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PubMed1992

Pronounced effects of the combination of a new thromboxane antagonist (GR32191) and heparin on bleeding time in man.

Potential pharmacokinetic and pharmacodynamic interactions between two oral doses of GR32191 (40 and 80 mg), a new thromboxane antagonist, and heparin (5,000 IU bolus + 1,000 IU/h for 3 h) were studied in eighteen healthy male volunteers using two separate double-blind, randomised, placebo-controlled, cross-over studies. Mean (range) bleeding time values were 8.4 min (7.5-9.7) during heparin/placebo, 12.1 min (9.2-18.6) (GR32191/placebo) and 16.3 min (11.5-21.4) (GR32191/heparin) in the 40 mg study, while these values were 8.7 min (5.5-15.5), 16.0 min (9.3 - greater than 36.0) and 23.8 min (10.7 - greater than 36.0), respectively in the 80 mg study. Compared to screening values, the combination of 80 mg of GR32191 and heparin had a greater effect on the bleeding time than the sum of the prolongations after the separate treatments (p = 0.05). In the 40 mg study this was not the case. Pharmacokinetics of heparin (as assessed by plasma anti-Xa and antithrombin activity) and GR32191 were unaltered during co-administration of the two drugs. GR32191 did not influence the effects of heparin on APTT. Heparin slightly diminished the inhibition of collagen induced platelet aggregation by 80 mg of GR32191 and the U-46619 (thromboxane A2-mimetic) induced platelet aggregation remained unchanged. Overall fibrinolytic activity (as evaluated by the fibrin plate test) was similar during all three treatments in the study with 80 mg. The combination of 80 mg of GR32191 and heparin caused a prolongation of the bleeding time which was more than expected on the basis of their individual effects.

Biphenyl Compounds↗

PubMed1996

Increased bleeding time after magnesium sulfate infusion.

Personal observation suggested that blood loss increased among patients with preeclampsia who received magnesium sulfate infusions. Bleeding time (modified Ivy) was checked before infusion of magnesium and at the completion of infusion for nine patients with preeclampsia and three who did not receive magnesium. Bleeding time more than doubled among patients who needed magnesium and did not change among controls.

Bleeding Time↗

PubMed1991

The interactive effects of Type A behavior and hostility on bleeding time thromboxane and prostacyclin formation.

Sixty-six male university students were classified as Type A or B on the basis of the Structured Interview of Rosenman and as hostile or non-hostile on the basis of the Cook-Medley scale. Vascular production of prostacyclin and platelet thromboxane in response to a standard vessel injury was evaluated. Basal thromboxane production, measured as the primary metabolite, thromboxane B2, in blood oozing from the bleeding-time site, was highest among hostile Type A subjects with significantly lower thromboxane production in hostile Type Bs and all non-hostile groups combined. Following an exercise treadmill test hostile subjects produced more thromboxane than non-hostile ones, and hostile Type As had significantly shorter bleeding times than hostile Type Bs. No significant differences on any measure were observed following a stressful color naming task. The observed interaction of hostility and Type A behavior on bleeding time thromboxane formation links behavior to an adverse aspect of a thrombosis-related parameter thought to be involved in the genesis of cardiovascular disease.

6-Ketoprostaglandin F1 alpha↗

PubMed1985

The prolonged bleeding time in hemophilia A: comparison of two measuring technics and clinical associations.

The authors simultaneously performed the Ivy (IBT) and the Simplate I (SBT) bleeding time in 17 volunteers with classic hemophilia A to determine whether a prolonged Simplate bleeding time was indeed indicative of impaired primary hemostasis, as has been postulated recently, or whether the technic itself accounted for the observed changes. They also assessed platelet function and Factor VIII-related activities on blood drawn that day. The SBT was prolonged in 11 patients, while the IBT was consistently normal. The platelet aggregation studies and the levels of Factor VIII-related antigen (VIII R:Ag) and ristocetin cofactor (VIII R:Rc) were normal, providing no evidence of von Willebrand's disease. The patients with a prolonged SBT were all younger than 20 years of age, bled two to three times more often than those with a normal SBT, and consumed more Factor VIII concentrate. A prolonged SBT with depressed VIII:C therefore is not indicative of von Willebrand's disease but is shared by a substantial proportion of hemophiliacs, who may be a greater risk of bleeding.

Adolescent↗

PubMed1997

Blockade of endogenous nitric oxide production results in moderate hypertension, reducing sympathetic activity and shortening bleeding time in healthy volunteers.

BACKGROUND: Short-term infusion of NG-monomethyl-L-arginine (L-NMMA) reversibly inhibits endogenous nitric oxide (NO) production in humans. We studied responses to more long-lasting (60 min) infusions, at doses high enough to cause effective inhibition of endogenous NO. METHODS: Eight healthy volunteers had catheters (pulmonary, arterial and venous) placed. Measurements included hemodynamics, endogenous NO levels in nasal air, bleeding time, and cyclic guanosine monophosphate (cGMP) and catecholamines in plasma. L-NMMA was infused at 0.3 mg.kg-1.min-1 during 30 min, followed by 0.15 (n = 6) or 0.3 (n = 2) mg.kg-1.min-1 during 30 min. RESULTS: L-NMMA significantly elevated mean arterial pressure by 12 +/- 3%, due to an increase in systemic vascular resistance. Cardiac output decreased by 23 +/- 3%, due to a decrease in stroke volume. Pulmonary vascular resistance (P < 0.05) increased, but mean pulmonary arterial pressure was stable. Forearm vascular resistance (P < 0.05) decreased. Bleeding time was shortened by 31 +/- 4% (P < 0.01). L-NMMA infusion reduced NO concentrations in nasal air by 64 +/- 2% (P < 0.01). Arterial pressure remained elevated and nasal NO remained depressed 90 min after the infusion, whereas most other responses were reversed at that time. Plasma cGMP showed only minor changes. Plasma norepinephrine decreased, suggesting reflexogenic inhibition of sympathetic activity, whereas epinephrine levels were low and stable throughout the experiment. CONCLUSION: Dosage of (13.5 mg.kg-1 in 60 min) L-NMMA infusion in humans was well tolerated. Pronounced and long-lasting inhibition of endogenous NO production, as evidenced by measurements in nasal air, resulted in unevenly distributed vasoconstriction, a transient decrease in cardiac output, and reflexogenic sympathetic withdrawal. Furthermore, bleeding time was shortened, suggesting platelet activation.

Adolescent↗

PubMed1979

The interaction of varying doses of dipyridamole and acetyl salicylic acid on the inhibition of platelet functions and their effect on bleeding time.

1 In normal volunteers maximum reductions in platelet functions, collagen aggregation, adhesion and PF4 availability, were achieved using combined doses of 50 mg three times daily dipyridamole + 180 mg ASA or 75 mg three times daily dipyridamole + 120 mg ASA daily. 2 These doses did not prolong the bleeding time. 3 A synergistic effect has been demonstrated with 25 mg dipyridamole three times daily and 60 mg ASA. 4 At higher doses the effects on platelet functions were additive up to the maximal response. 5 The effect of low doses of ASA on platelet function was cumulative. 6 As lower doses of ASA in the combination studied inhibit platelet functions maximally without altering the bleeding time and probably without inhibiting prostacyclin, we suggest that these combinations of dipyridamole and ASA merit consideration in future clinical trials.

Adult↗

PubMed1989

Abolition of in vivo platelet thrombus formation in primates with monoclonal antibodies to the platelet GPIIb/IIIa receptor. Correlation with bleeding time, platelet aggregation, and blockade of GPIIb/IIIa receptors.

We studied the dose-response effects of the F(ab')2 fragments of murine monoclonal antibodies to the platelet GPIIb/IIIa receptor (7E3 and 10E5) on in vivo platelet thrombus formation in a well-characterized monkey model in which the carotid artery is stenosed and thrombus formation is provoked and augmented by intimal damage and the infusion of subaggregating doses of epinephrine. Both antibodies abolished thrombus formation with a mean dose of -0.2 mg/kg. Ex vivo platelet aggregation was not always abolished at doses that abolished thrombus formation; similarly, bleeding times were only moderately prolonged (9.1 +/- 1.4 minutes) at these doses. Increasing the dose above that required to abolish thrombus formation consistently produced abolition of ex vivo platelet aggregation, marked prolongation of the bleeding time (14.2 +/- 1.5 minutes), and nearly quantitative blockade of GPIIb/IIIa receptors. We conclude that in a significant percentage of animals, the extent of GPIIb/IIIa blockade required to prevent vasoocclusive thrombus formation in this model is less than that required for abolition of platelet aggregation, and that the preservation of only a minority of functional GPIIb/IIIa receptors might be adequate to maintain a nearly normal bleeding time.

Animals↗

PubMed1981

High does epsilon-aminocaproic acid prolongs the bleeding time and increases rebleeding and intraoperative hemorrhage in patients with subarachnoid hemorrhage.

epsilon-Aminocaproic acid (EACA) has been used to prevent rebleeding in patients with intracranial aneurysms because it crosses the blood-brain barrier and is an inhibitor of fibrinolysis. Recommended doses have ranged from 24 to 48 g/day. We now describe an inhibitory effect on platelet function at the higher dose range. In vitro, a dose-dependent inhibition of adenosine diphosphate- and collagen-induced platelet aggregation was observed with concentrations of EACA beginning at 7.6 mM. In vivo, prolongation of the template bleeding time was observed in all eight patients receiving 48 g/day (greater than 20 minutes in four), in all five on 36 g/day (greater than 20 minutes in three), and in none of seven on smaller doses. More importantly, rebleeding and excessive intraoperative bleeding (requiring more than 1 litre of blood replacement) occurred predominantly in patients receiving the larger doses of EACA. Within 48 hours of the discontinuation of EACA, the bleeding times returned to normal values in all but one patient. We conclude that EACA exerts a dose-dependent inhibitory effect on platelet function and that patients receiving doses in excess of 24 g/day may be at risk of serious bleeding. Patients receiving EACA should be monitored with serial bleeding time tests.

Adult↗

PubMed1989

Ticlopidine in China: comparative study on the effect of two dose levels on bleeding time and platelet function in healthy volunteers.

The compared inhibitory effects of two dose levels of ticlopidine (250 and 500 mg/day) on bleeding time and platelet function in Chinese volunteers have been studied in a placebo-controlled study. Ticlopidine exerted several significant effects: namely prolongation of bleeding time, inhibition of ADP-induced platelet aggregation, reduction of the thromboxane B2 synthesis induced by collagen as well as by ADP. The daily dose of 250 mg did not show significantly different effects as compared to the western, usually recommended daily dose of 500 mg. At the daily dose of 500 mg, adverse reactions occurred more frequently than at the daily dose of 250 mg, but no serious side effects necessitating discontinuation of treatment, or abnormalities in hematological and liver function parameters were observed at these two dose levels. In Chinese people, ticlopidine therapy should be administered at a daily dose of 250 mg.

Adenosine Diphosphate↗

PubMed1993

Type A behavior and alcohol consumption: effects on resting and post-exercise bleeding time thromboxane and prostacyclin metabolites.

The vasoactive eicosanoids, prostacyclin and thromboxane, are thought to play an important role in the genesis of cardiovascular disease. Since an altered basal production of these eicosanoids among individuals exhibiting the Type A behavior pattern had previously been observed by the authors, the present study evaluated the extent to which the TABP-eicosanoid relationship would be altered by two lifestyle variables known to affect platelet activity: alcohol consumption and stressful physical activity. 55 male participants aged 18-25 years, participated in the study. They were classified as either Type A or Type B on the basis of the Structured Interview and as either moderate, heavy, or abstinent alcohol drinkers. Bleeding times were performed and bleeding time thromboxane and prostacyclin metabolites were measured in all subjects both before and following treadmill exercise. The results indicated that following exercise, Type A participants, who reported moderate alcohol intake, had decreased levels of thromboxane B2 formation relative to Type As reporting heavy consumption. Further, prostacyclin production, measured as the primary metabolite, 6-keto-prostaglandin F1 alpha, was significantly suppressed following exercise among drinkers as compared with participants reporting abstinence. These results were discussed in relation to the proposition that moderate alcohol consumption reduces coronary heart disease risk.

6-Ketoprostaglandin F1 alpha↗

PubMed1987

Use of a bleeding time determination in the evaluation of unexplained hematuria.

Although von Willebrand's disease is an unusual cause of gross hematuria in children, it is readily treatable with fresh frozen plasma or cryoprecipitate. We present 2 cases of recurrent, painless gross hematuria owing to this congenital factor VIII deficiency disorder. In each case the diagnosis was suggested first by the finding of a prolonged bleeding time. We suggest that the bleeding time determination be included as part of the screening hemostatic studies used in the evaluation of unexplained hematuria.

Bleeding Time↗

PubMed1984

Association between bleeding time and platelet adherence to artery subendothelium.

The efficacy of five different factor VIII-von Willebrand factor (FVIII-VWF) preparations in mediating adherence of blood platelets to damaged vessel walls was tested in an annular perfusion chamber utilizing human arteries and reconstituted blood. FVIII-VWF-purified by Sepharose CL-4B chromatography and von Willebrand factor prepared from this preparation by dissociation with 0.25 M CaCl2 followed by Sepharose CL-6B chromatography were equally effective in mediating platelet adherence as FVIII-VWF in cryoprecipitate and in plasma from normal subjects. A commercial concentrate of FVIII-VWF (Hemofil, Hyland) used for the treatment of haemophiliacs did not mediate platelet adherence at normal levels of FVIII-VWF related properties. A recently developed high-purity FVIII-VWF preparation (Concentrate II) containing multimers of high molecular weight normalized the platelet adherence. Platelet adherence in plasma obtained from two patients with von Willebrand's disease (VWD) was impaired, but plasma samples obtained following treatment with Concentrate II mediated normal platelet adherence. The normalization of platelet adherence paralleled the normalization of the bleeding time. This platelet adherence assay offers an inexpensive and efficient in vitro tool to test the efficacy of FVIII-VWF preparations designed for VWD patients. Preparations such as cryoprecipitate and Concentrate II mediated the platelet adherence and normalized the bleeding time. The commercial preparation did not mediate platelet adherence and had no effect on the bleeding time.

Antigens↗

PubMed1994

Molecular map of chromosome 19 including three genes affecting bleeding time: ep, ru, and bm.

The mouse ruby eye (ru) and pale ear (ep) pigment dilution genes cause platelet storage pool deficiency (SPD) and prolonged bleeding times. The brachymorphic (bm) gene, in addition to causing skeletal abnormalities, is also associated with prolonged bleeding times. All three hemorrhagic genes are found within 10 cM on Chromosome (Chr) 19. In this study, 15 microsatellite markers and five cDNAs, spanning 21 cM of Chr 19, were mapped in relation to the bm, ep, and ru genes in 457 progeny of an interspecific backcross utilizing the highly inbred strain PWK derived from the Mus musculus musculus species. Several markers were found to be closely linked to the three genes and should be useful as entry points in their eventual molecular identification.

Animals↗

PubMed1995

Effects of Visnea mocanera extracts on the bleeding time, gastrointestinal transit and diuresis in rodents.

The present study examined the effect of several extracts of Visnea mocanera L. on the bleeding time and gastrointestinal transit in mice using the Duke test and charcoal meal method, respectively; they were also investigated in order to examine their renal effects. Results showed that V. mocanera extracts significantly inhibited both the bleeding time and gastrointestinal transit in mice. No diuretic activity of these extracts were detected. In contrast, they significantly reduced the urine volume. The study provides experimental support to the therapeutic advocation of V. mocanera in ethnomedicine for the treatment of diarrhoea and the healing of wounds.

Animals↗

PubMed1991

The effects of hypnosis and of imagery on bleeding time: a brief communication.

2 studies are reported, one using hypnotized Ss selected on hypnotizability and one using Ss selected on imagery vividness, whose purpose is to examine whether non-patient Ss can control their bleeding in a laboratory setting. All Ss were cut on both arms with the "Surgicutt" device, an instrument that automatically makes a cut that will bleed from 2 to 10 minutes. Results suggest that Ss, who are instructed to reduce the bleeding time in one arm and to let the other arm bleed normally, are not able to control bleeding time.

Adult↗

PubMed1999

Tranexamic acid inhibits fibrinolysis, shortens the bleeding time and improves platelet function in patients with chronic renal failure.

BACKGROUND: A defect in platelet function is the main determinant of the prolonged bleeding time in chronic renal failure (CRF). We previously reported a significant correlation between platelet abnormalities and elevated plasma markers of plasmin and thrombin generation. Our aim was to explore the effect of inhibiting both plasmin action with tranexamic acid (TA) and thrombin production with low molecular weight heparin (LMWH), on the bleeding time (BT) and platelet function in patients with CRF. METHODS: 37 patients with CRF (mean creatinine 8.6 +/- 4.4 mg/dl) under conservative treatment, with prolonged BT, entered this study and received TA during 6 days, with (n = 24) and without LMWH (n = 13). BT, platelet aggregation/secretion, platelet granule contents, von Willebrand factor and parameters of coagulation and fibrinolysis were recorded before and at the end of treatment. RESULTS: The BT was shortened in 26/37 (67%) patients. This effect was associated with significant improvement of platelet aggregation and secretion, with decrease to a normal range of fibrin/fibrinogen degradation products, mild increase in plasmin-antiplasmin complexes and pronounced reduction of circulating plasminogen. No differences were seen among patients with or without LMWH. No serious side effects or complications were observed. INTERPRETATION: These findings indicate that the activation of fibrinolysis plays a significant role in the defect of primary hemostasis in patients with CRF. Inhibition of plasmin activity with TA shortens the BT and improves platelet function in the majority of patients with severe disease.

Antifibrinolytic Agents↗

PubMed1993

Studies of thromboxane B2, platelet factor 4, and fibrinopeptide A in bleeding-time blood of patients deficient in von Willebrand factor, platelet glycoproteins Ib and IIb-IIIa, and storage granules.

The blood volumes and concentrations of thromboxane B2 (TxB2), platelet factor 4 (PF4), and fibrinopeptide A (FPA) were measured every 30 seconds in bleeding-time blood in normal subjects and in patients with idiopathic thrombocytopenic purpura (ITP), delta and alpha delta storage pool deficiency (SPD), Bernard-Soulier Syndrome (BSS), thrombasthenia (TSA), and von Willebrand's disease (vWD). Data were fitted to second-order (TxB2, PF4, and FPA) or third-order (volumes) polynomials. Average values for various parameters over fixed-time intervals were determined by numerical methods. The bleeding time was greater than 15 minutes in all patient groups and the initial bleeding, as reflected by the initial slope of the fitted blood volume curves, was increased in ITP, BSS, and SPD (delta-SPD in particular), but not in vWD and TSA. The increased values for both the initial slope and the volume of blood collected after 2 minutes in SPD suggest that vascular tone may be modulated, in part, by dense granule substances such as adenosine triphosphate (ATP) or serotonin. In TSA, uniquely, both platelet (TxB2 and PF4) and coagulation (FPA) values were increased in early bleeding samples (initial slope). In vitro studies of TxB2 production, together with previous flow studies of fibrin formation, also suggest enhanced activation and coagulant properties of thrombasthenic platelets. In other patients, reduced values of all substances at later times may reflect impaired platelet-fibrin plug formation in the high-shear regions at the ends of transected blood vessels. However, the initial slopes of the fitted curves for both TxB2 and PF4 were normal in vWD, suggesting that the early appearance of these substances may typically be from platelets that are adherent to collagen within the lower shear environment of the wound surface. The finding that FPA values were not decreased initially in any patient group, including ITP, but were decreased at later times (except for TSA), suggests that early fibrin formation occurs independently of platelets in the low-shear environment of the wound surface, whereas at later times fibrin is formed in a platelet-dependent manner in the high-shear regions at the ends of transected vessels.

Adult↗

PubMed1998

Effect of dialysis on bleeding time in chronic renal failure.

Renal failure is associated with severe haemorrhagic complications. Platelets play an important role in coagulation and their dysfunction may be responsible for the bleeding tendency in these patients. Sixty patients with advanced renal failure were investigated for bleeding tendency due to platelet dysfunction. The pre-dialysis platelet count was 46 to 325 x 10(9)/L) (mean 166 x 10(9)/L). Post-dialysis platelet count was 60 to 310 x 10(9)/L, (mean 172 x 10(9)/L) Pre-dialysis mean bleeding time (BT) was 4.95 +/- 0.27 minutes (range 1.30 to 20 minutes). Thirty-three patients (55%) had prolonged BT before dialysis. Mean BT in all patients after dialysis was 2.46 +/- 0.24 minutes (range 1.15 to 10 minutes). BT was corrected in 27 (81.8%) out of 33 patients with prolonged BT before dialysis. In 6 patients (10%) it remained prolonged. This improvement in BT after dialysis was statistically significant (p value < 0.001). Both peritoneal and hemodialysis resulted in significant improvement in bleeding time.

Adolescent↗