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PubMed1997

Dietary fatty acids in human thrombosis and hemostasis.

The effects of fatty acids on hemostasis are controversial. It has been difficult to show convincing effects of saturated or monounsaturated fatty acids that are clearly related to hemostatic variables in humans. Unsaturated fatty acids alter platelet aggregation and processes related to coagulation and fibrinolysis. Indirect evidence exists that n-6 polyunsaturated fatty acids may exert favorable effects on thrombotic processes in vivo, but large clinical trials have failed to show benefits of 5-6 g linoleic acid (18:2n-6) or linolenic acid (18:3n-3)/d. Only long-chain n-3 fatty acids prolong the template bleeding time, and they may exert some beneficial effect on erythrocyte flexibility. It appears unlikely that n-3 fatty acids lower fibrinogen or interact with the fibrinolytic system directly. One prospective secondary prevention trial showed benefits that may have resulted from either an improved hemostatic profile or an antiarrhythmic effect. A similar time course of clinical improvement was noted with reduced rates of cardiac mortality and postoperative thrombosis in Norway during World War II, and this was associated with a drastic dietary alteration involving increased consumption of n-3 fatty acids and reduced consumption of saturated fatty acids. Further work is needed to develop better tools to examine in vivo hemostasis so that the mechanisms and eventual clinical utility of n-3 fatty acids can be elucidated in well-designed clinical trials.

Blood Coagulation↗
PubMedDate not supplied

Viruses and hemostasis.

The great majority of viral infections are not associated with significant alterations in hemostasis. Occasionally, common viral pathogens lead to illnesses in which hemostatic impairment is an important feature. In these instances, two clinical syndromes usually are present: thrombocytopenic purpura and disseminated intravascular coagulation. Immune mechanisms are implicated in the first, while the second is associated with severe disease. Hepatitis viruses produce hemorrhage by a third mechanism. In cases of fulminant hepatitis, hepatocellular injury leads to decreased production of multiple coagulation factors and impairment of other hepatic functions that modulate hemostasis. A small number of viruses stand apart by virtue of the frequency with which they cause hemorrhage. These are the hemorrhagic fever viruses. Much more needs to be learned about how these viruses cause disease and induce hemorrhage. The first line of therapy in viral infections complicated by hemorrhage is early treatment with an antiviral agent. Unfortunately, effective antiviral therapy is usually not available. There is little useful information and no controlled studies on the efficacy of therapy aimed directly at correcting hemostatic impairment.

Blood Coagulation Factors↗
PubMed1990

Impaired hemostasis and platelet function in rats fed low zinc diets based on egg white protein.

Zinc-deficient rats exhibit impaired hemostasis, a pathological sign related to defective platelet function. The original observation was made in rats fed a low zinc diet based on soy protein. The present study was designed to test the effect of feeding a low zinc, egg white-based diet on bleeding time and platelet aggregation. The reversibility of the defect and the response of washed platelets from rats fed low zinc (less than 1 mg/kg) and control (100 mg/kg) diets were also assessed. Immature male rats were fed the respective diets for 11 d, the controls being both ad libitum- and pair-fed. To test reversibility, rats depleted for 11 d were then fed the control diet for an additional 7 d. Saline bleeding time was increased, and aggregation of platelet-rich plasma (PRP) from rats of low zinc status was impaired. The rate of the secondary phase of aggregation was significantly less than that of controls, but it was not different from that of controls after 7 d of zinc repletion. Aggregation of washed platelets was also impaired by low zinc status, showing that the defect is associated with the platelet, not the plasma. Egg white as a source of protein in the low zinc diet resulted in abnormal hemostasis and platelet aggregation, including a defective response of washed platelets.

Animals↗
PubMed1994

Platelet thrombus formation and hemostasis are delayed in the microcirculation of copper-deficient rats.

The role of dietary copper in platelet thrombus formation and hemostasis was studied in the cremaster muscle microcirculation. Male weanling Sprague-Dawley rats were fed purified diets that were either copper-adequate (94 mumol Cu/kg diet) or copper-deficient (0 mumol Cu/kg diet) for 1, 3 or 5 wk. The rats were anesthetized with pentobarbital, and the cremaster was spread in a Krebs-filled tissue bath. Fluorescein isothiocyanate tagged to bovine serum albumin (FITC-BSA) was injected intra-arterially. After a 20-min equilibration, blue light (1.8 W/cm2, 450-490 nm) was used to activate the FITC-BSA and induced platelet thrombus formation within the vasculature. In vivo television microscopy was used to quantify the thrombus formation. In rats fed the copper-deficient diet for 3 or 5 wk, platelet thrombus formation induced by photoactivation was significantly (P < 0.05) delayed and prothrombin time was significantly longer but the number of circulating platelets was significantly greater than in age-matched rats fed the copper-adequate diet. Bleeding time, measured after micropuncture of a second-order venule, was significantly longer but hematocrit was significantly lower in rats fed the copper-deficient diet than in those fed the copper-adequate diet. The results demonstrate that platelet-mediated hemostasis is depressed in dietary copper deficiency and that this may be due to a decrease in hematocrit, a decrease in the activity of a coagulation factor and/or an alteration of platelet function.

Animals↗
PubMed1995

Gene targeting and gene transfer studies of the plasminogen/plasmin system: implications in thrombosis, hemostasis, neointima formation, and atherosclerosis.

The plasminogen/plasmin or fibrinolytic system with its physiological triggers, tissue-type plasminogen activator, and urokinase-type plasminogen activator has been presumed to participate in normal and pathological processes of the vessel wall such as blood clot dissolution (thrombolysis), hemostasis, aneurysm formation, neovascularization, restenosis, and atherosclerosis. The implied role of the fibrinolytic system in vivo is, however, deduced from correlations between fibrinolytic activity and (patho)physiological phenomena, which does not allow establishing a cause/consequence relationship. Gene targeting and gene transfer technologies allow establishment of the in vivo role of gene products more conclusively. This article reviews briefly the findings of such studies on thrombolysis/thrombosis, hemostasis, neointima formation, atherosclerosis, and associated effects on survival.

Arteriosclerosis↗
PubMed1996

Methods for monitoring hemostasis during and following cardiac surgery.

The challenges in cardiac surgical hemostasis continue to plague the clinician. Rapid analysis and interpretation of coagulation tests are crucial in identifying coagulopathies that include both hemorrhagic and thrombophilic conditions. An understanding of the hemostatic mechanism, combined with a knowledge of pharmaceutical and transfusion interventions, is necessary to develop effective therapeutic plans. The coagulation tests that provide the most useful information include both end-point determinants and kinetic tests of clot formation. Future evaluation of the efficacy of coagulation tests in meeting these challenges will move beyond quantification of changes within various intermediates of hemostasis and rest with the correlation of these measured values with specific, outcome-directed indicators for optimizing patient care.

Blood Coagulation↗
PubMed1989

Serum lipids, lipoproteins, hemodynamics, and hemostasis in doxazosin-treated monkeys.

The effect of doxazosin administration on hemodynamics, hemostasis, and serum lipid and lipoprotein levels was investigated in cynomolgus monkeys (Macaca fascicularis) with diet-induced hypercholesterolemia. Acute administration of doxazosin (1 and 5 mg/kg) reduced resting mean arterial pressure by 20% without affecting heart rate, and completely inhibited the pressor response to phenylephrine. Platelet aggregation, prothrombin time, and activated partial thromboplastin time were not altered by the drug. Long-term doxazosin administration (1, 10, and 20 mg/kg/day) was associated with significant reductions in levels of total serum cholesterol (13%), very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) cholesterol (14%), and apolipoprotein B (15%) without any significant effects on high-density lipoprotein (HDL) cholesterol and apolipoprotein A-1. A 76% reduction in serum triglycerides, independent of drug level, was also seen in doxazosin-treated monkeys. In monkeys removed from drug treatment, serum cholesterol initially exceeded and then returned to pretreatment levels, whereas serum triglycerides remained low for 3 weeks. In our hypercholesterolemic monkey model, the administration of doxazosin resulted in beneficial changes in lipid and apolipoprotein profiles, hemostasis, and hemodynamics.

Adrenergic alpha-Antagonists↗
PubMed2000

Blood hemostasis in exercise and training.

Formation of the blood clot is a slow but normal physiological process occurring as a result of the activation of blood coagulation pathways. Nature's guard against unwanted blood clots is the fibrinolytic enzyme system. In healthy people, there is a delicate dynamic balance between blood clot formation and blood clot dissolution. Available evidence suggests that exercise and physical training evoke multiple effects on blood hemostasis in normal healthy subjects and in patients. A single bout of exercise is usually associated with a transient increase in blood coagulation as evidenced by a shortening of activated partial thromboplastin time (APTT) and increased Factor VIII (FVIII). The rise in FVIII is intensity dependent and continues into recovery. The effects of acute exercise on plasma fibrinogen have yielded conflicting results. Thus, the issue of whether exercise-induced blood hypercoagulability in vitro mirrors an in vivo thrombin generation and fibrin formation remains disputable. Exercise-induced enhancement of fibrinolysis has been repeatedly demonstrated using a wide range of exercise protocols incorporating various exercise intensities and durations. Moderate exercise appears to enhance blood fibrinolytic activity without a concomitant activation of blood coagulation mechanisms, whereas, very heavy exercise induces simultaneous activation of blood fibrinolysis and coagulation. The increase in fibrinolysis is due to a rise in tissue-type plasminogen activator (tPA) and decrease in plasminogen activator inhibitor (PAI). The mechanism of exercise-induced hyperfibrinolysis is poorly understood, and the physiological utility of such activation remains unresolved. Strenuous exercise elicits a transient increase in platelet count, but there are conflicting results concerning the effect of exercise on platelet aggregation and activation. Few comprehensive studies exist concerning the influence of exercise training on blood hemostasis, making future investigation necessary to identify whether there are favorable effects of exercise training on blood coagulation, fibrinolysis, and platelet functions.

Exercise↗
PubMed2004

Effect of dealcoholized beer (Bitburger Drive) consumption on hemostasis in humans.

BACKGROUND: The beneficial effect of moderate alcohol consumption in lowering the risk of cardiovascular disease has been shown in several epidemiologic studies. Such studies have also shown, however, that the protective effect of alcoholic beverages like wine and beer is not only due to the ethanol content but also to the presence of nonalcoholic constituents. The positive effect of alcoholic beverages has been attributed to changes in lipoprotein metabolism, but there is substantial evidence that effects on hemostasis play an important role. Whether the effects of alcoholic beverages on hemostasis are due exclusively to ethanol or are due, in part, to nonalcoholic components, is still under debate. METHODS: We have examined the hemostatic effects of 3 liters of beer, dealcoholized beer, and ethanol/water (v/v 4%), consumed over a period of 3 hr, in 12 young healthy volunteers. Platelet parameters CD62, PAC-1, and monocyte platelet aggregates were analyzed using flow cytometric measurements. The activity of factor VII was determined with a prothrombin time (PT) assay and plasminogen activator inhibitor activity using a chromogenic substrate. Thrombin generation was determined according to the method of Hemker. RESULTS: All three fluids administered, dealcoholized beer, beer, and ethanol, reduced the expression of activated fibrinogen receptor, the platelet activation marker CD62, and the formation of monocyte-platelet-aggregate. In addition, dealcoholized beer also showed significant inhibitory effects on thrombin generation, whereas beer and ethanol showed procoagulatory effects. CONCLUSIONS: This study has shown that the acute consumption of dealcoholized beer inhibits thrombogenic activity in young adults. This action could have a beneficial effect on the development of coronary artery disease. Thus, the consumption of dealcoholized beer could provide cardiovascular benefit without the negative effects of alcohol.

Adult↗
PubMed2006

The complementary Erlangen active simulator for interventional endoscopy training is superior to solely clinical education in endoscopic hemostasis--the French training project: a prospective trial.

BACKGROUND: The Erlangen Active Simulator for Interventional Endoscopy (EASIE) using ex-vivo porcine organs was introduced in 1997. The present study should analyze whether repeated EASIE simulator training in endoscopic hemostasis led to superior performance compared with a traditionally educated group. The results were compared with a similar project in New York. METHODS: Thirty-five French GI fellows were enrolled. Baseline skills evaluation was performed in four disciplines (manual skills, injection/coagulation, clip application and variceal ligation) using the compactEASIE-simulator equipped with an upper gastrointestinal organ package for bleeding simulation. The same, translated evaluation forms (from the prior New York project) were used. Subsequently, fellows were randomized into group A (n=17, only clinical education) and group B (n=18, additional three simulator trainings). Group B was trained the next day and after 4 and 7 months by experts of the French Society of Gastrointestinal Endoscopy. Both groups performed routine and emergency endoscopies at their home hospitals during the study period. Both groups were re-evaluated blindly after 9 months. RESULTS: The learning curve for group B showed a significant improvement in all disciplines (P<0.004) whereas group A improved significantly in only two of four disciplines at blinded final evaluation (manual skills P=0.02, injection/coagulation P=0.013). The direct comparison of groups B and A at blinded final evaluation showed significantly superior ratings for group B in all disciplines (P<0.006) and significantly shorter performance times in two disciplines (P=0.016 each). The comparison with the similar 'New York project' revealed that preexisting differences in skills were adjusted by the training. CONCLUSION: Complementary trainings (three workshops in 7 months) in endoscopic hemostasis using the compactEASIE improved skills compared with a solely clinical education. The results of the 'New York project' were confirmed and benefits were independent from the medical educational system.

Animals↗
PubMed2005

The plastic surgeon's guide to drugs affecting hemostasis.

The plastic surgeon is encountering an unprecedented population of aging individuals who both desire cosmetic or reconstructive surgery and may require the use of medications that alter hemostasis. The increasing use of anticoagulants and platelet inhibitors in particular can create challenges for the plastic surgeon. The purpose of this review is to familiarize the surgeon with the medications that can affect hemostasis and to suggest strategies for their use in the perioperative period. Specific case examples are presented.

Adult↗
PubMed2004

Mechanisms of poly-N-acetyl glucosamine polymer-mediated hemostasis: platelet interactions.

BACKGROUND: Investigations were performed to determine whether poly-N-acetyl glucosamine (p-GlcNAc) induces hemostasis by the activation of platelets. METHODS: Platelets were isolated from human blood, fixed in the presence poly-N-acetyl glucosamine fibers, and visualized with scanning electron microscopy. Platelet activation surface markers were measured by fluorescence multiphoton microscopy. Platelet aggregation in the presence of p-GlcNAc fibers and integrin receptor blockers was measured. RESULTS: Scanning electron microscopy indicated that contact of platelets with poly-N-acetyl glucosamine fibers resulted in platelet activation. Fluorescent microscopy showed that contact of platelets with the marine polymer increased intracellular levels of free calcium and resulted in surface exposure of platelet phosphatidylserine, P selectin, and the alphaIIbbeta3 integrin. Antibody inhibitors of the platelet alphaIIbbeta3 integrin inhibited p-GlcNAc to stimulate fibrin polymerization. CONCLUSION: Poly-N-acetyl glucosamine fiber material promotes hemostasis by the activation of platelets.

Acetylglucosamine↗
PubMed2004

Impaired hemostasis and protection against thrombosis in protease-activated receptor 4-deficient mice is due to lack of thrombin signaling in platelets.

Platelets from protease-activated receptor 4 (PAR4)-deficient mice are unresponsive to thrombin, and Par4-/- mice have prolonged bleeding times and are protected against thrombosis. However, in addition to its role in platelets, PAR4 contributes to thrombin signaling in cells in the blood vessel wall that might participate in hemostasis and thrombosis, such as endothelial cells. To determine whether the hemostatic and thrombotic phenotypes of Par4-/- mice were due to loss of PAR4 function in hematopoietic vs. other cell types, tail bleed times and thromboplastin-induced pulmonary embolism were examined in lethally irradiated mice reconstituted with Par4+/+ or Par4-/- bone marrow. In Par4+/+ and Par4-/- mice reconstituted with Par4+/+ marrow, the median tail bleed times were 2.0 and 1.7 min, respectively, vs. > 10 min for both Par4+/+ and Par4-/- mice reconstituted with Par4-/- marrow. In the pulmonary embolism model, Par4+/+ and Par4-/- mice reconstituted with Par4+/+ marrow survived a median of 3.7 and 2.8 min, respectively, after administration of thromboplastin, vs. > 20 min for both Par4+/+ and Par4-/- mice reconstituted with Par4-/- marrow. Further, the phenotype of mice reconstituted with Par4-/- marrow was almost as dramatic as that seen in Nf-e2-/- mice, which lack platelets. These data strongly suggest that increased tail bleed times and protection against thrombosis in Par4-/- mice are accounted for by lack of PAR4 function in platelets, emphasize the importance of thrombin signaling in platelets among the multiple pathways and cell types that govern hemostasis and thrombosis.

Animals↗
PubMed2005

Factor V Leiden improves in vivo hemostasis in murine hemophilia models.

The role of factor V Leiden (FVL) as a modifier of the severe hemophilia phenotype is still unclear. We used mice with hemophilia A or B crossed with FVL to elucidate in vivo parameters of hemostasis. Real-time thrombus formation in the microcirculation was monitored by deposition of labeled platelets upon laser-induced endothelial injury using widefield microscopy in living animals. No thrombi formed in hemophilic A or B mice following vascular injuries. However, hemophilic mice, either heterozygous or homozygous for FVL, formed clots at all injured sites. Injection of purified activated FV into hemophilic A or B mice could mimic the in vivo effect of FVL. In contrast to these responses to a laser injury in a microvascular bed, FVL did not provide sustained hemostasis following damage of large vessels in a ferric chloride carotid artery injury model, despite of the improvement of clotting times and high circulating thrombin levels. Together these data provide evidence that FVL has the ability to improve the hemophilia A or B phenotype, but this effect is principally evident at the microcirculation level following a particular vascular injury. Our observations may partly explain the heterogeneous clinical evidence of the beneficial role of FVL in hemophilia.

Animals↗
PubMed1977

Alteration of primary hemostasis in hemophiliacs after treatment with lyophilized antihemophilic globulin.

Seven patients with classic hemophilia A had alteration of primary hemostasis after treatment with lyophilized antihemophilic globulin (LAHG). The following test results, which were normal before treatment, became abnormal after treatment: bleeding time, bleeding intensity, and platelet adhesiveness. In two patients, the fibrin-fibrinogen-degradation products increased to more than 40 microgram/ml. In three patients, the bleeding symptoms became worse with LAHG therapy although no inhibitor against Factor VIII was demonstrated. In one of these patients, the bleedings symptoms disappeared when the use of LAHG was discontinued and prednisone was given; at the same time, the altered primary hemostasis returned to normal. In the remaining two patients, prednisone did not have any effect. In these two patients, however, the bleeding stopped, and the bleeding time became normal immediately after freshly prepared blood-group compatible cryoprecipitate was given.

Adolescent↗
PubMed1997

Decidual cell regulation of hemostasis during implantation and menstruation.

Progesterone stimulation of the estradiol (E2)-primed human endometrium initiates DZ of the stromal cells around the spiral arterioles. Under continued steroid stimulation, DZ spreads wave-like to establish the decidual cell as a major cell type of the luteal phase and pregnant endometrium. Because of their widespread distribution throughout the endometrium and concentration at perivascular sites, decidual cells are spatially and temporally positioned to mediate the opposing requirements of maintaining hemostasis during endovascular trophoblast invasion, yet promoting menstrual hemorrhage in the absence of implantation. The experimental results summarized in this review indicate that the paradoxical properties manifested by endometrial stromal/decidual cells are controlled by several proteins with either hemostatic or ECM-degrading or vasoactive activity, and that their expression is altered in response to changes in levels of circulating ovarian steroids during the menstrual cycle. These conclusions are drawn primarily from studies with a well-characterized in vitro model of DZ using monolayers of stromal cells derived from specimens of predecidualized endometrium. Thus, progestins modify the expression of several DZ-related markers in the cultured stromal cells, and E2 enhances these effects despite the lack of response to E2 alone. These responses are consistent with the differential actions displayed by E2 and progesterone in vivo, by which E2 primes the endometrium for the decidualizing effects of progesterone by elevating progesterone receptor levels. Accordingly, during steroid-induced in vitro DZ, a marked increase in the expression of stromal cell TF and PAI-1 and reciprocal inhibition of tPA activity suggest mechanisms to account for the absence of hemorrhage during invasion of the endometrial vasculature by implanting trophoblasts. In contrast to steroid-induced DZ, the events of menstruation are initiated in response to a decline in circulating levels of ovarian steroids. Accordingly, subjecting in vitro decidualized stromal cells to steroid withdrawal results in pronounced reversal in the expression of all of the end points listed above. Consequently, the local hemostatic environment is transformed into a hemorrhage-promoting milieu. Taken together with vascular injury resulting from ischemia induced by spiral artery vasoconstriction, the net effect is attainment of two prerequisites for menstrual hemorrhage, vascular injury and inadequate hemostasis.

Decidua↗
PubMed1988

Role of platelet-activating factor in primary hemostasis.

To determine whether platelet-activating factor (PAF) has a physiological role in the process of primary hemostasis in the rabbit, we measured skin bleeding times in animals given orally a specific PAF-receptor antagonist L-652,731. One hour after the administration of L-652,731 (20 or 40 mg/kg), a significant prolongation of bleeding time was observed. Parameters known to interfere with the process of primary hemostasis were not altered by PAF-receptor antagonist. In addition, no changes were observed in platelet count and vessel wall arachidonic acid metabolism, as revealed by serum thromboxane B2 levels, vascular 6-ketoprostaglandin F1 alpha generation, and by aspirin experiment. The fact that aspirin alone did not induce prolongation of bleeding time in rabbits is probably due to the simultaneous inhibition of platelet thromboxane A2 and vascular prostacyclin. [3H]PAF binding to washed platelets of rabbits given L-652,731 showed a significant reduction in maximum number of detectable binding sites in comparison with values found in the same animals before the L-652,731 administration. The results suggest that the bleeding-time prolongation observed after L-652,731 administration results from its ability to selectively inhibit PAF bioactivity. Thus locally released PAF appears to exert a physiological role in the process of platelet plug formation that follows a skin incision in the rabbit.

Animals↗