients had not been pregnant and had not received blood transfusions or because the reactivity of the serum with the patient's own platelets was demonstrated. The platelets of 28 patients with thrombocytopenia not due to a platelet defect or decreased thrombopoiesis were investigated. In the platelets of 15 (54%) of these, significant differences in fluorescence were found with anti-immunoglobulin conjugate as well as with anti-IgG, -IgA, -IgM, or -complement reagents. It was concluded that in these patients in vivo sensitization of the platelets with autoantibody was demonstrated. In two patients an indication of the in vivo sensitization of the megakaryocytes was also obtained.

Antibodies, Anti-Idiotypic↗
PubMed1980

HLA antigens of platelets. IV. Influence of "private" HLA--B locus specificities on the expression of Bw4 and Bw6 on human platelets.

Quantities of the HLA--B antigens B5, B7, B8, B13, B27, and Bw44 were determined on platelets of subjects heterozygous for those markers using an assay based on inhibition of antibody-mediated 51Cr release from lymphocytes. In confirmation of previous studies, Bw44 was found to vary about 35-fold and B8 about 8-fold. In contrast, B5, B7, B27, and B13 varied only 2--3-fold. Expression of each of the six antigens was proportional to that of its associated broad specificity, Bw4 or Bw6. The antigens Bw4 and Bw6, when measured directly on platelets of 62 normal heterozygous subjects, were found to vary 32-fold and 20-fold, respectively. Bw4 was strongly expressed on platelets carrying B5 or B27 (P less than 0.001), was weakly expressed in the presence of B13 (P less than 0.001) and was variable, possibly bimodal, in the presence of Bw44. Bw6 was strongly expressed on platelets carrying B7, Bw15.1, or Bw35 (P less than 0.01) but was weak on platelets carrying B8 or B14 (P less than 0.01). Little or no variation in Bw4 or Bw6 was observed on lymphocytes of the same donor population. These findings are consistent with the possibility that private HLA--B locus specificities influence the expression of part or all the HLA--B molecule on the platelet surface through an undetermined mechanism. The atypical behavior of Bw44/Bw4 on platelets suggests the possibility that Bw44 consists of two subspecificities not yet detectable with available serologic reagents. Variability of HLA markers in tissues other than platelets could have important immunobiologic implications which seem deserving of further investigation.

Blood Platelets↗
PubMed1996

Coagulation factor activation in stored platelet concentrates is modulated by the platelets.

To assess alterations in coagulation proteins in stored platelet concentrates, we used a series of platelet parameters and measures of coagulation activation to compare samples collected before unit donation, during the processing of platelet concentrates (PC) from CPDA-1 blood, and in storage up to 5 days as well as stored platelet-poor plasma (PPP). Storage-dependent increases in activated partial thromboplastin time and prothrombin time were seen in both PC and PPP. However, FVII, FXI, FXII, kallikrein activity and prothrombin F1.2 levels remained unchanged in stored PC. Surprisingly, in stored PPP, significant alterations in FXII, FVII, kallikrein and prothrombin F1.2 levels were seen. Platelet morphology and surface marker studies demonstrated platelet activation during storage. These data suggest that the presence of platelets in the CLX storage container partially suppresses coagulation activation at significant cost to platelet viability.

Blood Coagulation↗
PubMed1981

The human platelet as a model for the glutamatergic neuron: platelet uptake of L-glutamate.

L-Glutamate uptake into human platelets revealed two components: a high-affinity system (KmH = 3.1 microM), which was sodium-dependent, and a low-affinity site (Km = 88 microM) displaying temperature rather than sodium dependency. These kinetic properties were similar to those found in crude synaptosomal preparations and brain slices. However, Vmax values were far higher in brain (VmaxH = 325 +/- 96, VmaxL = 3759 +/- 1116 pmol/mg wet weight per min) than in platelets (VmaxH = 14 +/- 6, VmaxL = 313 +/- 63 pmol/mg platelet protein per 10 min), indicating a denser population in brain than in platelets of qualitatively similar sites. Pharmacological analysis substantiated the resemblance of nerve endings and platelets: the specific uptake inhibitors threo-3-hydroxy-DL-aspartate and DL-aspartate-beta-hydroxamate as well as D- and L-glutamate and L-aspartate showed similar--though not identical-- IC50 values in both preparations; a spectrum of compounds devoid of inhibitory effects in synaptosomes also did not interfere with glutamate uptake in platelets. Uptake parameters were studied in a population of human volunteers to determine the variability of platelet glutamate uptake. Whole blood could be stored up to 6 h after venipuncture without any appreciable change in experimental values. Percentage of variation between 0.09 and 0.28 for three repetitive (weekly) assays in single subjects indicated that glutamate uptake measurements in human platelets are sufficiently suited for future clinical studies.

Animals↗
PubMed1968

Platelet adhesiveness: the effect of centrifugation on the measurement of adhesiveness in platelet-rich plasma.

Platelet adhesiveness has been measured in citrated whole blood and in platelet-rich plasma obtained from normal subjects, splenectomized patients, and from patients in whom the diagnosis of recurrent venous thrombosis had been made. The duration of centrifugation used in the preparation of platelet-rich plasma was found to have a profound effect on the measurement of platelet adhesiveness because the figure for platelet adhesiveness measured in platelet-rich plasma obtained by centrifugation was considerably lower than that found in citrated whole blood. This effect was particularly marked when platelet-rich plasma was obtained from subjects in whom platelet adhesiveness measured in whole blood was increased.

Blood Cell Count↗
PubMed1981

Biochemical abnormalities of platelets in renal failure. Evidence for decreased platelet serotonin, adenosine diphosphate and Mg-dependent adenosine triphosphatase.

The platelet content of adenosine triphosphate (ATP), adenosine diphosphate (ADP), serotonin and ouabain-insensitive, magnesium-dependent adenosine triphosphatase (ATPase) was determined in patients with chronic renal failure, patients on chronic hemodialysis, and kidney transplant recipients. Platelet ATP content was normal in all. By contrast, ADP content, expressed in mumol/10(11) platelets, was significantly lower in renal failure: 1.82 +/- 0.96 compared to 2.51 +/- 0.97 in normals (p less than 0.05), but not in dialyzed or transplanted patients; 2.27 +/- 0.96 and 1.87 +/- 0.87, respectively. The mean content of serotonin was also significantly lower in renal failure patients: 0.52 microgram/10(9) platelets as compared to 0.90 microgram/10(9) platelets in normals (p less than 0.05) but was not significantly different in dialyzed and transplanted patients. ATPase was significantly lower in renal failure: 3.13 +/- 1.2 mumol Pi/10(9) platelets in whole suspension and 0.71 +/- 0.22 Pi/mg protein/h in membrane preparation compared to 4.74 +/- 1.1 and 1.18 +/- 0.19, respectively, in normals, and was significantly lower in dialyzed and transplanted patients. Experimental azotemia (BUN 65-86 mg/100 ml), induced by the oral ingestion of urea 2-3 g/kg body weight over 24 h, failed to induce any of these abnormalities. The abnormality in platelet ADP and serotonin content in renal failure paralleled the functional platelet defects which characterize these patients and were reversible following dialysis and transplantation.

Adenosine Diphosphate↗
PubMedDate not supplied

Effect of pre-incubation at 37 degrees C of platelet concentrates on the post-transfusion platelet adhesion capacity to collagen and fibrinogen.

The effect of warming (37 degrees C) of stored platelet concentrates (PC) on the post-transfusion platelet function as measured by the adhesion capacity in a rectangular perfusion system under flow conditions was analyzed in 22 patients undergoing transfusion for stable thrombocytopenia. Nine patients received a PC stored at 22 degrees C and incubated at 37 degrees C for 1 h before transfusion, 10 patients received a non-warmed PC, 3 patients received both a pre-warmed and a non-warmed PC. In the PC the platelet adhesion capacity to collagen was higher in the pre-warmed PC than in the non-warmed PC (33 +/- 5.9% coverage vs. 22 +/- 4.7% coverage, respectively, in a selected group with the same platelet concentration). The adhesion capacity to collagen of the platelets in the patient's blood, measured 10 min after transfusion, had increased considerably in both patient groups and 4 h later the adhesion capacity in both patient groups was similar to that of the pre-warmed PC before transfusion. We conclude that though pre-warming of stored PC had a beneficial effect on the adhesion capacity to collagen of the platelets in the PC, the clinical significance is questionable because already 10 min after transfusion the adhesion capacity to collagen of stored non-warmed platelets had improved to the level of the pre-warmed platelets and 4 h after transfusion this improvement was still present.

Adult↗
PubMed1986

Role of platelets and platelet inhibitors in aortocoronary artery vein-graft disease.

To study the prevention of occlusion of aortocoronary-artery bypass grafts, we conducted a prospective, randomized, double-blind trial comparing long-term administration of dipyridamole (begun 2 days before operation) plus aspirin (begun 7 hr after operation) with placebo in 407 patients. Results at 1 month and at 1 year showed a reduction in the rate of graft occlusion in patients receiving dipyridamole and aspirin. On the basis of our clinical trial and our experimental studies in dogs and pigs, we describe four consecutive phases of aortocoronary artery bypass vein-graft disease: an early postoperative phase of platelet thrombotic occlusion, which is significantly prevented by platelet inhibitor therapy when started in the perioperative period; in addition, occlusion rates are presently decreasing, perhaps related to better surgical and technical experience; an intermediate phase of platelet-related intimal hyperplasia, within the first postoperative year, which is not prevented with platelet inhibitor therapy; a late phase of occlusion, toward the end of the first postoperative year, in which intimal hyperplasia or complicating platelet thrombi superimposed on the intimal hyperplasia may contribute to occlusion; platelet inhibitor therapy is of significant benefit in the prevention of this thrombotic type of occlusion; a phase of atherosclerotic disease, after the first postoperative year, in which the role of platelets and of platelet inhibitor therapy is under investigation.

Animals↗
PubMed1991

Enhancement of platelet reactivity and modulation of eicosanoid production by intact erythrocytes. A new approach to platelet activation and recruitment.

Erythrocytes are known to influence hemostasis. Bleeding times are prolonged in anemia and corrected by normalizing the hematocrit. We now demonstrate that intact erythrocytes modulate biochemical and functional responsiveness of activated platelets. A two-stage procedure, permitting studies of cell-cell interactions and independently evaluating platelet activation and recruitment within 1 min of stimulation, was developed. Erythrocytes increased platelet serotonin release despite aspirin treatment, enzymatic adenosine diphosphate removal, protease inhibition, or combinations thereof. The data suggested that erythrocyte enhancement of platelet reactivity can reduce the therapeutic effectiveness of aspirin. Erythrocytes metabolically modified platelet arachidonate or eicosapentaenoate release and eicosanoid formation. They promoted significant increases in cyclooxygenase and lipoxygenase metabolites upon platelet stimulation with collagen or thrombin. However, with ionophore, erythrocytes strongly reduced platelet lipoxygenation. These erythrocyte modulatory effects were stimulus-specific. Activated platelet-erythrocyte mixtures, with or without aspirin, promoted 3-10-fold increases in extracellular free fatty acid, which would be available for transcellular metabolism. Erythrocyte-induced increases in free eicosapentaenoate may contribute to antithrombotic and anti-inflammatory effects of this fish oil derivative. These results provide biochemical insight into erythrocyte contributions to thrombosis and hemostasis, and support the concept of thrombus formation as a multicellular event.

Adenosine Diphosphate↗
PubMed1993

Low shear stress can initiate von Willebrand factor-dependent platelet aggregation in patients with type IIB and platelet-type von Willebrand disease.

Platelets exposed to shear stress aggregate in the absence of exogenously added agonists, utilizing distinct platelet membrane receptors and ligands depending upon the level of shear stress applied. Using a modified cone and plate type viscometer, we previously demonstrated that, under low shear stress (18 dyn/cm2), aggregation is mediated by platelet membrane glycoprotein (GP) IIb-IIIa and fibrinogen, whereas aggregation induced by high shear stress (108 dyn/cm2) requires the binding of von Willebrand factor (vWF) to both GPIb-IX and GPIIb-IIIa (Ikeda, Y., M. Handa, K. Kawano, T. Kamata, M. Murata, Y. Araki, H. Anbo, Y. Kawai, K. Watanabe, I. Itagaki, et al. 1991. J. Clin. Invest. 87:1234-1240). Here we report that vWF-dependent aggregation occurs under low shear stress in citrated platelet-rich plasma (PRP) from two types of congenital bleeding disorders, platelet-type von Willebrand disease (vWD) and type IIB vWD, in both of which ristocetin-induced aggregation is known to be heightened. Aggregation induced by low shear stress was enhanced in both types of disorders compared to normal controls, and the enhancement was completely abolished by anti-vWF monoclonal antibody NMC-4, which blocks the GPIb-binding site on vWF. Under high shear stress, the extent of maximal aggregation was not different between controls and the patient groups although maximal aggregation was reached much more quickly in the latter. When citrated PRP was exposed to a gradient of shear stress (6 to 108 dyn/cm2 over a 5-min period), vWF-dependent aggregation, as judged from the inhibitory effect of NMC-4, first occurred at 14 dyn/cm2 in platelet-type vWD and at 10-12 dyn/cm2 in type IIB vWD, as compared with more than 81 +/- 20.1 dyn/cm2 in control platelets. These results suggest that an abnormality in either vWF or GPIb-IX triggers the aggregation-inducing interaction of the two molecules under low shear stress, which might explain the intravascular platelet clumping, that presumably underlies the thrombocytopenia observed in these bleeding disorders.

Humans↗
PubMed1985

Evidence of enhanced platelet aggregation and platelet sensitivity in migraine patients.

In fourteen untreated migraine patients with a mean age of 40 years platelet sensitivity to 5HT, EN and ADP was investigated during the prodromal phase (three patients), 12-48 h after headache (three patients) and during the headache-free period (eight patients). Platelet sensitivity was tested using an optical density method and was calculated by the percentage of disaggregation (%DA) occurring 3 min after the peak aggregation. Platelet release reaction was assessed using beta-thromboglobulin (beta-TG) as an indicator. Platelet sensitivity to low concentrations of 5HT, EN and ADP (0.3 X 10(-9) M/ml) was most marked during the headache and prodromal phases. The least platelet sensitivity in migraineurs was detected during the headache-free interval, but was still higher than in the control group. beta-TG levels were increased during the headache phase indicating platelet release reaction. A general hyperaggregability of platelets in migraineurs has been demonstrated and in addition a varying sensibility of platelets to low concentrations of 5HT, EN and ADP has been established.

5-Hydroxytryptophan↗
PubMed1978

Platelet-mediated pulmonary hypertension and hypoxia during pulmonary microembolism: reduction by platelet inhibition.

The literature indicates that vasoactive substances released from platelets contribute to the pulmonary pressor response and hypoxemia during pulmonary microembolism. Hence, removal of the platelets or inhibition of their function should reduce these effects. The purpose of this study was, therefore, to investigate the pulmonary effects of experimental embolism with glass beads in dogs rendered thrombocytopenic with platelet antiserum and to compare these effects to the effects in dogs pretreated with sulfinpyrazone (Anturane) or heparin, both substances that affect the function of platelets, probably by inhibiting the release of platelets. In all three groups the pulmonary hypertension was reduced by more than half, and hypoxemia was lessened or abolished. The results of this study indicate the platelets contribute to the effects of pulmonary microembolism and that administration of sulfinpyrazone or heparin reduces the embolism-induced pulmonary hypertension to the same extent as the depletion of platelets. Platelet-inhibiting drugs might therefore be useful prophylactically in human pulmonary microembolism.

Animals↗
PubMed1984

Determination of low affinity platelet factor 4 in frozen and thawed human platelets by the newly developed enzyme immunoassay system.

By the use of a newly developed sandwich enzyme immunoassay method for low affinity platelet factor 4 (LA-PF4), the effects of repeated freeze-thawing on the contents of this protein in platelets were determined and compared with those of Triton-X 100 lysed platelets. The assay system consisted of polystyrene balls covered with immobilized antibody fragments F(ab')2 and the same antibody Fab' labeled with beta-D-galactosidase from E. coli. The assay was specific to LA-PF4 with no significant cross-reactivity with platelet factor 4. Coefficients of variation within-run and between-run for the assay of LA-PF4 were less than 12%. The results obtained with this enzyme immunoassay correlated well with those of a radioimmunoassay of beta-thromboglobulin which is immunologically identical with LA-PF4 (r = 0.961, slope = 1.056, y-intercept = -3.739 ng/ml; n = 22). The contents of LA-PF4 per 10(9) Triton-X 100 lysed platelets in platelet-rich plasma were 23.65 +/- 3.14 micrograms (mean +/- S.D.). The contents of LA-PF4 in platelets were increased from 46% to 95% of Triton-X 100 values by repeated freezing and thawing 1 to 7 times. The present data indicate that the freeze-thawing technique should be done carefully to obtain the reliable determination of LA-PF4 in platelets.

Blood Coagulation Factors↗
PubMed1985

Monomeric and polymeric collagen-induced platelet aggregation in citrated and heparinized platelet-rich plasma.

The physical and chemical properties of Type I bovine collagens were studied in relation to their platelet aggregating activity in citrated and heparinized human platelet-rich plasmas (PRP). Despite close similarities in physical and chemical properties, significant differences were found in platelet aggregating potency between two monomeric atelocollagens. Skin atelocollagen was a potent and corneal atelocollagen was a very weak inducer of platelet aggregation in citrated and heparinized PRP. In a polymeric form, however, corneal atelocollagen was a stronger platelet aggregating agent than monomeric skin acid-soluble or atelocollagen. Removal of the telopeptides altered some of the characteristics of the platelet aggregation induced by monomeric skin collagen. The rate and maximum extent of aggregation were the same with skin acid-soluble (intact) and atelocollagens in either type of PRP, but the lag periods and aggregation times were longer in citrated and somewhat shorter in heparinized PRP with skin atelocollagen than with acid-soluble collagens. The possible mechanisms leading to the differences observed in platelet aggregating activity of collagens in different physical states and from different tissues, and their distinct platelet aggregation patterns in differently anticoagulated PRP, are discussed.

Adult↗