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Results for “Bleeding Time”

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At least 343 records · Page 19Linked to original sources

PubMed1979

The effect of prostacyclin (PGT2) on platelet behaviour. Thrombus formation in vivo and bleeding time.

Prostacyclin (PGI2) infused intravenously into anaesthetized rabbits inhibited electrically-induced thrombus formation in the carotid artery, increased bleeding time and inhibited ex vivo platelet aggregation induced by ADP or arachidonic acid. The increase in bleeding time and the inhibition of ex vivo platelet aggregation lasted for as long as the infusion of PGI2 was maintained but rapidly disappeared after infusion was stopped. Prostacyclin is a more potent inhibitor of platelet function, in vivo than prostaglandin E1 (PGE1) or prostaglandin D2 (PGD2). The effects of prostacyclin on all parameters studied except blood pressure were potentiated by the concomitant administration of theophylline, a phosphodiesterase inhibitor.

Animals↗

PubMed1992

Prolonged bleeding time in patients with lupus anticoagulant.

Platelet adhesion to collagen under flow conditions was studied in 18 patients with lupus anticoagulant, seven of which showed a prolonged bleeding time in the presence of a normal platelet count. The effect of patient plasma, IgG and purified anticardiolipin antibodies on platelet adhesion was also examined. We found a significant reduction of platelet adhesion in patients with lupus anticoagulant, which was more evident in patients with prolonged bleeding time. This platelet adhesion defect could be attributed to a plasma factor. In fact, patients' platelets regained normal adhesion when mixed with normal plasma, whereas controls' platelets showed abnormal adhesion in the presence of patient plasma. A causative role of antiphospholipid antibodies was demonstrated in experiments using purified immunoglobulins and anticardiolipin antibodies.

Adult↗

PubMed1997

Characterization of a novel bleeding disorder with isolated prolonged bleeding time and deficiency of platelet microvesicle generation.

Platelet prothrombinase activity and microvesicle (MV) generation were measured in four patients from three unrelated families with a life-long bleeding disorder associated with slightly prolonged bleeding time and isolated defective serum prothrombin consumption, without platelet function abnormality or von Willebrand factor defect. MV generation was reduced in all the patients either after thrombin plus collagen or A23187 calcium ionophore stimulation, whereas, at variance with Scott syndrome, prothrombinase activity was normal. This abnormality constitutes a new bleeding disorder, which provides new insights into the possible role of platelet microvesicles in health and disease. Furthermore, the results of this study suggest that MV generation should be investigated in patients with a bleeding history and apparently isolated prolonged bleeding time when prothrombin consumption in serum is defective and all other investigations are normal.

Adult↗

PubMed1987

[In vitro bleeding time].

An in vitro model of primary haemostasis, in vitro bleeding time (BT) according to Kratzer and Born, was studied. There was a significant correlation with in vivo BT. The in vitro BT may be easily repeated in the same patient, facilitating the control of haemostasis. It may also permit studying the effect in vitro and/or ex vivo of drugs on primary haemostasis.

Bleeding Time↗

PubMed1988

Decrease of bleeding time by a peptide fraction from bovine factor VIII in laboratory animals.

A peptide fraction of low molecular weight prepared from bovine Factor VIII by enzymatic hydrolysis (Vueffe) reduces bleeding time in laboratory animals. In this study the haemostatic action in mice, rats and rabbits was investigated using different experimental conditions. This action was observed in animals with either normal or experimentally prolonged bleeding time, thus suggesting better efficacy in pathological situations. The evidence obtained following different routes of administration confirmed the activity of the compound. The efficacy was present at very low doses in all animal species without interfering either with platelets or with blood coagulation.

Animals↗

PubMed1986

Controlled trial of desmopressin in liver cirrhosis and other conditions associated with a prolonged bleeding time.

The synthetic vasopressin derivative desmopressin (DDAVP) shortens a prolonged bleeding time (BT) in patients with uremia, congenital platelet dysfunction, and von Willebrand disease. To establish the limits of the clinical usefulness of DDAVP, a controlled randomized study was carried out in 53 patients and ten volunteers with different conditions that have in common a prolonged BT. DDAVP significantly shortened the BT in 21 cirrhotics (P less than .01), in eight patients with unclassified prolonged BT (P less than .05) and in ten volunteers taking the antiplatelet drugs aspirin (P less than .05) and ticlopidine. The BT changes were not statistically significant in 15 patients with severe thrombocytopenia nor in nine with congenital platelet dysfunction, even though a few patients with storage pool deficiency responded with a marked BT shortening. Our findings indicate that DDAVP might be given when biopsies or other surgical procedures must be carried out in patients with prolonged BT. However, the compound is often ineffective in patients with thrombocytopenia or congenital platelet dysfunction.

Adolescent↗

PubMed1976

Bleeding times, platelet adhesion, and aspirin.

The effects of aspirin on well-standardized commercially produced platelet adhesiveness devices and template bleeding times were simultaneously studied in 19 normal volunteers. As expected, there was significant prolongation of the bleeding time after aspirin, but there was no change in platelet adhesion. Reason for the different effects of aspirin on the two tests are discussed. In addition, the normal range of platelet adhesion was further defined utilizing commercially prepared glass-bead columns.

Adult↗

PubMed1985

Dangerous rises in blood pressure upon heating of trigeminal rootlets; increased bleeding times in patients with trigeminal neuralgia.

During radiofrequency (RF) heating of trigeminal rootlets, we regularly measured blood pressure rises to 250 to 300 mm Hg, confirming two previous reports. We also found abnormally increased bleeding times in 12% of 127 patients awaiting operation for trigeminal neuralgia. These two facts probably explain 6 fatalities and 2 lasting hemiplegias from intracranial bleeding unrelated to vascular puncture by the needle electrode during RF procedures for trigeminal neuralgia. We recommend correction of the abnormal bleeding time and control of the blood pressure rises by i.v. sodium nitroprusside.

Arrhythmias, Cardiac↗

PubMed1984

Clinical evaluation of a new test of hemostasis: the Filter Bleeding Time.

The clinical value of a new in vitro test of hemostasis, which we have called Filter Bleeding Time (FBT), was determined in 59 patients referred because of a suspected bleeding disorder. FBT is based on the progressive slowing of the drop rate of citrated blood through a filter of woven Dacron under constant pressure as platelet aggregates occlude the filter. The value for FBT is defined as the time when the blood drop interval has reached 1 minute. The Mayo modification of the Ivy bleeding time (IBT) was performed in all patients; platelet response to ADP, collagen, epinephrine and arachidonate was performed in 24 patients. In 30 normal volunteers FBT measured 1-3 hr after venipuncture was 2.8 +/- 1.5 (means +/- 1SD) min. The FBT was prolonged in 3 of 3 patients with Glanzmann's thrombasthenia, 2 with disseminated intravascular coagulation, 1 with chronic lymphocytic leukemia, 1 with myelofibrosis, and 1 who had taken aspirin. In 6 patients FBT was prolonged while IBT was normal: 4 after taking aspirin, 2 with polycythemia vera. All 6 had reduced platelet aggregation (PA) to ADP (5 microM), collagen (2 mg/ml), epinephrine (5 microM) and/or arachidonate (1.7 mM). In 3 patients FBT was normal while IBT was abnormal: 1 with disseminated intravascular coagulation, 2 undiagnosed; 1 of these 3 had abnormal PA. Of 6 patients with von Willebrand's disease, FBT was prolonged in 5 and borderline in 1; IBT was prolonged in 3, normal in 1, and not done in 2 infants.(ABSTRACT TRUNCATED AT 250 WORDS)

Arachidonic Acids↗

PubMed1982

A possible method to control prolongations of bleeding time under antiplatelet therapy with ticlopidine.

The interactions of oral and i.v. administrations of corticosteroids with the effects of ticlopidine were studied, in a search for an antidote for possible excessive prolongations of bleeding time induced by antiaggregating agents. Indeed, the results show that an i.v. injection of methylprednisolone or an oral treatment with prednisolone counteract the prolongation of bleeding time but do not interfere with the inhibition of platelet aggregation brought about by ticlopidine. This could be ascribed to a vasoconstrictive effect of corticosteroids, possibly through reduction of vascular prostacyclin release. If this mode of action was confirmed, this useful finding would essentially apply to ticlopidine, but not to cyclooxygenase inhibitors such as aspirin which, by themselves, abolish prostacyclin production.

Adenosine Diphosphate↗

PubMed2005

Short-term, moderate dosage Vitamin E supplementation may have no effect on platelet aggregation, coagulation profile, and bleeding time in healthy individuals.

OBJECTIVE: To investigate the in vivo effect of short-term, moderate dosage synthetic dl-alpha-tocopherol acetate supplementation on platelet aggregation, coagulation profile, and simulated bleeding time in healthy individuals. alpha-tocopherol is the most biologically active isomer of Vitamin E, traditionally promoted as an antioxidant and therapeutic agent in cardiovascular disease. In vitro studies have suggested that alpha-tocopherol plays a role in the inhibition of platelet aggregation. However, further investigations into the effect of alpha-tocopherol on bleeding in vivo have not duplicated these findings. MATERIALS AND METHODS: A total of 42 healthy volunteers complied with a 2-week abstinence period from the use of anti-platelet agents followed by determination of baseline platelet aggregation properties and coagulation studies using citrated whole blood. Moderate dosage Vitamin E (800 IU of dl-alpha-tocopherol acetate) was then self-administered for 14 days with reevaluation of platelet aggregation and coagulation profile, and simulated bleeding time after 14 days of Vitamin E supplementation. RESULTS: Forty subjects completed the 4-week study period. All 40 subjects demonstrated normal baseline coagulation studies and all had collagen-stimulated platelet aggregation assessment performed in triplicate. After Vitamin E supplementation, no significant difference was demonstrated in any study parameter. CONCLUSIONS: Dietary supplementation with moderate dosage synthetic dl-alpha-tocopherol acetate did not significantly prolong bleeding or platelet aggregation in vivo. The affect of Vitamin E on platelet aggregation in vitro does not appear to be reproducible in vivo. Therefore, peri-operative discontinuation of Vitamin E may not be necessary.

Adenosine Diphosphate↗

PubMed1982

Prolongation of rat tail bleeding time caused by oral doses of a thromboxane synthetase inhibitor which have little effect on platelet aggregation.

N (7-carboxyheptyl) imidazole is an inhibitor of platelet thromboxane synthetase that has no effect on the cyclooxygenase activity. An oral dose of the substance to rats (10 mg/kg) prolonged tail bleeding time from 170 +/- 13 sec to 284 +/- 22 sec. This oral dose also inhibited platelet thromboxane B2 production induced by collagen ex vivo but had little effect on the aggregation dose response curve. There was no effect on thrombin-induced aggregation. Neither the thrombocytopenia induced by the Arthus reaction nor thrombus formation on an implanted cotton thread were inhibited by oral doses of carboxyheptylimidazole up to 30 mg/kg. Similarly neither the prothrombin nor activated partial thromboplastin time were affected. It is postulated that this thromboxane synthetase inhibitor prolongs bleeding time nor by inhibiting platelet aggregation or blood coagulation but rather by preventing the vasoconstriction which would normally be caused by thromboxane A2.

6-Ketoprostaglandin F1 alpha↗

PubMed1995

Blocking of tissue factor pathway inhibitor (TFPI) shortens the bleeding time in rabbits with antibody induced haemophilia A.

Tissue factor (TF)/FVIIa initiates coagulation by activating factor IX (FIX) and factor X (FX). Tissue factor pathway inhibitor (TFPI)-FXa complexes form and inhibit TF/FVIIa. Blocking of TFPI may facilitate haemostasis initiated by FVIIa/TF thereby compensating for impaired FIX/FVIII-dependent coagulation. This hypothesis was tested in a study using rabbits made temporarily haemophilic by the injection of antibodies against FVIII. These rabbits were given i.v. injections of anti-TFPI IgG antibodies and 40 min later bleeding was initiated by cutting the nail including the apex of the cuticle. Injection of anti-TFPI IgG shortened the bleeding time significantly from 26 min to 11 min (normal mean bleeding time in non-haemophilia rabbits: 5 min). Treatment with anti-TFPI IgG also resulted in a shortening of the haemophilic aPTT to a level slightly longer than the normal aPTT. In addition, the prolonged dilute TF clotting time was shortened by the anti-TFPI IgG treatment. Thus, both bleeding and coagulation parameters indicated that blocking of TFPI may be potentially haemostatic in haemophilia.

Animals↗

PubMed1994

Effect of cryoprecipitate and plasma on plasma von Willebrand factor multimeters and bleeding time in Doberman Pinschers with type-I von Willebrand's disease.

We determined whether administration of cryoprecipitate or fresh-frozen plasma (FFP) would enhance glass bead platelet retention and shorten the bleeding time in von Willebrand factor (vWf)-deficient Doberman Pinschers. Plasma concentration of vWf was < 15% of the reference value in these dogs and, on the basis of multimeric analysis of vWf, these dogs had type-I von Willebrand's disease (vWd). Concentration of vWf in cryoprecipitate (prepared from FFP of clinically normal dogs) was enriched almost 20 times, and the preparation was a concentrate of the largest and most physiologically active multimers. Administration of a dose of cryoprecipitate calculated to increase plasma vWf concentration of recipient dogs to 50 U/dl increased plasma vWf concentration in recipient dogs to about 40 U/dl. Mean buccal mucosal bleeding time (BMBT) shortened from 6.7 minutes before treatment to 3.8 minutes at 2 hours after treatment. Cryoprecipitate from donor dogs treated with deamino-8-D-arginine vasopressin (1 micrograms/kg of body weight) effectively shortened mean BMBT from 6.4 minutes to 3.1 minutes. Administration of cryoprecipitate from vWf-deficient dogs prolonged, rather than shortened, the BMBT. After FFP (450 ml) infusion, plasma vWf concentration increased in recipient dogs, but the BMBT did not shorten. Glass bead platelet retention did not change after administration of cryoprecipitate or FFP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1980

Prolonged bleeding time in children and young adults with hemophilia.

Of 49 patients with hemophilia A or B, who had not received replacement transfusions for at least 72 hours, ten were demonstrated to have a prolonged value for the bleeding time. None had evidence of von Willebrand's disease or prior aspirin ingestion, and only one was found to have an associated intrinsic platelet defect. It appears that the bleeding time, generally thought to be a measurement of platelet-subendothelium interaction, may also sometimes be prolonged in congenital coagulation disorders in which platelet function is normal.

Adolescent↗

PubMed1976

Antihemophilic factor concentrate therapy in von Willebrand disease. Dissociation of bleeding-time factor and ristocetin-cofactor activities.

Treatment of von Willebrand disease with two plasma antihemophilic factor (AHF) concentrates, cryoprecipitate and glycine-precipitated AHF, was compared. Both concentrates were equally effective in immediately raising the plasma levels of factor VIII, the factor VIII-related antigen, and the ristocetin-related von Willebrand factor (vWF) and in stimulating a secondary rise in plasma factor VIII. Given either concentrate, the vWF activity, the antigen, and factor VIII levels were normalized in a patient with von Willebrand disease. However, correction of the prolonged bleeding time and control of bleeding occurred only with the cryoprecipitate. The bleeding-time corrective factor and the ristocetin-related vWF or platelet-aggregating factor are dissociable, distinct activites.

Antigens↗

PubMed1984

The effect of radiographic contrast agents on bleeding time and platelet aggregation.

The purpose of this study was to determine whether the use of relatively small amounts of radiographic contrast agents may impair hemostasis. Before and after injection of contrast agents, we measured the template bleeding time, platelet count in whole blood and platelet-rich plasma, platelet aggregation induced by epinephrine and adenosine diphosphate (ADP), and percent disaggregation of ADP-induced platelet aggregates in platelet-rich plasma of 18 patients. Ten patients received 50-100 ml of sodium iothalamate (66.8%) for intravenous urography and 8 patients received 125-200 ml of a combination of meglumine diatrizoate (66%) and sodium diatrizoate (10%) for coronary angiography and left ventriculography. Neither group demonstrated a statistically significant mean difference (p greater than 0.05) for any parameter measured before and after administration of the contrast agents. However, 2 patients who received diatrizoate had lengthening of their bleeding times to greater than twice the baseline value without any change in in vitro platelet aggregation. Physicians should be aware of this potential cause of bleeding which could be of particular danger to patients undergoing cardiopulmonary bypass with its inherent hemostatic defects.

Bleeding Time↗

PubMed1985

Desmopressin and bleeding time in patients with cirrhosis.

Desmopressin acetate 0.3 microgram/kg was given intravenously to nine patients with chronic liver disease and to a further six such patients in a double blind controlled study versus placebo. Desmopressin acetate significantly shortened the bleeding time compared with basal values in both groups and compared with placebo. There was also a significant decrease in partial thromboplastin time (but not prothrombin time) and significant increases in factor VIII and its components, von Willebrand factor and ristocetin cofactor activity, but not in factors VII, IX, X, XI, or XII. Increased fibrinolysis could be blocked by concomitant administration of tranexamic acid. No important side effects were seen. The multimer pattern of von Willebrand factor was studied for the first time in chronic liver disease. It was normal, but after administration of desmopressin acetate the percentage of multimers of higher molecular weight increased significantly. This may be an important mechanism in the shortening of the bleeding time in cirrhosis, as has been shown in uraemia and other conditions after administration of desmopressin acetate. Desmopressin acetate may be useful in correcting defects in primary haemostasis in chronic liver disease.

Bleeding Time↗