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PubMed1989

An in vitro bleeding time test.

A new conical plastic device and method, the Platelet-Stat test, has been developed to measure in vitro bleeding time. Ten milliliters of citrated blood, collected by venipuncture, was used. The in vitro bleeding time test was validated by several criteria. Eight volunteers tested had a mean bleeding time of less than 1 minute. Different anticoagulants were evaluated, and the test performed optimally with citrate. Within-run precision had a mean time of 39 +/- 6.7 seconds with a coefficient of variation of 17%. An aspirin study was done on eight volunteers. Preaspirin in vitro bleeding time was less than 1 minute, whereas postaspirin times were more than 7 minutes at 18-24 hours. This test is a reproducible method of performing the bleeding time with greater precision than the in vivo test.

Anticoagulants↗
PubMed1997

Prolongation of bleeding time by acute hemolysis in rats: a role for nitric oxide.

The present study was aimed at clarifying the interaction between red blood cell trauma and bleeding observed in some clinical conditions. Acute hemolysis provoked by distilled water injection was followed by a significant prolongation of the "template" bleeding time in rats. Comparable effects were observed after injection of an isotonic lysate of washed red blood cells. N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) formation from L-arginine, normalized bleeding time when given to rats before hemolysis induction. The occurrence of hemolysis decreased ex vivo platelet adhesion to collagen without affecting platelet aggregation and induced a transient drop in blood pressure, the latter occurring during the first minute after injection. L-NAME pretreatment increased ex vivo platelet adhesion but did not affect either platelet aggregation or fall in blood pressure. All the effects of L-NAME were blunted by treating the animals with the NO precursor L-arginine but not D-arginine. Incubation of the erythrocyte lysate with apyrase prevented the prolongation of bleeding time induced by the hemolysate. Moreover, ADP administration, at doses that did not increase hemoglobin levels, induced effects similar to those observed after hemolysis (on template bleeding time and ex vivo platelet adhesion), which were also reversed by L-NAME and restored by L-arginine. ADP is abundantly released from (hemo)lysed red blood cells and is known to stimulate release of NO, a potent vasodilator and inhibitor of platelet adhesion. ADP-dependent NO release could be responsible for bleeding time prolongation, due to abnormalities in platelet-vessel wall interaction, during acute hemolysis. Lysis of white blood cells may also contribute to prolongation of bleeding time. Because ADP could not be detected in these cells, we postulate that other mechanisms also can be involved in bleeding time prolongation after blood cell activation in vivo.

Adenosine Diphosphate↗
PubMed2000

Performing and interpreting the bleeding time in the neonatal intensive care unit.

In summary, the bleeding time is a helpful clinical tool to detect and investigate certain hemostatic defects in neonates and to evaluate the adequacy of treatments. A prolonged bleeding time alone is sometimes not sufficient to diagnose specific conditions requiring further investigations. Platelet hyporeactivity in the first days of life, gestational age, platelet dysfunction secondary to various neonatal or maternal pathologic conditions, neonatal or maternal drug administration, and hematocrit must be considered for the correct interpretation of the bleeding time test in neonates. In addition, reliable test results can be ensured only by the scrupulous execution of the procedure.

Bleeding Time↗
PubMed1986

Platelet von Willebrand factor: an important determinant of the bleeding time in type I von Willebrand's disease.

We studied 17 patients with moderate to mild type I von Willebrand's disease (vWd) and correlated the bleeding time with the plasma von Willebrand factor antigen (vWf Ag), the plasma vWf activity (ristocetin cofactor), the platelet vWf Ag, and the platelet vWf activity. We found an excellent correlation between the bleeding time and the platelet vWf activity and, to a lesser extent, between the bleeding time and the platelet vWf Ag. The length of the bleeding time was inversely proportional to the level of the platelet vWf (P less than .001) or, to a lesser extent, the platelet vWf Ag (P less than .05). The plasma vWf Ag and activity did not correlate significantly with the bleeding time. These studies indicate that the platelet vWf is one of the important bleeding time factors in type I vWd and that the platelet vWf plays an important role in the early steps of hemostasis.

Bleeding Time↗
PubMed1990

Evaluation of an automated bleeding time device in the newborn.

Sick infants frequently developed impaired hemostasis as a secondary event. Abnormal platelet-vessel wall interaction contributes to the hemorrhagic side effects. Currently, the bleeding time is the best measure of in vivo platelet participation in small vessel hemostasis. Bleeding times in the newborn have been previously determined with an automated device designed for the adult or with nonautomated devices. The automated bleeding time device for the adult is not suitable for the infant (length 5 mm, depth 1 mm). We evaluated the performance of an automated bleeding time device designed specifically for the newborn making a cut 2.5 mm in length and 0.5 mm in depth. The results with the automated device showed a strong correlation with the modified template bleeding time device previously used for the newborn. The normal range was shorter and the sensitivity to abnormal vessel wall interaction was greater with the automated device. As well, the ease of determining the bleeding time with the automated device was considerably improved over the template device.

Bleeding Time↗
PubMed1999

Prolonged bleeding time in experimental cirrhosis: role of nitric oxide.

BACKGROUND/AIMS: Nitric oxide is a powerful in vitro inhibitor of platelet adhesion and aggregation. Our aim was to investigate whether the in vivo inhibition of nitric oxide release shortens bleeding time, in rats with cirrhosis induced by chronic bile duct ligation. METHODS: Mean arterial pressure and bleeding time were measured under basal conditions and 5, 15 and 30 min after administration of vehicle (0.9% saline) or an inhibitor of nitric oxide synthesis, Nw-nitro-L-arginine (5 mg/kg, iv). Mean arterial pressure was measured with an intra-arterial catheter and bleeding time with a standardized Simplate device. RESULTS: Cirrhotic rats showed a lower mean arterial pressure (116+/-4 mmHg) and a prolonged bleeding time (177+/-40 s) compared to control animals (133+/-6 mmHg and 95+/-12 s, respectively, p<0.01). In cirrhotic rats, Nw-nitro-L-arginine significantly increased mean arterial pressure (from 116+/-5 to 141+/-11 mmHg, p<0.05) and completely normalized bleeding time (from 170+/-39 to 103+/-21 s, p<0.05) 15 min after administration. Pretreatment with L-arginine (300 mg/kg, iv) prevented the hemodynamic and hemostatic changes induced by Nw-nitro-L-arginine. A trend to normalize platelet adhesion was observed in cirrhotic rats after the inhibition of nitric oxide production. In control animals, Nw-nitro-L-arginine increased mean arterial pressure, while no effect on bleeding time was observed. CONCLUSIONS: These findings support the concept that nitric oxide may be a mediator in the bleeding time abnormalities associated with experimental cirrhosis.

Animals↗
PubMed1985

Low haematocrit and prolonged bleeding time in uraemic patients: effect of red cell transfusions.

This study demonstrates that a low haematocrit is the main determining factor of the prolonged bleeding time often encountered in uraemic haemodialysed patients. Thirty-three patients submitted to regular haemodialysis and having a platelet count greater than 100 X 10(9)/l were investigated with the following tests: simplate bleeding time, blood cell count, platelet aggregation induced by ADP, collagen and sodium arachidonate, arachidonate induced MDA synthesis, tests for detection of an acquired storage pool disease, and factor VIII complex level. The results were compared to two other groups; one of uraemic patients not yet subjected to haemodialysis and another of healthy volunteers. The results were basically identical in the two groups of uraemic patients. The only consistent abnormality was a 30-35% reduction in the platelet MDA synthesis in comparison with control subjects. There was a negative correlation between the log bleeding time and the haematocrit (r = 0.78, P less than 0.01). Fourteen uraemic patients having a prolonged bleeding time were submitted to a red cell transfusion programme and were investigated a second time under identical conditions. There was no change in any of the platelet function tests or in the factor VIII complex level, but the bleeding time was normalized when the post-transfusion haematocrit was over 26% (nine patients). This study emphasizes the role of anaemia in the pathogenesis of the prolonged bleeding time in uraemia and suggests that red cell transfusion can be a long-term efficient therapeutic measure to stop bleeding in these patients.

Adolescent↗
PubMed1984

A comparative study of the effects of aspirin and paracetamol (acetaminophen) on platelet aggregation and bleeding time.

In a double blind, randomised trial, the effects of 1 g aspirin and 1 g paracetamol were compared on bleeding time and platelet aggregation in 40 volunteers (20 females). Also investigated was the relationship between plasma aspirin esterase activity and both bleeding time and platelet aggregation after aspirin. Following 1 g aspirin there was a significant increase in bleeding time at 24 h (p less than 0.01). A significant reduction (P less than 0.01) in platelet aggregation with collagen was observed at 1, 6 and 24 h after aspirin, but no significant reduction (P greater than 0.05) was observed with ADP. Paracetamol had no effect on bleeding time or platelet aggregation. Plasma aspirin esterase activity ranged from 0.26-0.6 mumol/ml/min. A significant negative correlation (R = -0.55, P less than 0.001) was observed between percentage increase in bleeding time (24 h) and plasma aspirin esterase activity. Further significant correlations were observed between plasma aspirin esterase activity and change in platelet aggregation with collagen at 1 h (R = 0.68, P less than 0.001), 6 h (R = -0.73, P less than 0.001) and 24 h (R = -0.67, P less than 0.001). These results suggest that it might be possible to predict an individual's haemostatic response to aspirin from knowledge of their plasma aspirin esterase activity.

Acetaminophen↗
PubMed1992

Bleeding time and antiplatelet agents in normal volunteers.

Clinical trials have shown that antiplatelet agents are effective in the prevention of thrombosis in arterial diseases and increase bleeding time. To compare the effects of three such drugs [acetylsalicylic acid (ASA) at two dose levels, ticlopidine and indobufen] on bleeding time, we performed a randomized cross-over study on 12 normal subjects. All received the four treatments (ASA 300 mg daily and 500 mg twice daily, ticlopidine 250 mg twice daily and indobufen 200 mg twice daily, each for 6 days plus one dose on day 7) in a sequential manner with a washout period of 15 days between the treatments. Bleeding time was measured using a Surgicut device (Ortho, Milan, Italy) before treatment, 2 and 24 h after the first administration, and before and 2, 24, 48 and 72 h after the last administration. ASA (at both doses) and indobufen quickly induced a significant prolongation of bleeding time, but the effect of indobufen soon wore off after the treatment was stopped, unlike that of ASA. In contrast, ticlopidine treatment prolonged bleeding time only after the first 24 h, and after 7 days the mean value was significantly higher than with ASA (both doses) and indobufen. This significant difference in bleeding time between ticlopidine and the other drugs was still present 48 h after the end of treatment.

Adolescent↗
PubMed1993

Assessment of the hemostatic effectiveness of human platelets treated with aminomethyltrimethyl psoralen and UV A light using a rabbit ear bleeding time technique.

The photochemical aminomethyltrimethyl psoralen (AMT), in conjunction with UV A light (UVA), has been shown to inactivate human immunodeficiency virus-1 and model viruses in platelet suspensions under conditions that have only a minimal effect on in vitro platelet properties. A rabbit ear bleeding time technique was used to assess the hemostatic effectiveness of human platelet suspensions treated with AMT/UVA. New Zealand White rabbits were made thrombocytopenic by a combination of irradiation and heterologous antirabbit platelet antiserum. Reticuloendothelial function in these rabbits was suppressed by the intravenous administration of ethyl palmitate. The hemostatic function of 1- and 5-day-old human platelet suspensions (14.5% plasma) that had been treated on day 1 with 40 micrograms/mL AMT and 24 kJ/m2 UVA (1 x UVA) was evaluated by measuring microvascular bleeding times after a standard incision. Comparable bleeding times were observed after infusion with both control and AMT/UVA-treated platelets stored for either 1 or 5 days. With the transfusion of AMT/1 x UVA-treated platelets stored for 5 days, the mean (+/- SD) bleeding time was 156.3 +/- 39.2 seconds (n = 10). With untreated platelets (no AMT/no UVA), stored for 5 days, the mean bleeding time was 189.2 +/- 36.4 seconds (n = 10). Neither AMT nor 1 x UVA treatment alone influenced the observed bleeding times. In contrast, the hemostatic effectiveness of human platelet suspensions was diminished if they were exposed to three times the standard UVA dose (72 kJ/m2) on day 1 and stored for 4 more days, regardless of whether AMT was present, with the mean bleeding time increasing to 442.2 +/- 122.6 seconds (n = 15, AMT present) or 396.0 +/- 45.9 seconds (n = 10, AMT absent). These results are consistent with data obtained from in vitro studies and indicate that virucidal AMT/1 x UVA treatment does not influence platelet hemostatic function. However, the final conditions to achieve these results must be carefully controlled.

Animals↗
PubMedDate not supplied

A comparison of thromboelastogram and template bleeding time in the evaluation of platelet function after aspirin ingestion.

STUDY OBJECTIVE: To compare template bleeding time (TBT) with thromboelastography (TEG) in human subjects after aspirin ingestion. DESIGN: Healthy volunteers were given a single 650 mg dose of aspirin or a dose of 650 mg of aspirin on three successive days. TBT and TEG studies were performed prior to aspirin ingestion and 4, 24, 72, and 168 hours after ingestion. SETTING: Inpatient operating room support area at the UCLA Center for Health Sciences. VOLUNTEERS: Residents and nurses who were in good general health, had not taken aspirin for 2 weeks, had normal platelet counts, and had no evidence of bleeding or coagulation disorders. INTERVENTION: TBT and TEG studies were performed prior to and after the ingestion of aspirin. MEASUREMENTS AND MAIN RESULTS: TBT studies were significantly prolonged at 4, 24, and 72 hours compared with controls. Maximum bleeding time prolongation occurred 24 hours after aspirin ingestion. Bleeding time returned to control values by the end of 168 hours (1 week). No TEG parameter was significantly changed by aspirin ingestion. CONCLUSION: TEG results may not identify patients who have an increased bleeding time as a result of aspirin ingestion.

Adult↗
PubMed1981

Effects of 11-week increases in dietary eicosapentaenoic acid on bleeding time, lipids, and platelet aggregation.

The effect of a diet rich in eicosapentaenoic acid (EPA) on platelet phospholipid fatty acid composition, platelet aggregation, and bleeding time was studied in 10 healthy men, whose usual diet was partly replaced by fish for 11 weeks. This diet provided 2-3 g EPA per day. Two doses (3.5 and 10 mg/kg body-weight) of acetylsalicylic acid (ASA) were given before and during the diet. The fish diet prolonged bleeding time (by 42%) and decreased platelet aggregability. The changes in platelet phospholipid fatty acid composition consisted of increases in the omega-3 series (C20:5 and C22:6) and decreases in the omega-6 series (C18:2 and C20:3). The reduction in platelet aggregation induced by collagen and ADP did not parallel the changes in platelet membrane phospholipids and bleeding times. Diminished platelet aggregation induced by collagen lasted only 3 weeks (while subject was still on the diet), whereas the decreased sensitivity to ADP persisted for at least 11 weeks after the volunteers had resumed their normal diet. ASA taken before the diet prolonged bleeding time by as much as did the diet itself. ASA taken during the diet prolonged bleeding time by more than the sum of the increases in bleeding time caused by ASA and by the EPA diet separately, but the synergism was not significantly more than additive. The findings suggest that a diet rich in omega-3 polyunsaturated fatty acids reduces tha interaction between platelets and the vessel wall by mechanisms which are more complex than just a reduction in susceptibility of platelets to the naturally occurring agents collagen and ADP, or an imbalance between proaggregatory and anti-aggregatory prostaglandin derivatives.

Adult↗
PubMed1990

Bleeding times in rats treated with heparin, heparin fragments of high and low anticoagulant activity and chemically modified heparin fragments of low anticoagulant activity.

A template bleeding time study in the rat was undertaken to see if it is possible to correlate bleeding times with the molecular weight, anticoagulant activity or chemical composition of heparin or heparin-derived compounds. Heparin from porcine intestinal mucosa (PM-heparin) and from bovine lung (BL-heparin) as well as heparin fragments from these sources were compared. Heparin fragments of low anticoagulant activity were prepared by affinity chromatography on immobilized antithrombin as well as by chemical modification. A heparin fragment of high affinity for antithrombin (HA-fragment) caused a marked and dose-dependent increase in bleeding time while the corresponding heparin fragment with low affinity for antithrombin (LA-fragment) had a marginal and non-dose dependent effect on the bleeding time. Similar results were also obtained with PM-heparin with high and low affinity for antithrombin. A high anti-FXa activity was not always correlated with a marked bleeding tendency. Provided that a fragment was devoid of activated partial thromboplastin time (APTT) activity, it was not possible to provoke a bleeding time of 20 min or longer, although the compound was administered at a dose of 1,088 U/kg (anti-FXa activity). On the other hand, a N-acetylated chemically oversulphated heparin fragment, with a very low anti-FXa activity (1 U/mg) and with an APTT activity of 34 U/mg, caused a bleeding time of 20 min or longer in 70% of the animals after injection of the same number of APTT units, 1,088 U/kg. These data indicate that the APTT activity is a better and more sensitive indicator of the bleeding than is the anti-FXa activity.

Acetylation↗
PubMed1993

[Bleeding time in patients with chronic liver diseases].

In 105 patients with chronic liver diseases, bleeding time was studied by Ivy method. A statistically significant difference was found in the bleeding time between patients with chronic hepatitis and controlled cirrhosis and patients with uncontrolled cirrhosis. In 10 out of 26 patients with prolonged bleeding time with platelet count over 100,000/mcl and prothrombin index value over 60%, clinical signs of haemorrhagic diathesis were observed. We believe that the evaluation of platelet function by measuring the bleeding time by Ivy method should enter the set of routine laboratory tests in patients with chronic liver disease.

Chronic Disease↗
PubMed1997

A comparison of the effects of aspirin on bleeding time measured using the Simplate method and closure time measured using the PFA-100, in healthy volunteers.

AIMS: The aim of this study was to compare the effects of aspirin on platelet function as measured by the 'classical' template bleeding time with a new ex vivo method measuring closure times using the PFA-100 machine. Platelet aggregation in response to arachidonic acid was also measured ex vivo. METHODS: The trial was a randomized, double-blind, placebo-controlled crossover design, with each volunteer taking 750 mg aspirin (BP) or placebo, three times a day for 5 days, with an 18 day wash-out period between treatments. Bleeding times and closure times were measured before the first dose on the first day and 0.5 h after the last dose on the fifth day of each treatment period. They were also measured 2 weeks after the last day of the trial. RESULTS: Baseline bleeding times (pre-placebo) were 415 s using the Simplate, whilst baseline closure times were 115 s using the PFA-100. Aspirin treatment caused an increase of both the template bleeding time (61%) and the closure time of the PFA-100 (79%) when compared with the effects of placebo. The platelet aggregatory response to arachidonic acid was completely inhibited following aspirin treatment and was unaffected following placebo. Two weeks after the end of the trial, all values had returned to pre-treatment levels. The template bleeding time was unaltered in 1 of the 12 volunteers during aspirin treatment and was significantly prolonged in 3 of the 12 volunteers during placebo treatment. The PFA-100 closure time was unaltered in 1 of the 12 volunteers during aspirin treatment and was prolonged in 1 subject during placebo treatment. CONCLUSIONS: The change in closure time using the PFA-100 is as sensitive and reproducible to the effects of aspirin on platelet function as is the template bleeding time test. However, the PFA-100 produced less variable effects with fewer false positive results.

Adult↗
PubMed1984

Prolongation of rat tail bleeding time by ketanserin: mechanisms of action.

Serotonin (5-HT) may play a regulatory role in platelet-vessel wall interaction. This can be reliably investigated by measuring bleeding time. Ketanserin is a recently developed selective 5-HT2 receptor antagonist, reportedly effective against both platelet and vascular 5-HT activation. Ketanserin (5-10 mg/kg) significantly prolonged tail bleeding time measured in conscious rats by two different techniques. While mianserin (a 5-HT2 receptor antagonist exhibiting alpha-adrenolytic activity) also prolonged bleeding time, methysergide, metergoline and cyproheptadine did not. All three compounds acted as 5-HT2 receptor antagonists with appreciable affinity for 5-HT1 receptors. On the other hand, bleeding time was prolonged by either prazosin (a selective alpha 1-adrenoceptor antagonist) or labetalol (an alpha 1- and beta-receptor antagonist). In contrast it was not affected by phentolamine or nicergoline (alpha 1-alpha 2-receptor antagonists) nor by propranolol (a beta-receptor antagonist). The effect of prazosin was significantly increased by combining it with either ketaserin or metergoline. Depletion of platelet serotonin by reserpine did not result in any modification of bleeding time, unless reserpine was combined with an inhibitor of 5-HT synthesis. Platelet activation by 5-HT was neither potentiated by norepinephrine nor prevented by prazosin or phentolamine whereas ketanserin and methysergide were equally effective inhibitors. These findings argue against a role of platelet and/or vascular 5-HT2 receptors in the antihemostatic effect of ketanserin in rats. This drug prolongs bleeding time by antagonising vascular adrenoceptors (prazosin-like effect) and/or by preventing a synergistic interaction between 5-HT and catecholamines at the vascular level.

Animals↗
PubMed1983

Warfarin-induced factor VII deficiency and the bleeding time.

The effect of warfarin-induced factor VII deficiency on the skin bleeding time was investigated in 10 consecutive patients with mean prothrombin times of 33 sec and factor VII levels of 7%. Bleeding times in all but one subject were entirely within the normal range. We conclude that warfarin administration, even to the point of prolonging the prothrombin time beyond the therapeutic range, is not associated with an abnormal bleeding time. Furthermore, from the above evidence and a review of the literature, it is considered doubtful that factor VII plays a major role in primary hemostasis.

Bleeding Time↗
PubMedDate not supplied

Preoperative test of bleeding time in ear surgery.

In 300 patients subjected to ear surgery the bleeding time according to Ivy was determined preoperatively. In 25 cases prolonged bleeding time was found. Further investigations revealed mild thromboasthenia in 4 cases and enhanced fibrinolytic activity in one instance. In 10 patients the cause was intake of drugs containing acetylsalicylic acid. During operation the patients were treated with AMCA and in two cases fresh blood also was given. Even slightly enhanced bleeding can affect the results in microsurgery of the ear. We therefore suggest that bleeding time should be determined as a preoperative routine in order to detect the patients in need of specific treatment. Patients also should be recommended to avoid drugs containing acetylsalicylic acid for a fortnight before surgery.

Adolescent↗