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PubMed1987

Effects of treadmill and pacing stress testing on peripheral arterial thromboxane, platelet function and catecholamine activities in patients with chronic coronary artery disease.

Two different methods of causing myocardial oxygen demand and supply imbalance; symptom limited treadmill exercise and right atrial pacing stimulation, were used to examine the alteration of hemodynamics and the effects upon sympathetic nerve activities, platelet functions and prostaglandin synthesis in patients with coronary artery disease (CAD). Age and sex distributions, the cardiothoracic ratio, left ventricular end-diastolic pressure, ejection fraction and coronary artery obstructions of the patients did not differ significantly between the two tests. Arterial blood samples were obtained to assay for plasma catecholamine, beta-thromboglobulin (beta TG), platelet factor 4 (PF4), TXB2 (thromboxane B2) and 6 keto-PGF1-alpha (6 ketoprostaglandin F1-alpha) without any difficulties before and immediately after testing. The arterial systolic pressure and pressure rate product (PRP) were changed more significantly by treadmill exercise than pacing, while the DPTI/TTI (diastolic pressure time index/tension time index) ratio and ST segment deviations showed similar changes with both tests. The plasma NE (norepinephrine) level, beta TG, PF4, and TXB2/6 keto-PGF1-alpha were significantly elevated by treadmill exercise, but not by pacing. 6 keto-PGF1-alpha was not markedly affected by either tests. There were no significant differences between the patients with and without anginal pain either in hemodynamics or metabolites. Significant relationships were observed between changes in plasma NE levels and the PRP (r = 0.76, n = 26, p less than 0.01) and also changes in the arterial systolic pressure (r = 0.64, n = 26, p less than 0.01), but there were no significant correlations between any other hemodynamic parameters with plasma NE, platelet function, prostaglandin activity, or between each metabolite.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed2000

Anesthetic implications of the grey platelet syndrome.

PURPOSE: To describe the obstetrical anesthetic care provided to two sisters with a rare qualitative platelet disorder, the grey platelet syndrome (GPS). CLINICAL FEATURES: Both patients manifested thrombocytopenia prior to delivery without previous history of a bleeding diathesis or other abnormal laboratory tests of coagulation function. The first required emergency Cesarean section due to fetal bradycardia. Due to the thrombocytopenia and the emergency nature of the procedure, general anesthesia was used. During the C-section, 1.5-2 litres of old blood was noted in the abdominal cavity which was attributed to an old splenic capsular tear of unknown etiology. Work-up for the thrombocytopenia revealed large platelets on the peripheral smear with abnormal aggregation on platelet function studies. Electron microscopy of the platelets revealed absent alpha granules, diagnostic of GPS. The second patient, the sister of patient #1, presented in a similar fashion. However, at presentation, the platelet count was 112,000 x m(-3) and spinal anesthesia was provided without complication for Cesarean delivery. The same patient presented for a second delivery during which fetal bradycardia necessitated emergency C-section under general anesthesia. Despite administration of six units of platelets, blood loss was 5,200 mL. Her postpartum course was uncomplicated and she and the infant were discharged home on postoperative day #4. CONCLUSION: The primary concerns for the anesthesiologist looking after patients with qualitative platelet defects are related to defective coagulation which influences the need for perioperative replacement of blood products and limits the use of regional anesthesia.

Adult↗
PubMed2002

Hypertonic resuscitation and blood coagulation: in vitro comparison of several hypertonic solutions for their action on platelets and plasma coagulation.

Resuscitation with hypertonic saline (HS) appears to aggravate bleeding in a model of uncontrolled hemorrhage [J. Trauma 28 (1988) 751; J. Trauma 29 (1989) 79; Arch. Surg. 127 (1992) 93]. This property may be related to the anticoagulant effects of HS on plasma clotting factors and platelets [J. Trauma 31 (1991) 8]. The hypothesis in this study is that a hypertonic solution can be developed that would not disturb the blood coagulation mechanism and could be used as an alternative to hypertonic saline.HS and four different 2400 mosM solutions containing monosaccharides and/or glycine were screened for their in vitro effects on plasma clotting times and platelets. Significant prolongations falling outside the normal range were detected in prothrombin time (PT) and thrombin rime (TT) when only 5% of the volume of normal plasma is HS. Platelet function as measured by extent of shape change (ESC) induced by ADP and aggregation induced by thrombin were also critically impaired by HS at a 5% dilution. All alternative solutions-hypertonic glucose, sorbitol, glycine, glucose/glycine, glucose/mannitol/glycine, sorbitol/glycine-caused a significantly reduced impairment in platelet function and the plasma coagulation system. Hypertonic glycine showed a unique ability to fully preserve the function and integrity of the plasma coagulation system. Considering the pre-deposition of the trauma patient to coagulopathy, administration of HS which clearly is a potent anticoagulant and anti-platelet risks further aggravating the coagulopathy. In contrast, hypertonic glycine preserves the blood coagulation mechanism and exhibits the potential for numerous therapeutic applications. Therefore, prompt evaluation of hypertonic glycine as a resuscitative fluid is highly desirable.

Blood Coagulation↗
PubMed2003

A new platelet parameter, the mean platelet component, can demonstrate abnormal platelet function and structure in myelodysplasia.

The mean platelet component (MPC) is a new platelet parameter generated by the Bayer ADVIA 120 full blood count analyser as part of the routine complete blood count (CBC) test cycle. We report a case of myelodysplasia with bleeding complications and abnormal template bleeding time in whom low mean platelet component parameters were associated with partial platelet granule deficiency, demonstrated by transmission electron microscopy. We suggest that the mean platelet component is an inexpensive and rapid test to screen for platelet dysfunction related to ultrastructural abnormalities in myelodysplasia.

Blood Platelet Disorders↗
PubMed1997

Megakaryocytes and platelets in myeloproliferative disorders.

Increased megakaryocyte (MK) proliferation in bone marrow is a feature common to the three Ph-negative myeloproliferative disorders (MPDs), i.e. essential thrombocythaemia (ET), polycythaemia vera (PV), and myelofibrosis with splenic myeloid metaplasia (MMM), and to chronic myelocytic leukaemia (CML). Enlarged MKs with multilobulated nuclei and cell clustering in close proximity are the hallmark of all the Ph negative MPDs. Clonality of haematopoietic cells, based on X chromosome inactivation, can now be studied in a majority of female patients in all nucleated cell fractions as well as in platelets. Cytofluorometric studies have demonstrated a shift towards higher ploidy classes in PV and ET MKs which may be useful in discriminating between both primary and reactive thrombocytosis and CML patients which show a significant shift to lower MK ploidy values. The role of MK proliferation on the evolution of myelofibrosis common to MPDs has been firmly established. Implication of platelet-derived growth factor (PDGF) in myelofibrosis has already been demonstrated. More recently transforming growth factor beta (TGF beta) synthesized and secreted by MK has been implicated in fibroblasts stimulation. A significant increase in circulating colony-forming units of MKs (CFU-MK) has been repeatedly observed in MPDs as well as a spontaneous MK colony formation in a majority of ET patients. Hypersensitivity to thrombopoietin (TPO) in relation to a functional defect of the TPO-MPL pathway may play a major role in spontaneous MK growth. There is no currently available test of platelet functions able to predict the risk of occurrence of thrombotic or haemorrhagic complications in MPD patients. However, the role of platelet activation in the pathogenesis of ischaemic erythromelalgia has been established and a correlation between presenting haemorrhagic manifestations and platelet counts in excess of 1000 x 10(9)/l has been found.

Blood Platelets↗
PubMed1981

A practical approach to disorders of hemostasis.

Simple screening tests are available to detect abnormalities in the plasma coagulation system and platelet function. Prothrombin time reflects the integrity of the extrinsic system, while activated partial thromboplastin time indicates whether the intrinsic system is intact. Thrombin clotting time is a measure of the integrity of the end stage of clotting. Prothrombin time is also helpful in monitoring warfarin therapy; either of the latter two tests can perform a similar function in patients receiving heparin. Ivy bleeding time is the best screening test of platelet function. If bleeding time is prolonged but results of plasma coagulation tests are normal, specialized platelet function tests may be necessary.

Adult↗
PubMed1986

Platelet damage by protamine and the protective effect of prostacyclin: an experimental study in dogs.

Protamine is given after cardiopulmonary bypass to reverse the effect of heparin. However, the adverse effects of an overdose have not been fully evaluated. In this canine study, a standard dose of one bolus of heparin (300 IU per kilogram of body weight) was neutralized by an infusion of protamine hydrochloride in a 1:2 ratio. Platelet number and function were severely reduced by this overdose of protamine, and this finding correlated with a prolongation of the bleeding time. Giving a titrated dose of protamine hydrochloride to reverse heparin activity, measured by the activated clotting time, affected neither platelet number nor function. When prostacyclin (0.5 microgram/kg/min) was infused during administration of an overdose of protamine, platelets again were not affected by the excess of protamine.

Adenosine Diphosphate↗
PubMed2006

[Influence of raising oxygen content on function of platelet concentrate during preservation].

To explore the influence of raising oxygen (dissolved oxygen) content on function of platelet concentrate, the platelet concentrate was prepared by a CS-3000 plus blood cell separator. Experiments were divided into 2 groups: test group and control group. After raising oxygen content in platelet plasma under sterile operation, the platelet samples of two groups were preserved in oscillator with horizontal oscillation at 22 +/- 2 degrees C. The platelet count, platelet aggregation rate, lactic acid content and CD62p expression level of platelet were detected on 0, 1, 2, 3, 4, 5 days of platelet preservation. The results showed that the platelet count and platelet aggregation rate decreased with prolongation of preserved time, while the lactic acid content and CD62p expression level of platelet increased gradually. Compared with control group, there were significant differences in aggregation rate of platelet preserved for 2-3 days, and in CD62p expression level of platelet preserved for 1-3 days, while significant difference was found in lactic acid content of platelet preserved for 1-3 days. It is concluded that raising content of oxygen in platelet plasma can provide more oxygen to compensate oxygen supply deficiency for platelet metabolism and improve the efficiency of platelet oxygenic metabolism and the quality of platelet during preservation.

Blood Platelets↗
PubMed2005

The platelet function analyzer (PFA-100): an update on its clinical use.

The platelet function analyzer, PFA-100, is a relatively new method which has been developed as a quantitative, simple and rapid in vitro tool of assessing primary hemostasis. The aim of this review is to summarize the published studies reporting on the utility of the PFA-100 device as a screening tool for primary hemostasis. Data were identified by searches of the published literature, including PubMed, references from reviews and abstracts from the most important meetings on this topic. The literature data document that the PFA-100 is a useful screening tool for the investigation of von Willebrand's disease and various acquired and congenital intrinsic platelet function disorders. It is also useful for evaluating primary hemostasis before surgical procedures and for monitoring desmopressin therapy in patients with type 1 von Willebrand's disease. Moreover, recent studies have shown its potential for therapeutic monitoring of the effectiveness of anti-platelet medications in cardiovascular disease management. Given its high sensitivity, speed and simplicity of use, we conclude that the PFA-100 could replace the in vivo bleeding time as a screening test for primary hemostasis in routine clinical practice.

Blood Platelet Disorders↗
PubMedDate not supplied

[Effect of ethyl alcohol on selected parameters of the hemostasis system in vitro].

Alcohol produces several disorders in all components of hemostasis system. However, its mechanism of action is not clear. Therefore, an effect of ethyl alcohol on the selected parameters of both platelet and plasma hemostasis has been examined in vitro. Blood aggregation induced by ADP and PAF and platelet-leucocytic aggregates have been determined in vitro in the group of 45 healthy volunteers. Out of plasma parameters the selected factors of blood coagulation and fibrinolysis have been examined. Results suggest that the examined concentrations of ethyl alcohol mainly affect platelet function decreasing platelet aggregation. Alcohol does not affect significantly blood coagulation and fibrinolysis occurring in vitro.

Adult↗
PubMed1987

[Diagnostic problems in disorders of thrombocyte functions].

Numerous specific methods have been introduced lately in the clinical practice allowing the determination of the exact defect in platelet functions of the patient. Those methods are divided in five groups: global methods in vivo and in vitro, methods reflecting the platelet adhesiveness, platelet aggregation, platelet secretion, platelet participation in coagulation. The author is one of the first that introduced the study on platelet aggregation and secretion by aggregometer as well as the study of factor VIII antigen and von Willebrand factor. The author, based on his experience, proposes a diagnostic constellation of tests for establishing the nature of platelet defect.

Blood Platelet Disorders↗
PubMed2006

Is chronic fatigue syndrome associated with platelet activation?

Chronic fatigue syndrome (CFS) is a debilitating condition that has no known aetiology or pathophysiology. Recent investigations by other workers have suggested that individuals with CFS may have a hypercoagulable state. This study investigated various aspects of platelet activation and function in 17 patients with CFS and in 16 age-matched and sex-matched healthy controls. Platelet aggregation, platelet volume and coagulation tests were performed. Platelet aggregation was investigated by means of the photometric changes using citrated platelet-rich plasma, whole blood aggregation was calculated as the percentage fall in single platelet counts and the coagulation tests were performed on an automatic microcentrifugal analyser.A trend was observed for the patients to have lower aggregation results and a reduced mean platelet volume. However, this only reached statistical significance for one result; the rate of the aggregation slope by 1.0 microg/ml collagen [CFS patients, 18 (9-28) versus controls, 32.5 (19-36); Mann-Whitney U test, P = 0.029]. No significant differences were found for any of the measurements of coagulation. These results are in contrast to previously reported findings. However, due to the heterogeneous nature of the disease, and the resulting lifestyles of the patients, caution should be taken when comparing one group of patients with another. Nevertheless, we certainly found no evidence of increased platelet activation or of a hypercoagulable state in patients with CFS and, on the basis of these results, anti-platelet or anti-coagulant therapy is not warranted.

Adult↗
PubMed1985

Long-term antiplatelet activity and safety of indobufen in patients with cardiovascular disease. Italian Multicenter Study Group.

An open collaborative study was performed to assess the long-term platelet inhibiting activity, tolerability and safety of indobufen, a new inhibitor of platelet aggregation. The drug was given orally to 151 patients with cardiovascular disease for a period ranging from 6 to 24 months (mean 12.5 months). Extensive clinical examination, laboratory investigations and platelet function studies were carried out before the treatment and at 1, 2, 3, 4, 5, 6, 8, 10, 12, 15, 18, 21 and 24 months. Indobufen, 200 mg b.i.d., exerted a prompt inhibitory effect on platelet adhesiveness and aggregation, normalized circulating platelet aggregates and slightly prolonged bleeding time. Five patients were withdrawn from the study due to the occurrence of drug-related, untoward clinical events. For the remaining patients there were no appreciable changes in standard laboratory tests. Gastrointestinal symptoms, generally minor and transient, were the most common complaints recorded during treatment. Compliance with therapy was excellent, as judged by residual tablet counts and platelet function studies. The data obtained in this study indicate that indobufen, 200 mg b.i.d., is associated with a marked inhibition of platelet function and the treatment is well tolerated and safe. Indobufen therefore may prove to be a useful drug in the management of patients with cardiovascular disease.

Adult↗
PubMed2006

Effects of external electrical stimulation on laser-beam-induced experimental thrombosis.

External electrical stimulation (EES) has demonstrated venous antithrombotic properties. The aim of this investigation was to study its antithrombotic properties using unfractionated heparin (UFH) as a reference in arterial and venous mesenteric microvessels. For this purpose a rat model of laser-beam-induced thrombosis was used. Four groups of rats were investigated (n = 7): control, UFH (5 mg /kg), UFH (2.5 mg/kg) and electrical stimulation [e-vascular, E = 10, alternate polarity, in two protocols: (i) 30 min before and during thrombosis induction and (ii) only 30 min before thrombosis induction as preventive stimulation]. This effect was tested in arterial and venous microvessels in the four groups using the continuous protocol and only in arterial microvessels using the preventive protocol. Three parameters were studied: the number of laser beams needed to induce platelet thrombus formation, the number of emboli and the duration of embolization. Induced hemorrhagic time (IHT), platelet aggregation induced by ADP and coagulation tests (activated partial thromboplastin time, aPTT, prothrombin time, pTT, and fibrinogen level) were also determined. Continuous electrical stimulation decreased the number of emboli and the duration of embolization both in arterioles and in venules. It also significantly reduced the amplitude and velocity of the ex vivo platelet aggregation induced by ADP. Contrary to UFH, neither aPTT nor pTT were affected in platelet-poor plasma collected after the induction of thrombosis by laser beam, nor did it modify IHT. Preventive electrical stimulation produced similar results with fewer effects on induced venous thrombosis. These data suggest that EES has a potent antithrombotic effect on arterial and venous thrombosis without any hemorrhagic adverse effects, making it a very promising tool in the prevention and treatment of venous and arterial thromboembolic complications.

Animals↗
PubMed1995

Techniques for evaluating the cause of bleeding in the ICU. Diagnostic clues and keys to interpreting hemostatic tests.

Begin by obtaining both a bleeding and a family history to help ascertain whether the disorder is acquired or inherited. On physical examination, look for multiple bleeding sites or profuse bleeding; these can indicate a systemic bleeding diathesis. Order hemostatic tests. Prolonged aPTT points to a defect in the intrinsic or common coagulation pathway; prolonged PT, to a defect in the extrinsic or common pathway. Thrombin time is abnormal when hypofibrinogenemia, afibrinogenemia, or thrombin inhibitors are present. Bleeding time is prolonged in thrombocytopenia, platelet dysfunction, severe hypofibrinogenemia, and von Willebrand's disease. Factor assays also may be needed to further define the defect.

Blood Coagulation Tests↗