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PubMed1988

[Thrombocyte function in essential thrombocythemia and reactive thrombocytosis].

Blood of 16 patients with essential thrombocythemia (ET), 9 patients with reactive thrombocytosis (RT) and 13 healthy persons was used for platelet aggregation studies. When the aggregation was induced with adenosine diphosphate (0.01 microM), collagen (0.1 micrograms/ml) or platelet activating factor (PAF 0.5 microM) the plasma of the patients with ET showed significantly decreased aggregation (35%-44% of the value for the control groups). Independent of inhibitors of platelet aggregation, thrombin (0.05 U/ml) caused similar aggregation in healthy controls and patients with ET; patients with RT showed an increase aggregation. Adrenalin-induced aggregation discriminated best between patients with ET and controls. Adrenalin in concentrations ranging from 0.01 micrograms/ml to 100 micrograms/ml caused comparable dose-related amounts of aggregation in healthy controls and patients with RT. Over the whole concentration range, patients with ET showed significantly decreased aggregation (28%-34% of the value for the control groups). This difference proved to be independent of the influence of inhibitors of platelet aggregation. Though concentrations of alpha1-acid glycoprotein never reached inhibitory levels in the plasma of patients with ET (n = 12) they were significantly higher compared with those in normal plasma (n = 12). Fibrinogen concentrations in plasma of ET-patients (n = 12) were in the normal range. Cellular adenosine 3'-5'-cyclic monophosphate concentrations in ET (n = 10) are comparable with normal values (n = 5). The significance of the results for diagnosis and better pathophysiological understanding of ET is discussed.

Blood Platelets↗
PubMed1993

The influence of aspirin on plasma and platelet catecholamine levels, and platelet function in normal man.

The aim of the study was to determine whether aspirin influences sympathoadrenal output in normal human subjects. Plasma and platelet adrenaline and noradrenaline levels were measured before and after chronic administration of oral aspirin (300 mg per day for 7 days). Catecholamine concentrations measured immediately following aspirin did not differ from control (pre-treatment) values. Platelet noradrenaline and plasma adrenaline levels were, however, significantly increased 2 weeks after cessation of treatment. Platelet TxB2 generation was significantly reduced following aspirin treatment indicating that platelet cyclooxygenase had been inhibited. Catecholamine concentrations did not correlate with TxB2 generation. In vitro platelet aggregation induced by ADP, adrenaline and collagen was reduced after aspirin providing additional confirmation of cyclooxygenase inhibition. However, the in vivo markers of platelet function, beta-TG and PF4 were unaffected. These data do not provide convincing evidence for an action of aspirin on sympathoadrenal outflow, either directly or via a prostaglandin (thromboxane) mediated effect, although this does not exclude a later, delayed effect. There was no evidence for interactions between thromboxane, catecholamine levels in plasma and platelets, and platelet function.

Adenosine Diphosphate↗
PubMed1983

Plasma levels of acetylsalicylic acid and salicylic acid after oral ingestion of plain and buffered acetylsalicylic acid in relation to bleeding time and thrombocyte function.

Buffered acetylsalicylic acid (Alka Seltzer, B-ASA) and plain aspirin (P-ASA) tablets were compared as to their effects on bleeding time and platelet function in eight healthy male volunteers. Two doses (500 and 1000 mg) of each preparation were investigated in a cross-over design, each volunteer being his own control in each dose group (n=4). Both preparations disturbed platelet aggregation to the same extent. Bleeding time increased after both preparations, though significantly more after the buffered preparation than after plain acetylsalicylic acid, irrespective of the dosage. The 1000 mg dose prolonged bleeding time significantly more than the 500 mg dose, irrespective of the preparation. Kinetic analysis showed that B-ASA gave higher peak plasma levels of acetylsalicylic acid (ASA) and accordingly salicylic acid peak levels were also higher after the buffered preparation. It is concluded that B-ASA in equi-analgesic doses prolongs bleeding time more than the plain preparation. Since it is less agressive on the gastro-intestinal mucosa, its use may be advantageous in situations where acetylsalicylic acid induced loss of platelet aggregation is desired. However, the risk of prolonged bleeding--e.g. after tooth extractions--is probably higher after the buffered preparation.

Adult↗
PubMed1989

Fish oil diet rich in eicosapentaenoic acid increases bleeding time in the rat by interaction with sympathetic transmitters.

The influence of a diet supplemented with MaxEPA (a fish oil concentrate, rich in eicosapentaenoic acid = EPA) on bleeding time in small mesenteric arteries of the rat and on formation of thromboxane B2 (TXB2) by ADP-stimulated platelets was investigated. Since EPA has been found to antagonize noradrenaline (NA) - induced vasoconstriction, the influences on bleeding time of the alpha-receptor antagonist phentolamine and of the adrenergic neuron blocking agent guanethidine alone as well as during dietary supplementation with MaxEPA were studied. Bleeding time slowly increased during the MaxEPA diet over a period of 12 weeks resulting in a final prolongation of about 75%. Indomethacin which dose-dependently increased bleeding time in control rats, further increased the already prolonged bleeding time in rats on the MaxEPA diet. Guanethidine prolonged bleeding time strongly in control animals but caused no further increase in those on the MaxEPA diet. Indomethacin also further increased the bleeding time prolonged by guanethidine, just as it did in animals on MaxEPA diet. In contrast to guanethidine, phentolamine prolonged bleeding time only slightly. The ability of platelets from rats on the diet to generate TXB2 was reduced to 59.5% but was more drastically reduced (to 26.7%) from rats pretreated with indomethacin. The results indicate that MaxEPA feeding prolongs bleeding time by a mechanism other than that of indomethacin. We speculate that EPA prolongs bleeding time rather by antagonizing the vasoconstrictor effect of sympathetic transmitters at the site of the injured vessel than by a reduced formation of TXA2.

Animals↗
PubMed1991

Hemostatic studies in patients with infective endocarditis: a report on nine consecutive cases with evidence of coagulopathy.

Local and generalized changes in coagulation may be important in the genesis of vegetations and embolism in infective endocarditis. To characterize such alterations, serial hematological investigations were performed on nine consecutive patients who satisfied the inclusion criteria. Platelet survival was measured by Indium111 labeling. Acute and convalescent samples were analyzed for fibrinogen, factor VIIIc, antithrombin III (AT III), fibrin/fibrinogen degradation products (FDPs), and platelet aggregation. The results suggest that in the active stage of the disease: (1) hypercoagulability may be caused by a rise in acute phase reactants, (2) an acceleration of coagulation and fibrinolysis may supervene, and (3) in some cases there is a reduction in platelet aggregation, possibly as a result of continued circulation of previously activated "exhausted" platelets.

Adult↗
PubMed1989

The effect of exercise on bleeding time and local production of prostacyclin and thromboxane.

Exercise at a heart rate corresponding to 30% VO2max for 15 min was associated with an increase in the volume of bleeding time blood from a mean of 133 microliters before exercise to a mean of 218 microliters during and immediately after the exercise. There was similarly an increase in thromboxane B2 production from 6.40 nmol.l-1 before to 11.50 nmol.l-1. Most subjects also showed an increase in the length of the bleeding time and in the production of bleeding time 6-keto-PGF1 alpha. The extent of increase in the bleeding time and in production of 6-keto-PGF1 alpha was quite variable, with subjects showing the largest increases in bleeding time also demonstrating the greatest increases in 6-keto-PGF1 alpha (r = 0.76, P = 0.004). The ingestion of aspirin before exercise markedly inhibited basal bleeding time thromboxane B2 production and blocked the exercise-associated increments in thromboxane B2 and 6-keto-PGF1 alpha production. While the aspirin itself increased the length of the bleeding time, there was not any further increase associated with exercise. In contrast to the effects of acute short-term exercise, long-distance running was associated with a significant decrease in bleeding time, but no change in bleeding time blood volume, bleeding time thromboxane B2, or bleeding time 6-keto-PGF1 alpha. The results show that acute low-level exercise can be associated with significant changes in the volume of blood oozing from a bleeding time incision and in the amount of thromboxane production stimulated at the incisional site. Following exhaustive exercise of long duration, the above changes are no longer seen.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Clinical application of a new in vitro bleeding time device on surgical patients.

A new in vitro bleeding time (BT) device was applied to various surgical patients. After setting the optimal assay condition, the normal in vitro bleeding time (T2) and volume (V2) were obtained from healthy volunteers, being 114.7 secs +/- 25.8 (SD) and 272.2 microliter +/- 69.1 (SD), respectively. When the T2 was below 210 secs, the platelet count was inversely proportional to the T2 and V2 of the in vitro BT with p less than 0.01. The value of the in vitro BT was not affected by heparin. Agents, which modify platelet functions, such as PGI2, DN9693 (an inhibitor of phosphodiesterase) and aspirin, prolonged the in vitro BT (T2, V2) dose-dependently. Administration of aspirin (660 mg) to volunteers prolonged the T2 from 108 to over 300 secs and the V2 from 253 to over 600 microliter but ticlopidine (500 mg/day for 3 days) had no effect. In 8 patients with liver cirrhosis who underwent hepatectomy, one patient with a prolonged T2 (260 secs) and a normal skin BT bled postoperatively, however, 3 patients with a prolonged skin BT (greater than 15 min) and a normal T2 had no hemorrhagic complications. From these observations it was concluded that in vitro BT is a convenient and useful tool to examine primary hemostasis or platelet function.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2005

Effects of total flavone of Abelmoschl Manihot L. Medic on the function of platelets and its mechanism.

OBJECTIVE: To study the effects of total flavone of Abelmoschl Manihot L. Medic (TFA) on the function of platelets and to explore its mechanism. METHODS: Rat models of artery-veins bypassing thrombus formation were used. The platelets of rabbits were collected. Platelet aggregation was induced by collagen and intracellular calcium ion concentration ([Ca(2+)]i) was assayed by Fura-2 method. RESULTS: TFA (25, 50, 100 mg/kg) significantly and dose-dependently reduced the weight of thrombus. TFA (0.025, 0.05, 0.1 mg/ml) possessed dose-dependant inhibitory effects on rabbits' platelet aggregation induced by collagen. TFA significantly reduced the resting and CaCl(2)-induced increase of free intracellular calcium concentration ([Ca(2+)]i) in rabbit platelet in vitro. CONCLUSION: TFA has an antiplatelet effect via the inhibition on the influx of Ca(2+).

Animals↗
PubMed2006

[Heparin-induced thrombocytopenia].

Heparins are in widespread use as anticoagulants for the prophylaxis and therapy of thromboembolisms. A dangerous side-effect is heparin-induced thrombocytopenia type II (HIT type II) with the paradox of thromboembolic venous and arterial vascular occlusions. HIT type II is an immunological disease which results in activation of platelets and plasma coagulation. The main symptom is an acute onset of thrombocytopenia with a fall in thrombocytes to less than 50% of the initial value with or without newly arising thromboembolic complications between days 5 and 14 after the start of heparin therapy. Surgery patients are more often affected by subclinical antibody formation as well as by symptomatic HIT type II than clinical patients. In this review we will discuss the difficult diagnosis and the differential diagnosis with special emphasis on postoperative intensive care patients, as well as preventive measures and management on occurrence of HIT type II and associated thrombotic complications.

Anticoagulants↗
PubMed1997

[Ultrasound examination of the liver in HELLP syndrome].

A 33-year-old multiparous woman in the 34th gestational week presented with severe upper abdominal pain, nausea and vomiting. Clinical examination revealed severe epigastric tenderness. Abdominal ultrasound examination showed geographical areas with increased echogenicity in the right lobe of the liver. Through haematological examination, we found severe thrombocytopenia and fibrinolysis. The diagnosis of HELLP syndrome was suspected and a caesarean section was performed. We suggest that obstetrical patients with upper abdominal pain and abnormal liver sonography should immediately be haematologically investigated to exclude the life-threatening condition of the HELLP syndrome.

Adult↗
PubMed2000

Sonoclot signature during normal pregnancy.

OBJECTIVE: The Sonoclot analyser provides global measurement of haemostasis, including plasma coagulation, platelet function and fibrinolysis. Benefits of its use in cardiovascular and hepatic surgery are well-documented and it may be useful in managing obstetric complications. The aim of this study was to determine ranges of the Sonoclot variables for normal pregnancy. DESIGN: Prospective and longitudinal study. SETTING: Antenatal outpatient clinic, university hospital. PATIENTS: Forty-seven healthy women were studied; forty-two completed normal pregnancies and gave birth to healthy infants. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Sonoclot signatures were performed at 10-15, 32-34 and 38-40 weeks of gestation and at 8 weeks postpartum. Haemoglobin concentration, haematocrit, platelet count, fibrinogen and activated partial thromboplastin time (APTT) were analysed with normal results. Sonact time and peak time were significantly decreased and clot rate and secondary rate were significantly increased during pregnancy compared with 8 weeks postpartum, indicating hypercoagulability. There were no significant changes in these variables during pregnancy. There were no changes in peak amplitude and downward rate. A significant correlation was found between sonact time and APTT, and between clot rate and APTT. CONCLUSIONS: We found the Sonoclot analyser simple to handle and the signatures easy to interpret. The ranges for the Sonoclot variables apply throughout pregnancy. The ranges for sonact time, clot rate, secondary rate and peak time during pregnancy differed from the ranges at 8 weeks postpartum.

Adult↗
PubMed1997

Does continuous heparinization influence platelet function in the intensive care patient?

OBJECTIVE: To study the influence of continuous administration of heparin on platelet function in intensive care patients. DESIGN: Prospective, serial investigation. SETTING: Clinical investigation on a surgical and neurosurgical intensive care unit in a university hospital. PATIENTS: The study included 45 patients: 15 postoperative with patients sepsis (Acute Physiology and Chronic Health Evaluation II score between 15 and 25), 15 trauma patients (Injury Severity Score 15 to 25), and 15 neurosurgical patients. INTERVENTIONS: Management of the patients was carried out according to the guidelines for modern intensive care therapy. Sepsis and trauma patients received standard (unfractionated) heparin continuously [aim: an activated partial thromboplastin time (aPTT) approximately 2.0 times normal value; sepsis-heparin and trauma-heparin patients], whereas neurosurgical patients received no heparin (neurosurgical patients). MEASUREMENTS AND RESULTS: From arterial blood samples, platelet aggregation was measured by the turbidimetric method. Platelet aggregation was induced by adenosine diphosphate (ADP; 2.0 mumol/l), collagen (10 micrograms/ml), and epinephrine (25 mumol/l). Measurements were carried out on the day of diagnosis of sepsis or 12 h after hemodynamic stabilization (trauma and neurosurgery patients) (baseline) and during the next 5 days at 12.00 noon. Standard coagulation parameters [platelet count and fibrinogen and antithrombin III (AT III) plasma concentrations] were also monitored. Heparin 4-10 U/kg per h (mean dose: approximately 500 U/h) was necessary to reach an aPTT of about 2.0 times normal. Platelet count was highest in the neurosurgical patients, but it did not decrease after heparin administration to the trauma and sepsis patients. AT III and fibrinogen plasma levels were similar in the three groups of patients. In the sepsis group, platelet aggregation variables decreased significantly (e.g., epinephrine-induced maximum platelet aggregation:-45 relative % from baseline value). Platelet function recovered during the study and even exceeded baseline values (e.g., ADP-induced maximum platelet aggregation: +42.5 relative % from baseline value). Continuous heparinization did not blunt this increase of platelet aggregation variables. In the heparinized trauma patients, platelet aggregation variables remained almost stable and were no different to platelet aggregation data in the untreated neurosurgical patients. CONCLUSIONS: Continuous administration of heparin with an average dose of approximately 500 U/h did not negatively influence platelet function in the trauma patients. Recovery from reduced platelet function in the sepsis group was not affected by continuous heparinization. Thus, continuous heparinization with this dose appears to be safe with regard to platelet function in the intensive care patient.

APACHE↗
PubMed2001

Decreased circulating levels of von Willebrand factor after intravenous administration of a rapidly degradable hydroxyethyl starch (HES 200/0.5/6) in healthy human subjects.

OBJECTIVE: Impairment of haemostasis has been described with slowly degradable medium molecular weight hydroxyethyl starch (MMW-HES), whereas rapidly degradable MMW-HES is generally considered to have no important effects on blood coagulation. This study was undertaken to investigate the effects of a rapidly degradable MMW-HES plasma substitute on primary haemostasis and blood coagulation in human subjects. DESIGN: Randomised, cross-over study. SETTING: Research unit of a university hospital. PARTICIPANTS: Nine healthy, adult male volunteers. INTERVENTIONS: A 60-min intravenous infusion of 1 l HES 200/0.5/6 (HAES-steril 6%) or 4% albumin (control). MEASUREMENT AND RESULTS: The infusion of HES resulted in decreased circulating levels of von Willebrand factor antigen (from 85+/-8% to 59+/-6% after HES vs from 80+/-7% to 69+/-8% after albumin, p<0.05) and ristocetin cofactor activity (from 93+/-4 to 67+/-4% after HES vs from 79+/-5 to 75+/-5% after albumin, p<0.01). This was associated with an impairment of in vitro platelet function as determined with the PFA-100 platelet function analyser (closure time with collagen/epinephrine from 120+/-7 to 159+/-14 s after HES vs from 121+/-7 to 137+/-10 s after albumin, p<0.05; with collagen/ADP from 88+/-3 to 116+/-9 s and from 103+/-4 to 114+/-7 s after HES and albumin, respectively, p=0.01). CONCLUSIONS: The infusion of 1 l of HES 200/0.5/6 in healthy human subjects results in moderately decreased plasma levels of von Willebrand factor associated with impairment of platelet function.

Adult↗
PubMed2002

Effects of two preparations of 75-mg extended-release aspirin on platelet aggregation, prostanoids and nitric oxide production in humans.

OBJECTIVE: The lowest dose of aspirin shown to be effective in the secondary prevention of thrombotic accidents is 75 mg/day. Presystemic acetylation of cyclooxygenase and the formation of salicylic acid in the liver are fundamental to ensure optimum antithrombotic effects of aspirin. This study was designed to compare the effects of two forms of extended-release aspirin (at 75 mg/day) on prostanoid and nitric oxide synthesis in healthy volunteers. METHODS: The participants in this single-blind cross-over study (n = 6) were randomly assigned to receive one of three different formulations: plain-formulated aspirin (PF), extended-release aspirin that released acetylsalicylic acid steadily over 5 h (EX5) or an extended-release formulation that released 49% of the drug during the first 2 h after intake (EX2) and the rest of the dose during the subsequent 5 h. Laboratory analyses were done for platelet aggregation and thromboxane B2 (in whole blood), 6-keto-prostaglandin F1alpha (in leucocytes), neutrophil nitric oxide production and plasma nitrite/ nitrate levels. RESULTS: The PF and EX2 formulations inhibited platelet aggregation by 97% with no significant difference in effect between the two. In contrast, maximum inhibition of aggregation by the EX5 formulation was only 30%. Similar effects were found for platelet thromboxane production: PF and EX2 led to 99% inhibition, whereas EX5 led to 76% inhibition (P < 0.05). The inhibition of prostacyclin production differed in all three treatments (63% for PF, 40% for EX2 and 24% for EX5). The increase in leucocyte nitric oxide production also differed in all three treatments (1.01-fold the basal value with PF, 1.4-fold with EX5 and 3.6-fold with EX2). Both extended-release formulations maintained high levels of nitric oxide production 24 h after the last dose, whereas in the PF period nitric oxide concentration had returned to basal values after this time. The changes in plasma nitrite concentrations in each period of treatment were similar to those seen for leucocyte nitric oxide. CONCLUSION: The pharmacodynamic profile of the extended-release formulations was better than that of plain-formulated aspirin in terms of thromboxane/prostacyclin balance and nitric oxide production. However, the EX2 formulation inhibited platelet function more effectively than did the EX5 formulation.

6-Ketoprostaglandin F1 alpha↗