Topic
Bleeding time
About: Bleeding time is a research topic. Over the lifetime, 2644 publications have been published within this topic receiving 86543 citations.
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Papers
TL;DR: In this article, the authors showed that platelet surface P-selectin-positive (degranulated) platelets are rapidly cleared from the circulation, but continue to circulate and function.
Abstract: To examine the hypothesis that surface P-selectin-positive (degranulated) platelets are rapidly cleared from the circulation, we developed novel methods for tracking of platelets and measurement of platelet function in vivo. Washed platelets prepared from nonhuman primates (baboons) were labeled with PKH2 (a lipophilic fluorescent dye), thrombin-activated, washed, and reinfused into the same baboons. Three-color whole blood flow cytometry was used to simultaneously (i) identify platelets with a mAb directed against glycoprotein (GP)IIb-IIIa (integrin alpha 11b beta 3), (ii) distinguish infused platelets by their PKH2 fluorescence, and (iii) analyze platelet function with mAbs. Two hours after infusion of autologous thrombin-activated platelets (P-selectin-positive, PKH2-labeled), 95 +/- 1% (mean +/- SEM, n = 5) of the circulating PKH2-labeled platelets had become P-selectin-negative. Compared with platelets not activated with thrombin preinfusion, the recovery of these circulating PKH2-labeled, P-selectin-negative platelets was similar 24 h after infusion and only slightly less 48 h after infusion. The loss of platelet surface P-selectin was fully accounted for by a 67.1 +/- 16.7 ng/ml increase in the plasma concentration of soluble P-selectin. The circulating PKH2-labeled, P-selectin-negative platelets were still able to function in vivo, as determined by their (i) participation in platelet aggregates emerging from a bleeding time wound, (ii) binding to Dacron in an arteriovenous shunt, (iii) binding of mAb PAC1 (directed against the fibrinogen binding site on GPIIb-IIIa), and (iv) generation of procoagulant platelet-derived microparticles. In summary, (i) circulating degranulated platelets rapidly lose surface P-selectin to the plasma pool, but continue to circulate and function; and (ii) we have developed novel three-color whole blood flow cytometric methods for tracking of platelets and measurement of platelet function in vivo.
606 citations
TL;DR: It is indicated that 1-deamino-8-D-arginine vasopressin can be used for temporary correction of bleeding time and may prevent surgical bleeding in patients with uremia and factor VIII-related antigen and ristocetin cofactor.
Abstract: In a randomized double-blind cross-over trial we gave either 1-deamino-8-D-arginine vasopressin or placebo to 12 patients with uremia, hemorrhagic tendencies, and prolonged bleeding times. After vasopressin infusion, all patients had shortened bleeding times, with the effect lasting for at least four hours in most cases. Platelet count, platelet cyclic AMP levels, platelet retention on glass beads, plasma fibronectin, serum thromboxane B2 and residual prothrombin, hematocrit, and plasma osmolarity were unchanged after vasopressin. A consistent post-infusion increase in factor VIII coagulant activity and, to a lesser extent, in factor VIII-related antigen and ristocetin cofactor accompanied the shortening of bleeding time. In addition, vasopressin induced the appearance in plasma of larger von Willebrand-factor multimers than those present in the resting state. The compound was given to nine additional patients with acute or chronic renal failure and prolonged bleeding times, before major surgery or renal biopsy. In these patients, shortening of the bleeding time was associated with normal hemostasis. Our findings indicate that 1-deamino-8-D-arginine vasopressin can be used for temporary correction of bleeding time and may prevent surgical bleeding in patients with uremia.
597 citations
TL;DR: Data suggest that when a hypothermic patient bleeds without surgical cause, skin and wound temperature should be restored to normal before the administration of blood products that are not only expensive but may also transmit disease.
Abstract: Baboons that were subjected to systemic hypothermia at 32 C had an arm skin temperature of 27.3 C and bleeding time of 5.8 minutes. With local warming of the arm skin to 34 C, the bleeding time was 2.4 minutes. In normothermic baboons with arm skin temperature of 34.6 C, the bleeding time was 3.1 minutes. Local cooling of the arm skin to 27.6 C produced a bleeding time of 6.9 minutes. Increasing the skin temperature of the arm in hypothermic baboons to 38.9 C and in normothermic baboons to 40.1 C reduced bleeding times to 2.1 and 2.3 minutes, respectively. In both hypothermic and normothermic baboons there was a negative and significant correlation between the bleeding time and the arm skin temperature and the thromboxane B2 level in the shed blood obtained at the template bleeding time site. There was a significant positive correlation between the thromboxane B2 level in the shed blood and the arm skin temperature. Both in-vivo and in-vitro studies have shown that the production of thromboxane B2 by platelets is temperature-dependent, and that a cooling of skin temperature produces a reversible platelet dysfunction. Data also suggest that when a hypothermic patient bleeds without surgical cause, skin and wound temperature should be restored to normal before the administration of blood products that are not only expensive but may also transmit disease.
570 citations
TL;DR: It is shown that bleeding time depends on both platelet count and mean platelet volume, as well as platelet number, which should be considered as an index of haemostasis and its dysfunction, thrombosis.
508 citations
TL;DR: Constitutive expression of factor IX was observed, which resulted in the correction of the bleeding disorder over a period of over 17 months in mice, and as a preclinical model for gene therapy, recombinant adeno-associated viral vectors containing the human or canine factor IX cDNAs were infused into the livers of murine and canine models of hemophilia B.
Abstract: Hemophilia B, or factor IX deficiency, is an X-linked recessive disorder occurring in about 1 in 25,000 males. Affected individuals are at risk for spontaneous bleeding into many organs; treatment mainly consists of the transfusion of clotting factor concentrates prepared from human blood or recombinant sources after bleeding has started. Small- and large-animal models have been developed and/or characterized that closely mimic the human disease state. As a preclinical model for gene therapy, recombinant adeno-associated viral vectors containing the human or canine factor IX cDNAs were infused into the livers of murine and canine models of hemophilia B, respectively. There was no associated toxicity with infusion in either animal model. Constitutive expression of factor IX was observed, which resulted in the correction of the bleeding disorder over a period of over 17 months in mice. Mice with a steady-state concentration of 25% of the normal human level of factor IX had normal coagulation. In hemophilic dogs, a dose of rAAV that was approximately 1/10 per body weight that given to mice resulted in 1% of normal canine factor IX levels, the absence of inhibitors, and a sustained partial correction of the coagulation defect for at least 8 months.
480 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2025 | 5 |
| 2024 | 7 |
| 2023 | 18 |
| 2022 | 39 |
| 2021 | 33 |
| 2020 | 27 |