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At least 343 records · Page 19Linked to original sources
PubMed2000

Effects of HMG-CoA reductase inhibitor on hemostasis.

Clinical trials of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor (statin) therapy have demonstrated improvement in coronary atherosclerosis progression and reduction in risk of cardiovascular events. However, improvement in cardiovascular end-points is incompletely explained by the baseline or treated LDL cholesterol level. The beneficial effects of statins on clinical events may involve nonlipid mechanisms that modify hemostasis. Local activation of platelets and thrombus formation adjacent to atheromatous plaques, especially where ruptured or eroded, are now recognized to be of pathophysiological importance in the acute and chronic clinical expression of coronary heart disease. Thus, favorable effects of statins on hemostasis may be relevant to decreasing or delaying the progression and clinical manifestations of atherosclerosis.

Coronary Artery Disease↗
PubMed1998

Platelet receptors for the complement component C1q: implications for hemostasis and thrombosis.

Platelets participate in a variety of responses of the blood to injury (1). In addition to their well known role in hemostasis and thrombosis, platelets play a role in inflammation and react with components of the immune system. Immune complexes and aggregated IgG, for example, are known to activate platelets via ligation of Fc gamma RII receptors and induce the release of platelet granule contents, including biogenic amines and adenine nucleotides (2). Platelets also interact with the complement subcomponent C1q utilizing binding sites that are unrelated to C1s, a complement subcomponent which was originally suggested to support C1q binding to thrombocytes (3). The physiologic and pathologic consequences of platelet C1q receptor occupancy are incompletely understood. Platelet C1q receptors may contribute to immune complex localization and clearance, as has been suggested for C1q receptors on phagocytic cells (4), but considerable evidence is emerging to suggest that the interaction between C1q and platelets may influence hemostasis and perhaps, more profoundly, thrombotic complications resulting from immune injury. This review will summarize current concepts in C1q receptor biology as it relates to human platelet function and blood coagulation.

Animals↗
PubMed1999

The effect of chitosan (poly-N-acetyl glucosamine) on lingual hemostasis in heparinized rabbits.

PURPOSE: The purpose of this study was to evaluate the effect of chitosan on lingual hemostasis in rabbits whose coagulation pathway had been impaired by administration of intravenous heparin. MATERIALS AND METHODS: Bleeding times were measured for bilateral (15 mm x 2 mm) tongue incisions in 10 New Zealand white rabbits. Using a randomized, blinded experimental design, one incision in each animal was treated with chitosan, and the other was treated with the control vehicle without chitosan. Activated coagulation times and extraoral bleeding times were measured for each animal before, during, and after heparinization. RESULTS: Intravenous infusion of heparin more than tripled the mean activated coagulation time and increased mean systemic bleeding time by 40%. In this heparinized animal model, lingual incisions receiving the experimental substance showed a 43% improvement in bleeding time as compared with lingual incisions receiving the control solution (P< or =.001). Chitosan treatment brought bleeding time of the lingual incision for heparinized animals within the normal range. Scanning electron microscopic evaluation of the incisions treated with chitosan showed an altered red blood cell morphology and an unusual affinity between erythrocytes. CONCLUSIONS: Topical application of chitosan to lingual incisions effectively decreased intraoral bleeding time in a therapeutically anticoagulated (heparinized) rabbit model. Chitosan facilitated lingual hemostasis, possibly through interaction with erythrocytes, linking them together to establish a cellular clot or hemostatic plug.

Animals↗
PubMed1976

Post-extraction hemostasis during coumarin anticoagulant therapy with a locally applied coagulation-active substance.

A safe and simple method for the dento-alveolar attendance of patients on coumarin derivative therapy is reported. It eliminates the need to interrupt anticoagulant administration, while a physiologic coagulation-active substance consisting of fibrin, thrombin, and the patient's venous blood is used for hemostasis. This easy-to-prepare substance was applied following 53 extractions, two alveolar corrections and one resection of the third molar, and excellent hemostasis was observed without the occurrence of a secondary hemorrhage.

Administration, Topical↗
PubMed1987

Equine hemostasis. Description, evaluation, and alteration.

This is a review of equine hemostasis and is divided into three sections. The initial portion describes the normal hemostatic system and includes platelet function, coagulation, fibrinolysis and control processes. The second phase is devoted to laboratory tests of hemostasis, and the last section provides information on specific alterations.

Animals↗
PubMed2002

[Effects of plasma substitutes on hemostasis].

OBJECTIVE: Data synthesis on haemostasis effects of cristalloids and colloids and clinical implications for their use for plasma volume replacement. DATA SOURCES: Data were searched in the Medline database from 1954 to 2000 using the following key-words: cristalloids, colloids, albumin, gelatin, dextran, hydroxyethyl starch, haemostasis, von Willebrand disease, haemodilution. DATA EXTRACTION: Publications from 1954 to 1990 were selected depending on the quality of their methodology. Most of articles published after 1990 and all types including case report were accepted. DATA SYNTHESIS: Cristalloids induces a moderate hypercoagulable state with 10 to 30% haemodilution. Hypocoagulation is observed above 50% haemodilution. Albumin does not impair hemostasis except with a 50% or more haemodilution where hypocoagulation is observed. Dextran dramatically impairs haemostasis and fibrinolysis. With increasing dose, a progressive decrease of all von Willebrand multimers, mostly the largest, is observed. Till 50% haemodilution, gelatin has a moderate impact on hemostasis, but platelet aggregation is moderately modified. However this moderate impairment of haemostasis may potentiate the haemostatic effect of other colloids when used in association with gelatin. More than 30% haemodilution with hydroxyethyl starch (HES) has a serious effect in vitro on platelet function and fibrinoformation. In most studies in human, less than 20 ml.kg-1 plasma volume replacement has no clinical impact, but in some evaluations postoperative bleeding is more important with HES, particularly HES 450, in comparison to other colloids. With HES 450 and HES 200 highly substituted (0.6 of degree of substitution) intravascular cumulation of large molecules leads to type I von Willebrand syndrome when doses overtake 80 ml.kg-1. Dextran and HES are prohibited in patients with impaired haemostasis due to congenital disease (haemophilia and von Willebrand disease) or acquired defect (thrombocytopenia). Caution is required in patients with renal failure or receiving antithrombotic or non-steroidal anti-inflammatory agents. Patients without a haemorrhagic diathesis must not received more than 1.5 g.kg-1.j-1 of dextran and restrictive conditions of use must be respected with HES. CONCLUSION: Except isotonic cristalloids, all colloids induce haemostastic changes particularly for haemodilution over 30%. Effects are more pronounced with HES and dextran.

Blood Coagulation↗
PubMed2001

Tissue factor in the heart. Multiple roles in hemostasis, thrombosis, and inflammation.

Tissue factor (TF) is the primary cellular initiator of the coagulation protease cascade. It plays an essential role in hemostasis to limit hemorrhage in the event of vascular injury. Indeed, loss of TF is incompatible with life. Recent studies have suggested that TF also plays non-hemostatic roles in blood vessel development, tumor angiogenesis, tumor metastasis, cell migration, and inflammation. This review discusses the roles of TF in hemostasis, thrombosis, and inflammation in the heart as well as other potential roles of TF in the maintenance of cardiac muscle.

Endothelium, Vascular↗
PubMed1996

Drugs affecting hemostasis.

Most patients admitted to the PACU are closely observed for postoperative bleeding. Although some bleeding is to be expected, some patients may have alterations in the hemostatic process leading to excess blood loss. Hemostasis can be intentionally altered by drugs given preoperatively and/or intraoperatively. The effects of these drugs may contribute to the postoperative blood loss. This article reviews the normal hemostatic process as a foundation for discussing the commonly used drugs affecting hemostasis.

Anticoagulants↗
PubMed2003

Platelets in hemostasis and thrombosis: role of integrins and their ligands.

Platelet adhesion and aggregation at the site of vascular injury are two key events in hemostasis and thrombosis. The contribution of several platelet receptors and their ligands has been highlighted in these processes. In platelet adhesion, particularly at high shear stress, GP1b-von Willebrand factor (vWF) interaction may initiate this event, which is followed by firm platelet adhesion mediated by members of the integrin family, such as beta1 (alpha2beta1, alpha5beta1) and beta3 (alphaIIbbeta3) integrins. In platelet aggregation, although GP1b-vWF, P selectin-sulfatides, and other molecules, may play some roles, the process is mainly mediated by beta3 (alphaIIbbeta3) integrin and its ligands, such as fibrinogen and vWF. Recent studies with perfusion chambers and intravital microscopy have revised the dogma established with the static (low shear stress) conditions. It is intriguing that platelet adhesion and aggregation do still occur in mice lacking both vWF and fibrinogen, suggesting that other unexpected molecule(s) may also be important in hemostasis and thrombosis.

Animals↗
PubMed2005

Does body mass index, smoking, lipoprotein levels, surgically induced menopause, hormone replacement therapy, years since menopause, or age affect hemostasis in postmenopausal women?

BACKGROUND: Controversy still exists as to the relative importance of menopausal status and lifestyle factors for the risk of coronary heart disease in women. OBJECTIVE: The purpose of this study was to assess the influence of body mass index (BMI), smoking,lipoprotein levels, surgically induced menopause, hormone replacement therapy (HRT), years since menopause, and age on hemostasis in apparently healthy postmenopausal women. METHODS: Lipoproteins (total cholesterol [TC], low-density lipoprotein cholesterol, high-density lipoprotein cholesterol [HDL-C], triglycerides [TG]), and hemostatic factors (fibrinogen, von Willebrand factor antigen [vWFag], coagulation factors VIIag [FVIlag] and VIIa [FVIIa], plasminogen activator inhibitor 1 [PAI-1]) were each measured once. A forward, stepwise, multiple regression analysis was used to assess variations in hemostatic parameters. RESULTS: A group of 292 healthy Stockholm women recruited from the census register participated in the Stockholm Female Coronary Risk Study as controls. Of these women, 260 participated in the present study. BMI, smoking, lipoprotein levels, surgically induced menopause, and years since menopause (1-5 y) were found to be associated with a 31% increase in fibrinogen levels. A 7% increase in FVIIa levels was attributed to TC, BMI, and HRT. Years since menopause (1-15 y), TG, TC, BMI, and HRT were associated with an increase of up to 26% in FVIIag levels. A 9% increase in vWFag correlated with HDL-C and years since menopause (1-10, 11-14, and > or =15 y). BMI and TG explained a 21% and 3% increase, respectively, in PAI-1 levels. Neither the use of HRT nor years since menopause had any influence on hemostasis. CONCLUSION: BMI, high levels of TC and TG, and low HDL-C levels appear to be more important than hormonal status in their impact on hemostatic variables in healthy postmenopausal women.

Adult↗
PubMed2002

Vascular-platelet and plasma hemostasis regulators from bloodsucking animals.

Saliva of bloodsuckers (leeches, insects, ticks, vampire bats) contains various regulators of some hemostatic stages. This review summarizes information on their structural characteristics and mechanisms of action. Most bloodsuckers are shown to inhibit vascular-platelet hemostasis by blocking collagen-induced platelet adhesion/aggregation. Plasma hemostasis is inhibited by blocking activation of factor X or factor Xa directly.

Animals↗
PubMed1985

Pentosane polysulfate: the effect on hemostasis of a continuous 3-day infusion.

Pentosane polysulfate (PP) is a sulfated polysaccharide known to exhibit anticoagulant properties that are in part independent of antithrombin III activity. These effects have only been studied in vitro or after single injections in healthy subjects. Our objective was to evaluate the modification of hemostasis induced by a 3-day continuous infusion of PP (4 mg/kg body weight/24 hr) in 10 subjects. No hemorrhagic complication was observed in any patient. Bleeding time was not modified by the infusion, despite a slight decrease in the platelet number. Among the other parameters measured, the automated partial thromboplastin time, prothrombin time, and anti-Xa activity were the most affected by PP. The kinetics of their modifications were quite uniform: clotting times and the anti-Xa effect increased gradually until reaching steady state 24 hours after the start of the infusion. A progressive return to the pretreatment level was then observed during the 6 hours after the end of the infusion. A significant decrease in the factor V concentration was found at day 4. Finally, in contrast with other reported results, no activation of fibrinolysis was induced by PP under the conditions we used, which suggests that discontinuous administration or the route of administration of the drug influences the fibrinolytic effect. In conclusion, we show the excellent tolerance of continuous infusion of PP, detail the modifications in biologic parameters of hemostasis during and after PP infusion, and demonstrate that PP decreases factor V activity.

Adult↗
PubMed1997

Interesterification of fats in margarine: effect on blood lipids, blood enzymes, and hemostasis parameters.

OBJECTIVES: In 60 healthy humans, a blend of commonly used edible vegetable fats was compared with the same fat blend after random chemical interesterification, for their effects in terms of nutritional safety on blood lipids, blood enzymes and hemostasis parameters. DESIGN: Both fat blends were supplied double-blind at two energy levels (4 and 8% of energy) in margarine according to a parallel design. At either energy level, the two fat blends were consumed according to a cross-over design for two periods of three weeks, without an intermediate wash-out period. RESULTS: The 30 parameters studied revealed no statistically significant differences between the two fat blends, except for slightly (approximately 10%) lower D-dimers concentrations after consumption of the interesterified fat blend. CONCLUSIONS: Increased levels of the fibrin-degradation products D-dimers are positively associated with risk for coronary heart disease. Thus, it was concluded that the inclusion of a chemically interesterified vegetable fat blend in the diet of healthy people does not influence fasting blood lipids, blood enzymes and/or hemostasis parameters in an adverse way, when compared with a non-interesterified fat blend with the same fatty acid composition.

Adult↗
PubMed2003

Platelet chemokines and chemokine receptors: linking hemostasis, inflammation, and host defense.

Blood platelets play critical roles in hemostasis, providing rapid essential protection against bleeding and catalyzing the important slower formation of stable blood clots via the coagulation cascade. They are also involved in protection from infection by phagocytosis of pathogens and by secreting chemokines that attract leukocytes. Platelet function usually is activated by primary agonists such as adenosine diphosphate (ADP), thrombin, and collagen, whereas secondary agonists like adrenalin do not induce aggregation on their own but become highly effective in the presence of low levels of primary agonists. Current research has revealed that chemokines represent an important additional class of agonists capable of causing significant activation of platelet function. Early work on platelet alpha-granule proteins suggested that platelet factor 4, now known as CXCL4, modulated aggregation and secretion induced by low agonist levels. Subsequent reports revealed the presence in platelets of messenger RNA for several additional chemokines and chemokine receptors. Three chemokines in particular, CXCL12 (SDF-1), CCL17 (TARC), and CCL22 (MDC), recently have been shown to be strong and rapid activators of platelet aggregation and adhesion after their binding to platelet CXCR4 or CCR4, when acting in combination with low levels of primary agonists. CXCL12 can be secreted by endothelial cells and is present in atherosclerotic plaques, whereas CCL17 and CCL22 are secreted by monocytes and macrophages. Platelet activation leads to the release of alpha-granule chemokines, including CCL3 (MIP-1alpha), CCL5 (RANTES), CCL7 (MCP-3), CCL17, CXCL1 (growth-regulated oncogene-alpha), CXCL5 (ENA-78), and CXCL8 (IL-8), which attract leukocytes and further activate other platelets. These findings help to provide a direct linkage between hemostasis, infection, and inflammation and the development of atherosclerosis.

Blood Platelets↗
PubMed2001

Influence of ABO blood groups on primary hemostasis.

BACKGROUND: Recently, the in vitro bleeding time test (IVBT) was proved to be a very sensitive screening method for the detection of vWD, showing rather good correlation between the closure time and the level of vWF. The vWF levels have been found to be significantly lower in healthy humans who are group O than in those who belong to the other ABO blood groups (non-group O). The aim of this study was to detect whether these differences in vWF levels in normal persons correspond to differences in nonvascular primary hemostasis when investigated by the IVBT. MATERIAL AND METHODS: Healthy blood donors (n = 162) without evidence of hemostatic disorders, without ingestion of drugs for at least 2 weeks, and with normal in vivo bleeding time endpoints, normal factor VIII clotting activity levels, normal structure of vWF multimers, and normal ristocetin-induced platelet aggregation were examined by IVBT. IVBT was performed with two automated systems (Thrombostat 4000, VDG [TST]; and a platelet function analyzer (PFA-100, Dade Behring [PFA]). CaCl2 and ADP were used as aggregants for the two TST tests (TST-CaCl2 and TST-ADP), and ADP- or epinephrine (Epi)-coated membranes were used with the two PFA tests (PFA-ADP and PFA-Epi). RESULTS: Closure time in the IVBT significantly correlated with the blood groups, but in reverse order (as did blood volume; data not shown): TST-ADP (mean +/- SD): group O, 89 +/- 14.6 seconds versus non-group O, 82 +/- 13 seconds (p<0.01); TST-CaCl(2): group O, 154 +/- 28.9 seconds versus non-group O, 140 +/- 31.3 seconds (p<0.01); PFA-ADP: group O, 91 +/- 13.4 seconds versus non-group O, 86 +/- 11.9 seconds (p<0.05); PFA-Epi: group O, 112 +/- 15.4 seconds versus non-group O, 104 +/- 16.7 seconds (p<0.05). Donors with vWF < or =77.5 % had longer closure time than those with vWF >77.5 % (p<0.05). CONCLUSION: Significant ABO-group-specific differences in nonvascular primary hemostasis could be found by IVBT. The differences are small, however, and lie within the normal range. Whether these differences have any biologic relevance can only be speculated.

ABO Blood-Group System↗
PubMed2003

Mechanisms of glycosaminoglycan activation of the serpins in hemostasis.

Serpins are the predominant protease inhibitors in the higher organisms and are responsible, in humans, for the control of many highly regulated processes including blood coagulation and fibrinolysis. The serpin inhibitory mechanism has recently been revealed by the solution of a crystallographic structure of the final serpin-protease complex. The serpin mechanism, in contrast to the classical lock-and-key mechanism, involves dramatic conformational change in both the inhibitor and the inhibited protein. The final result is a stable covalent complex in which the properties of each component are altered so as to allow clearance from the circulation. Several serpins are involved in hemostasis: antithrombin (AT) inhibits many coagulation proteases, most importantly factor Xa and thrombin; heparin cofactor II (HCII) inhibits thrombin; protein C inhibitor (PCI) inhibits activated protein C and thrombin bound to thrombomodulin; plasminogen activator inhibitor 1 inhibits tissue plasminogen activator; and alpha2-antiplasmin inhibits plasmin. Nearly all of these reactions are accelerated through interactions with glycosaminoglycans (GAGs) such as heparin or heparan sulfate. Recent structures of AT, HCII and PCI have revealed how in each case the serpin mechanism has been fine-tuned by evolution to bring about high levels of regulatory control, and how seemingly disparate mechanisms of GAG binding and activation can share critical elements. By considering the serpins involved in hemostasis together it is possible to develop a deeper understanding of their complex individual roles.

Animals↗
PubMed1995

Platelet function analysis after in vitro treatment with hemostasis-affecting components.

An overall platelet function test in whole blood, which simulates conditions under arterial pressure, is useful in measuring the effect of polymer materials on blood hemostatic function. We performed biocompatibility tests with materials or plasma substitutes by interaction of blood from healthy volunteers and then subjected these blood samples to platelet function analysis (Thrombostat). We tested also the capacity of locally applied hemostatic agents for bleeding control by direct application of these agents onto the Thrombostat measuring cell. The biocompatibility tests with materials exposed to blood appeared very discriminating between compatible and noncompatible materials. The hemostatic capacity of blood exposed to noncompatible materials (assessed by binding of active thrombin) reduced markedly after one hour incubation of the material. The plasma substitutes did not affect hemostasis significantly. However, a blood dilution of 40%, as in cardiopulmonary bypass, increased the time required for closure of the measuring cell by a platelet plug exponentially. Local hemostatic agents could be selected according to their capacity to enhance platelet plug formation. In addition, ADP mixed with the hemostatic agent was most effective in improving capacity. We conclude that platelet function analysis contributes importantly to screening of materials and plasma substitutes with regard to their interaction with primary hemostasis.

Biocompatible Materials↗
PubMed2003

Basic mechanisms of hemostasis.

Hemostasis governs two essential processes of human life in that it maintains the fluidity of blood under physiological conditions and prevents excessive blood loss after injury. Hemostasis is regulated by components of the vessel wall and blood cells and by humoral coagulation factors. Under normal conditions, these components are involved in an active equilibrium through activation, propagation, and termination of the hemostatic pathways. This equilibrium is disturbed upon vascular injury, leading to a procoagulant response when needed. Unfortunately, pathological disturbances can occur as a result of inherited or acquired coagulation factor deficiencies that may lead to bleeding or thrombotic disorders.

Anticoagulants↗