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PubMed1986

Prolonged bleeding time, reduced platelet aggregation, altered PAF-acether sensitivity and increased platelet mass are a trait of asthma and hay fever.

In a case control study 31 asymptomatic patients with asthma and/or hay fever and 31 normal controls had their bleeding time measured using the Simplate II device and venostasis. Mean bleeding time in the atopic group (527 s) was significantly prolonged compared to the controls (393 s) (p less than 0.0005). Platelet aggregation to collagen and ADP (but not to PAF-acether) was significantly depressed in the atopics. Mean circulating platelet mass was significantly greater in atopics than in the controls (p = 0.006). Stepwise multiple regression analysis showed that within the control group bleeding time was best predicted by platelet mass (p = 0.007). No such relationship was found in the atopics. However stepwise multiple regression analysis showed that bleeding time in the atopics (but not in the controls) was best predicted by PAF-acether induced platelet aggregability (p less than 0.05). In neither group was bleeding time related to collagen induced platelet thromboxane B2 production. It is hypothesised that in respiratory atopy the depressed aggregatory function of platelets is not compensated for sufficiently by an increase in platelet mass, leading to prolongation of the bleeding time. This haemostatic imbalance, whose cause remains to be established, appears to constitute a trait of atopy.

Adenosine Diphosphate↗
PubMed1992

Effect of platelet count on the DDAVP-induced shortening of the bleeding time in thrombocytopenic Gaucher's patients.

As part of an investigative protocol requiring serial liver biopsies in patients with Type I Gaucher's disease who were receiving enzyme replacement therapy, we gave 11 patients a total of 15 infusions of DDAVP (0.3 micrograms/kg IV) and measured the Simplate bleeding time pre- and postin-fusion. All patients were thrombocytopenic (one patient 100-150,000; seven 66-99,000; and three 50-65,000/microliters). Nine of 15 infusions resulted in at least a 2-min shortening of the bleeding time; in 6/11 infusions in which the platelet count was greater than 65,000, the bleeding time shortened to less than or equal to 10 min, in 1/11 it shortened greater than or equal to 2 min but not to less than or equal to 10 min. In only 2/4 infusions given to patients with platelet counts less than 65,000 did the bleeding time demonstrate any significant shortening. None of the six liver biopsies performed in the patients whose bleeding time shortened to less than or equal to 10 min resulted in any significant bleeding; blood products were not transfused either pre- or postprocedure. These limited data demonstrate that a high percentage of patients with platelet counts of 65-100,000/microliters can manifest a significant shortening of bleeding time following a standard infusion of DDAVP, and that in approximately half of these patients the bleeding time will shorten enough to safely allow the performance of a liver biopsy without the need for prophylactic transfusion of blood products.

Adolescent↗
PubMed1986

Evaluation of the cuticle bleeding time in canine haemophilia A.

In this paper we describe our clinical experience and results with the cuticle bleeding time test in a colony of cross-bred Labrador retrievers with severe haemophilia A. The dogs have a severe bleeding tendency with a high incidence of fatal haemorrhages in the central nervous system. Homozygous females appeared to be especially prone to this lethal complication. Factor VIII recovery and half-life determinations yielded results similar to the data from human studies. The cuticle bleeding time proved to be a good measure of the coagulation defect. The prolongation of the bleeding time could be completely abolished by administration of 10 to 15 units of canine factor VIII per kg body weight. We conclude that the cuticle bleeding time in canine haemophilia provides us with a suitable model for the in vivo study of new therapeutic materials.

Animals↗
PubMed1989

DDAVP shortens the prolonged bleeding times of patients with severe von Willebrand disease treated with cryoprecipitate. Evidence for a mechanism of action independent of released von Willebrand factor.

After infusion of cryoprecipitate, the very prolonged bleeding time of patients with severe von Willebrand disease (vWD) is shortened but not always normalized in spite of normalization of plasma von Willebrand factor (vWF) levels. Therefore treatments that further improve primary hemostasis in severe vWD patients are needed. Since DDAVP shortens the bleeding time in a variety of bleeding disorders, we investigated in a double-blind, placebo-controlled crossover study the effects of the intravenous (IV) infusion of DDAVP (0.3 microgram/kg) on the bleeding times of 10 patients with severe vWD treated with cryoprecipitate. Their very prolonged bleeding times (greater than 30 minutes), partially corrected by the infusion of cryoprecipitate (14 +/- 2 minutes, mean +/- SEM), were further shortened by the administration of DDAVP (9 +/- 2 minutes, P less than .01) but not of saline (15 +/- 3 minutes, ns). Plasma vWF levels, raised from unmeasurable to normal values by cryoprecipitate, were not changed after DDAVP or saline. The defective deposition of platelets from eight patients onto human umbilical artery subendothelium was increased but not normalized by cryoprecipitate and was not significantly affected by DDAVP or saline. Therefore the infusion of DDAVP after cryoprecipitate may be of clinical benefit for management of bleeding episodes in severe vWD patients. Since severe vWD patients do not have releasable tissue stores of vWF, DDAVP must shorten their prolonged bleeding times independently of released vWF.

Bleeding Time↗
PubMed1985

Effect of incremental doses of aspirin on bleeding time, platelet aggregation and thromboxane production in patients with cerebrovascular disease.

Bleeding time, thromboxane production and inhibition of platelet aggregation were studied before and during administration of acetylsalicylic acid in doses of 50, 100, 325 an 1000 mg daily in eighteen patients with cerebrovascular disease. Inhibition of thromboxane production and platelet aggregation was almost complete at 50 mg acetylsalicylic acid daily, and median bleeding time had increased significantly from 5.5 to 6.5 min at this dose and reached a maximum of 7.5 min at 100 mg daily. Further increase of the dose resulted in a slight decrease in bleeding time. It appears that a strong effect on platelet function can be achieved by small doses of acetylsalicylic acid, and that higher doses might be less effective.

Adult↗
PubMed1990

Effects of a selective thromboxane receptor antagonist (GR32191B) and of glyceryl trinitrate on bleeding time in man.

1. GR32191B is a potent and selective thromboxane receptor antagonist. Glyceryl trinitrate (GTN) also inhibits platelet function in vitro. Both have been reported to prolong bleeding time. Since they may be used together in patients with coronary artery disease, we have investigated the possibility of an interaction between them. 2. Twenty-four healthy male volunteers were treated with GR32191B using a double-blind placebo-controlled crossover design. Bleeding times were determined before and after GR32191B or placebo and during co-administration of GTN. Plasma GR32191B concentration was measured. Platelet aggregation in response to adenosine diphosphate and to a thromboxane mimetic, U46619, was measured ex vivo. Urinary excretion of thromboxane (TX)B2 and 2,3-dinor-TXB2 was determined in 24 h urine samples. 3. Twelve hours after GR32191B (80 mg; p.o.), the plasma concentration was 36.6 +/- 2.7 nM (mean +/- s.e. mean) and bleeding time was increased by 66%. Ninety minutes after a second dose (40 mg; p.o.) the plasma concentration was 431.9 +/- 23.6 nM but bleeding time was not further prolonged. 4. Responses of platelets to U46619 were selectively antagonised following GR32191B. Urinary excretion rates of TXB2 and 2,3-dinor TXB2 were similar after treatment with GR32191B or placebo. 5. GTN (1 mg sub-lingually) had no significant effect on bleeding time 90-100 min following either placebo or GR32191B. 6. We conclude that GR32191B, in a dose that causes profound yet specific blockade of thromboxane receptors, causes only a modest prolongation of bleeding time that is unaffected by a therapeutic dose of GTN. This may prove advantageous when GR32191B is used in patients with ischaemic heart disease.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1998

Antithrombotic effect of YM-75466 is separated from its effect on bleeding time and coagulation time.

The antithrombotic effects of YM-75466 ([N-[4-[(1-acetimidoyl-4-piperidyl)oxy]phenyl]-N-[(7-amidino-2-nap hthyl)methyl]sulfamoyl]acetic acid monomethane sulfonate), a novel orally-active factor Xa inhibitor, and its effects on bleeding time and coagulation time were studied in rats and compared with those of warfarin. Both agents were orally administered. In the venous thrombosis model, YM-75466 and warfarin inhibited thrombus formation dose-dependently, with ID50 values of 3.3 and 0.56 mg/kg, respectively. Ex vivo study showed that both YM-75466 and warfarin prolonged prothrombin time dose-dependently, with doses, causing a two-fold prolongation of prothrombin time in the control group, of 89 and 0.38 mg/kg, respectively. In bleeding time studies, YM-75466 and warfarin prolonged bleeding time dose-dependently, with doses, causing a two-fold prolongation of bleeding time in the control group, of > 100 and 0.43 mg/kg, respectively. These results show that the antithrombotic effects of YM-75466 are markedly separate from its effects on bleeding time and coagulation time compared with warfarin.

Animals↗
PubMed1988

Aspirin dose, bleeding time, platelet adhesion and aggregation in cerebral thrombosis.

Bleeding time, platelet aggregation and platelet adhesiveness were measured before and after each of 11 consecutive therapeutic sequences in 17 patients who had recently suffered a cerebro-vascular accident of atheromatous ischemic origin. The first 10 sequences were each of 15 days duration and during the first 8 of these, aspirin was increased with each sequence from 300 mg/2 days to 3 g/day. During the 10th sequence a placebo was given. The final sequence (11th) lasted 3 months and during this time the dose of aspirin was fixed at 1 g/day. Significant modification of platelet aggregation was obtained with 300 mg/2 days, platelet adhesiveness was significantly modified with 500 mg/2 days while significant bleeding time modification required a minimum 500 mg/day. The results did not vary significantly with higher doses of acetylsalicylic acid (ASA). Only the results for the platelet aggregation were individually reproducible. There was no statistical correlation between the results of the tests. As far as the 3 tests are considered, the best efficiency is obtained with the therapeutic range of 500 mg to 1 g/day.

Adolescent↗
PubMed1999

Effect of dienogest on bleeding time, coagulation, fibrinolysis, and platelet aggregation in female rats.

We investigated the effect of dienogest on bleeding time, coagulation, fibrinolysis, and platelet aggregation in female rats compared with that of medroxyprogesterone acetate (MPA) and danazol, in order to elucidate the reason for relatively high incidence of bleeding in dienogest-treated patients with endometriosis. Dienogest caused no change in the bleeding time at a single dose of 100 mg/kg or at a repeated dose of 10 mg/kg per day for 2 weeks. The drug increased the fibrinogen level, coagulation factor II and V activities, and antithrombin III activity, but had no effect on fibrinolysis or on platelet aggregation at repeated doses of 1 and 10 mg/kg per day for 4 weeks. MPA significantly shortened the bleeding time at the same doses as dienogest. MPA increased the fibrinogen level and plasminogen activity, potentiated the platelet aggregation, and increased the platelet cholesterol-to-phospholipid ratio at a repeated dose of 10 mg/kg per day for 4 weeks. Danazol significantly shortened the bleeding time like MPA. Danazol increased the fibrinogen level, coagulation factor II, V, VII, VIII, IX, X, XI, and XII activities, and antithrombin III activity, but had no influence on the platelet aggregation at repeated doses of 10 and 100 mg/kg per day for 4 weeks. In comparison with MPA and danazol, dienogest may induce a relatively high incidence of bleeding in patients with endometriosis partially because of its minimal effect on hemostasis.

Animals↗
PubMed1985

The effects of low-fat diets rich in arachidonic acid on the composition of plasma fatty acids and bleeding time in Australian aborigines.

In the present study we measured the bleeding times in fourteen Aborigines (10 diabetic, 4 non-diabetic) before and after 2 weeks on a diet of tropical seafood (rich in both arachidonic acid and the omega 3 PUFA), followed by 3 weeks on a diet in which kangaroo and freshwater fish (linoleic and arachidonic acid-rich) were the major fat sources. Both diets were very low in fat. Bleeding times increased in all subjects after the 2 weeks of tropical seafood and continued to rise on the mixed diet. The increase over 5 weeks from 4.1 +/- 0.4 to 5.9 +/- 0.4 min was highly significant (p less than 0.01). Due to the extreme isolation of the study location it was only possible to measure the plasma fatty acid composition at the beginning and end of the study. The concentration of arachidonic acid in the plasma lipids doubled whereas that of linoleic acid was almost halved, despite the fact that the diet in the second part of the study contained considerably more linoleic than arachidonic acid. That there appeared to be preferential incorporation of arachidonic acid into the plasma lipids is further supported by the observation that the rise in arachidonic acid in the cholesterol ester and phospholipid fractions was almost exactly counter-balanced by the fall in linoleic acid. In conclusion, the present study demonstrated a rise in bleeding time associated with an increased concentration of arachidonic acid and decreased concentration of linoleic acid in plasma lipids, and suggests that the mechanism by which diet modulates haemostatic function may be more complex than currently assumed.

Animals↗
PubMed1998

Antithrombotic effects of YM-60828, a newly synthesized factor Xa inhibitor, in rat thrombosis models and its effects on bleeding time.

1. The effects of YM-60828, a newly synthesized factor Xa inhibitor, were investigated to analyse the relationship between its antithrombotic effects and its prolongation of template bleeding time in rats. YM-60828 was compared with argatroban, heparin and dalteparin. All agents were intravenously administered as a bolus. 2. In ex vivo studies, YM-60828 and argatroban prolonged both prothrombin time and activated partial thromboplastin time in a dose-dependent manner, while heparin and dalteparin prolonged only activated partial thromboplastin time. 3. In a venous thrombosis model, all agents exerted antithrombotic effects in a dose-dependent manner. The ID50 values of YM-60828, argatroban, heparin and dalteparin were 0.0081 mg kg(-1), 0.011 mg kg(-1), 6.3 iu kg(-1) and 4.7 iu kg(-1), respectively. 4. In an arterio-venous shunt model, all agents exerted antithrombotic effects in a dose-dependent manner. The ID50 values of YM-60828, argatroban, heparin and dalteparin were 0.010 mg kg(-1), 0.011 mg kg(-1), 10 iu kg(-1) and 4.2 iu kg(-1), respectively. 5. In bleeding time studies, all agents prolonged template bleeding time in a dose-dependent manner. ED2 values, the doses causing a 2 fold prolongation of bleeding time in the saline group, of YM-60828, argatroban, heparin and dalteparin were 0.76 mg kg(-1), 0.081 mg kg(-1), 18 iu kg(-1) and 25 iu kg(-1), respectively. 6. The ratio (ED2/ID50) of YM-60828 was more than 30 fold greater than that of heparin and more than 10 fold greater than those of argatroban and dalteparin. 7. These data show that YM-60828 can exert its antithrombotic effects with little prolongation of bleeding time compared with the other currently used anticoagulant agents.

Animals↗
PubMed1999

Anesthesia with sevoflurane, but not isoflurane, prolongs bleeding time in humans.

PURPOSE: Halothane has been shown to suppress platelet aggregation in vitro and ex vivo and to prolong bleeding time. In a previous in vitro study, we demonstrated that sevoflurane had a stronger suppressive effect on platelet aggregation than halothane. The present study investigated whether clinical use of sevoflurane affects bleeding time in vivo. METHODS: Thirty-four patients undergoing minor elective surgery were randomly assigned to sevoflurane or isoflurane. Anesthesia was induced with intravenous thiopental and maintained with sevoflurane or isoflurane with nitrous oxide. Bleeding time was measured by the Duke method. An initial (control) measurement was obtained in the operating room before the induction of anesthesia, and a second was obtained 5-10 min after endotracheal intubation but before starting the operation, when the end-expiratory concentration of sevoflurane or isoflurane had been stabilized at 1-1.5 times the minimum alveolar concentration (MAC), and the mean arterial pressures were between 80% and 120% of the preanesthetic values. RESULTS: Bleeding time was increased from the preanesthetic value of 2.07 +/- 0.82 min to 2.83 +/- 0.93 min (n = 15) in the sevoflurane group (P < 0.01) but was not significantly altered in the isoflurane group. CONCLUSION: Sevoflurane alters bleeding time in the clinical situation.

Clinical Trial↗
PubMed1992

Bleeding time: is it a useful clinical tool?

The bleeding times of five volunteers were assessed individually by each of 12 observers. The reliability of the measurements obtained was examined by comparing statistically the variability between subjects and between observers. This variability was found to be similar for both groups. Consequently, we suggest that the bleeding time estimation is an unreliable test and should not be used in isolation without reference to the salient features of a history and examination, when determining if an individual patient is at risk of haematoma formation as a complication of regional anaesthetic techniques.

Bleeding Time↗
PubMed2006

Platelets photochemically treated with amotosalen HCl and ultraviolet A light correct prolonged bleeding times in patients with thrombocytopenia.

BACKGROUND: Photochemical treatment (PCT) with amotosalen HCl with ultraviolet A illumination inactivates pathogens and white blood cells in platelet (PLT) concentrates. STUDY DESIGN AND METHODS: In a Phase II crossover study, 32 patients with thrombocytopenia received one transfusion of PCT and/or one transfusion of untreated (reference) apheresis PLTs. Hemostatic efficacy was assessed with the cutaneous template bleeding time and clinical observations. RESULTS: Paired bleeding time data for PCT and reference transfusions were available for 10 patients. Mean pretransfusion bleeding times were 29.2 +/- 1.6 minutes in the PCT group and 28.7 +/- 2.5 minutes in the reference group. After transfusion of a dose of PLTs of at least 6.0 x 10(11), mean 1-hour posttransfusion template bleeding times corrected to 19.3 +/- 9.5 minutes in the PCT group and 14.3 +/- 6.5 minutes in the reference group (p = 0.25). In 29 patients receiving paired PCT and reference transfusions, mean 1-hour posttransfusion PLT count increments were 41.9 x 10(9) +/- 20.8 x 10(9) and 52.3 x 10(9) +/- 18.3 x 10(9) per L for PCT and reference, respectively (p = 0.007), and mean 1-hour posttransfusion PLT corrected count increments (CCIs) were 10.4 x 10(3) +/- 4.9 x 10(3) and 13.6 x 10(3) +/- 4.3 x 10(3) for PCT and reference, respectively (p < 0.001). The time to next PLT transfusion was 2.9 +/- 1.2 days after PCT transfusions versus 3.4 +/- 1.3 days after reference transfusions (p = 0.18). Clinical hemostasis was not significantly different after PCT and reference transfusions. CONCLUSION: PCT PLTs provided correction of prolonged bleeding times and transfusion intervals not significantly different than reference PLTs despite significantly lower PLT count increments and CCIs.

Adolescent↗
PubMed1985

Influence of acetylsalicylic acid on bleeding time and serum thromboxane B2 in diabetes mellitus type I.

Basal and two hours after 600 mg acetylsalicylic acid (ASA) bleeding times were measured in 21 type I diabetic patients with retinopathy, 24 type I diabetic patients without retinopathy and 21 normal healthy volunteers. There were no significant differences either in basal or in after ASA bleeding times between these groups, but the percentage increase in bleeding time after ASA was significantly higher than normal in both diabetic groups. No correlation was found between basal--bleeding time and glucose, Hb A1 or lipid profile. TXB2 production by spontaneous blood clotting was drastically reduced by ASA in both diabetic and normal groups. Platelet hyperactivity in diabetes mellitus may be due, at least in part, to a predominance of the proaggregatory effects of TXA2 over the antiaggregatory effects of PGI2.

Adolescent↗
PubMed1985

Dose-related prolongation of the bleeding time by intravenous nitroglycerin.

The effects of intravenous nitroglycerin (NTG) upon the bleeding time, platelet aggregation response, and plasma 6-keto-PGF1 alpha concentration were measured in 17 patients about to undergo coronary bypass grafting. NTG produced a dose-related prolongation of the bleeding time that correlated with the accompanying decrease in systolic blood pressure. Platelet aggregation was not affected and measurements of 6-keto-PGF1 alpha failed to reveal detectable levels (less than 10 pg/ml) either before or after NTG infusion. This suggests that the prolonged bleeding time associated with NTG infusion may be due to vasodilation and increased venous capacitance, rather than altered vascular-platelet interaction.

Adult↗
PubMed1975

The bleeding time as a test of hemostatic function.

The vascular component of hemostatis is determined by the bleeding time as designed by Duke or by the Ivy modification, which is a combined bleeding time-tourniquet test. A prolonged bleeding time is observed: (1) in thrombopathic thrombocytopenia, which may be (a) hereditary or (b) acquired, as in the immune types or from depression of bone marrow, and (2) athrombocytopenically, as in von Willebrand's disease, Glanzmann's thrombasthenia, or from aspirin intolerance. The role of a specific bleeding time determinant in the plasma (labile bleeding time factor of Perkins) is discussed and its possible relation to platelets suggested.

Aspirin↗
PubMed2004

Prolonged bleeding time and lupus anticoagulant: a second paradox in the antiphospholipid syndrome.

OBJECTIVE: Systemic lupus erythematosus and antiphospholipid syndrome (APS) often appear concomitantly. Lupus nephritis and antiphospholipid antibody-related ischemic nephropathy cannot be distinguished clinically, although their etiology and treatment differ greatly. Examination of a renal biopsy sample is therefore essential in order to provide the correct treatment. We have observed that patients with lupus anticoagulant (LAC), a serologic marker for APS, often have a prolonged bleeding time, which is a contraindication for performing a percutaneous renal biopsy. We undertook this study to evaluate systematically the bleeding time in 27 consecutive patients. METHODS: The bleeding time was measured in 27 patients who were persistently positive for LAC and who were not exposed to aspirin or nonsteroidal antiinflammatory drugs. Platelet function and von Willebrand factor (vWF) parameters were subsequently assessed in patients with a prolonged bleeding time. RESULTS: Twenty-one of 27 patients (78%) had a prolonged bleeding time despite a normal platelet count in the majority of patients (81%). Platelet functioning and vWF parameters in these 21 patients were normal, except for those in 1 patient with a mild storage pool disease. CONCLUSION: With this study, we introduce yet another paradox in the phenomenon of APS. Although a prolonged bleeding time is generally accepted to be a sign of defective primary hemostasis, LAC is associated with thrombosis. Further studies are needed to elucidate the mechanism behind this disturbance of primary hemostasis.

Adult↗