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PubMed1983

Evidence for an ethanol mediated disruption of hemostasis.

Male Sprague-Dawley rats were given 1 ml intraperitoneal (i.p.) injections of saline, 5, 10 or 20% ethanol once daily for 7 days. Clotting times were determined for the PT, APTT, FIB, and factors II, V, VII, VIII, X, and XII. The platelet count (PLT) and the hematocrit (HCT) were also determined. Besides a uniform statistically significant decrease in the platelet count, the clotting times for the coagulation factors were also influenced by the alcohol injected. The data tends to indicate that when the concentration of alcohol was greater, that more clotting times were influenced. Detailed analysis of the data in reference to the total clotting cascade tends to suggest that ethanol principally prolongs the clotting times of the intrinsic pathway, while the extrinsic pathway appears to be unaffected by the treatment, and the common pathway is normal to accelerated in clotting times. This suggests that hemostasis as a whole was not affected by the treatment, but specific portions of the clotting cascade were, and development of abnormal hemostasis due to ethanol might depend on which part of the pathway was activated.

Animals↗
PubMed1985

Effects of acute ethanol intoxication combined with secobarbital abuse on hemostasis.

Male Sprague-Dawley rats were treated with 0.5 ml of 46% ETOH, 2.8 mg/kg of secobarbital or 14.3 mg/kg secobarbital or combinations thereof. Twenty-four hours following treatment, blood clotting data was determined. The data indicated that either ethanol or secobarbital alone is just as detrimental to hemostasis as is the combined abuse of both. Likewise, a lesser concentration of alcohol was just as disruptive on hemostasis as was the greater concentration of ethanol.

Alcoholic Intoxication↗
PubMed2006

Relationship of circulating biomarkers of inflammation and hemostasis with preclinical atherosclerotic burden in nonsmoking hypercholesterolemic men.

BACKGROUND: Relations of mediators of inflammation and hemostasis with preclinical atherosclerosis have been poorly analyzed. The aim of this study was to test potential associations of these blood markers with indicators of cardiovascular risk and atherosclerotic burden in asymptomatic, nonsmoking, hypercholesterolemic men. METHODS: A total of 87 men underwent cardiovascular risk assessment by means of 10-year Framingham risk calculation (median 9%) and atherosclerotic burden evaluation by means of ultrasonographic measurement of common carotid intima-media thickness and assessment of atherosclerotic plaques at three arterial sites (three-site plaques). RESULTS: Of the markers C-reactive protein, tumor necrosis factor-alpha, interleukin-10, factor VIIc, fibrinogen, plasminogen activator inhibitor-activator, soluble intercellular adhesion molecule-1, soluble P-selectin (sP-selectin), and von Willebrand factor, only sP-selectin was positively and independently associated with high Framingham risk score (>9%) (71.7 +/- 3.6 ng/mL, n = 33 v 59.6 +/- 2.8, n = 54; mean +/- SEM; P < .05) and with three-site plaques (75.4 +/- 5.7 ng/mL, n = 14 v 62.0 +/- 2.5, n = 73; P < .05). After adjustment for all of the above markers and for cardiovascular risk factors, odd ratios of having high Framingham risk and three-site plaques were 3.38 (1.43 to 10.21) and 5.23 (1.74 to 23.52) respectively, per 1-standard deviation increase in sP-selectin. CONCLUSIONS: These results confirm that among several hemostasis and inflammation mediators, only sP-selectin blood level was associated with preclinical atherosclerosis. It might confer to sP-selectin measurement a clinical usefulness for detecting and managing high cardiovascular risk in primary prevention.

Adult↗
PubMed2003

Glutathione-S-transferase genotypes, smoking, and their association with markers of inflammation, hemostasis, and endothelial function: the atherosclerosis risk in communities (ARIC) study.

Recent epidemiologic studies suggest that polymorphisms of glutathione-S-transferases M1 and T1 (GSTM1/GSTT1) modify the effects of cigarette smoking on risk of coronary heart disease (CHD). Since GSTs are able to detoxify numerous toxic compounds and products of oxidative stress, it is possible that GST genotypes may also modify the capacity of smoking to invoke a chronic inflammatory response. A cross-sectional analysis, using a subset of participants (n = 989) in a large (n = 15, 792) biracial cohort, was used to evaluate levels of nine markers of inflammation, hemostasis, and endothelial function by different combinations of GST genotypes and cigarette smoking status. Participants with the GSTM1 null (GSTM1-0) genotype and > or = 20 pack-years of smoking had the highest mean levels of CRP, fibrinogen, von Willebrand factor, ICAM-1, and VCAM-1 and lowest mean levels of albumin compared to other combinations of genotype and smoking. However, a formal test for interaction between GSTM1 genotype and smoking was statistically significant only for albumin. By contrast, participants who had the functional GSTT1 genotype (GSTT1-1) and smoked > or = 20 pack-years had the highest mean levels of only CRP and fibrinogen. The results of this study provide some limited evidence that GSTM1 and GSTT1 polymorphisms modify the effect of smoking on inflammation, hemostasis, and endothelial function.

Cohort Studies↗
PubMed2006

Hemostasis and aging.

Many changes in the vasculature, hemostasis and endothelium, including alterations of platelets, coagulation and fibrinolytic factors, occur during aging. While the increasing hypercoagulability observed with aging may account for the higher incidence of thrombotic cardiovascular disorders in the elderly, the lack of genetic protective factors against thrombosis in healthy centenarians suggests that little is yet known about the age-associated changes of hemostasis. The complex inter-relationships between inherited and acquired factors influencing the hemostatic system during aging are discussed in this review.

Aged↗
PubMed2004

Dietary fatty acids, hemostasis, and cardiovascular disease risk.

The cause of many myocardial infarctions is occlusive thrombosis, or a blood clot that stops blood flow in a coronary artery. Hemostasis involves a complex system of factors, which normally form and degrade blood clots, that work within a delicate balance. Emerging evidence suggests that some hemostatic factors, including factor VII, fibrinogen, and plasminogen activator inhibitor-1, are associated with increased risk for cardiovascular disease (CVD). Accumulating evidence suggests a relationship between dietary fatty acids and emerging hemostatic CVD risk factors, although much of this evidence is incomplete or conflicting. Dietary supplementation with marine n-3 fatty acids prolongs bleeding time and may decrease risk for thrombosis. Factor VII coagulant activity modestly decreases with reductions in saturated fatty acid (SFA) intake and thereby may contribute to the beneficial effects of low SFA diets. Large triglyceride-rich particles formed during postprandial lipemia can support the assembly and function of coagulation complexes and seem to play a role in the activation of factor VII, and thus may partially explain increased CVD risk associated with increased postprandial triglyceridemia. As our understanding of the role of dietary fatty acids and hemostasis evolves, it is likely that we will be able to make specific dietary recommendations to further decrease CVD risk. At this juncture, however, increasing marine n-3 fatty acids and decreasing certain SFAs are leading strategies to reduce hemostatic CVD risk factors. An array of dietary strategies that target multiple CVD risk factors could have a greater impact on CVD than a single risk factor intervention strategy.

Coronary Artery Disease↗
PubMed2003

Differential effects of progestins on hemostasis.

Recently large, prospective, randomized studies on hormone replacement therapy (HRT) have indicated that the progestin use might interfere with hemostasis and thus increase venous thrombotic events. Therefore, available publications were evaluated to determine whether progestins interfere with hemostasis, either when given alone via oral or parenteral routes or in combination with ethinylestradiol as synthetic estrogen or natural estrogens. There are indications that such interference is dependent upon the type and dose of the progestin, the route of application, the length of treatment and the type and dose of the estrogen with which it is combined. For natural progesterone, no negative effects on the hemostatic system were seen with either oral or parenteral application, in cyclic or continuous regimens, for the doses investigated. Similarly, no unwanted effects were seen with progestin only pills (POP), independent of the type and dose of progestin, or parenteral progestins. With the high-dose progestins used in gynaecological oncology, the increased activation of the hemostatic system resulting from the disease itself has to be taken into account when looking at any increased incidence of thromboembolic events in these patients. For estrogen/progestin combinations, the risk of venous thromboembolism is attributed to the estrogen used. Recent studies showed an increased rate of thromboembolic events in association with desogestrel-and gestodene-containing oral contraceptives, compared with those containing levonorgestrel. With HRT, a decrease in antithrombin factors could explain the increased rate of venous thrombotic events. In conclusion, progestins seems to have different effects on the hemostatic system due to their different pattern of biological activities. This was also shown in the arterial vascular system, where some progestins may reduce the endothelium-dependent vasodilating action of estrogens and stimulate intima proliferation and upregulate thrombin receptor expression while other progestins did not.

Contraceptives, Oral, Hormonal↗
PubMedDate not supplied

Hormone replacement therapy and hemostasis: effects in Brazilian postmenopausal women.

OBJECTIVE: To evaluate the impact that administration of transdermal estradiol gel combined with medroxyprogesterone acetate (MPA) has on hemostasis. METHODS: In this open prospective longitudinal study, thirty postmenopausal women received transdermal estradiol gel (1 mg/day) continuously combined with oral MPA (5 mg/day) for 12 days/month. The following parameters were determined: prothrombin time (PT), activated partial thromboplastin time (aPTT), factors VII, X, and XII activity, fibrinogen levels, thrombin-antithrombin complex levels, protein C and S antigen, antithrombin activity, plasminogen activator inhibitor type 1 (PAI-1) antigen, tissue-type plasminogen activator (t-PA) antigen, plasminogen activity and fibrin degradation products (FbDP) antigen. They were evaluated before and after 6 months of treatment. RESULTS: There was a significant decrease in factor VII activity (P=0.001), factor X activity (P=0.016), protein C antigen (P=0.022), antithrombin activity (P=0.025), plasminogen activity (P=0.023), t-PA antigen (P=0.043) and FbDP antigen (P=0.048) compared with baseline values. CONCLUSION: The results suggest that the treatment with transdermal estradiol gel combined with MPA avoids any major activation of coagulation and does not produce any overall effect on fibrinolysis. Therefore, this treatment might provide interesting effects on hemostasis in postmenopausal Brazilian women.

Administration, Oral↗
PubMed2005

A capillary hemostasis mechanism regulated by sympathetic tone and activity via factor VIII or von Willebrand's factor may function as a "capillary gate" and may explain angiodysplasia, angioneurotic edema, and variations in systemic vascular resistance.

The sympathetic nervous system (SNS) may directly or indirectly govern the release of von Willebrand's factor (VWB), which may be a hormone, from the vascular endothelium, which may be a gland. VWB is known to stabilize the labile VIIIC component of Factor VIII complex, and may thereby determine its half-life and activity level in the blood. Rising blood levels of Factor VIII may increase the speed of thrombin production during the "propagation" phase of blood coagulation and thereby elevate peak levels and duration of thrombin activity to produce and stabilize insoluble fibrin in quantities necessary to initiate clot formation. At the capillary level, microvascular receptor sites may bring fibrinogen and fibronectin, which are basic "building blocks" of insoluble fibrin, into close proximity with rising levels of Factor VIII to facilitate insoluble fibrin production and serve as binding sites for an expanding mass of insoluble fibrin that adheres to blood components to cause capillary hemostasis. Capillary hemostasis may serve as a "capillary gate mechanism" (CGM) that increases systemic vascular resistance and blood pressure and decreases cardiac output in accord with increased tone and activity levels of the SNS by obstructing capillary bed flow. Angiodysplasia may be caused by persistent defects in the VWB molecule that impair CGM function and cause visible capillary damage. Angioneurotic edema may be caused by sudden complement system attack on VWB that results in widespread paralysis of CGM function and sudden shift of blood from arteries and arterioles to capillaries to cause tissue edema and hypotension. The hypothesis may offer improved insight into the nature of circulatory physiology, the surgical stress syndrome, "vasoactive" drugs, and numerous disease states. It may be tested by using videomicroscopy to monitor changes in bowel capillary flow in response to stepwise increases of VWB or Factor VIII intravenous boluses in animals anesthetized using combined epidural-general technique to minimize SNS activity levels.

Angiodysplasia↗
PubMed2005

Impaired primary hemostasis with normal platelet function in Duchenne muscular dystrophy during highly-invasive spinal surgery.

A defective, normal or enhanced hemostasis has been reported in Duchenne muscular dystrophy (DMD). A retrospective analysis of intra-and postoperative (up to 36 h) estimated blood losses was performed in 156 patients undergoing spinal surgery for: DMD (n = 31), idiopathic scoliosis (IS) (n = 70), poliomyelitis (n = 10), cerebral palsy (CP) (n = 28), spinal muscular atrophy (SMA) (n = 17). Platelet aggregation and bleeding times were also investigated in DMD patients. Immunohistochemistry for dystrophin was performed in platelets, megakaryocytes and blood vessels of normal tissues. DMD patients showed significantly higher intraoperative estimated blood losses (DMD: 3495+/-890 ml; IS: 2269+/-804 ml; poliomyelitis: 2582+/-1252 ml; CP: 2071+/-683 ml; SMA: 2464+/-806 ml; P < 0.05), while postoperative blood losses were similar among different groups. Higher estimated blood losses in DMD were independent of the duration of surgery, body weight, gender, age, vertebral levels or preoperative Cobb angle. DMD children had significantly prolonged bleeding times, but retained normal platelet function. From control samples dystrophin was expressed in vascular smooth muscle cells, but not in platelets. DMD appears to be characterized by immediate bleeding during highly-invasive surgery and increased bleeding time without platelet abnormalities. Considering dystrophin expression in normal vascular smooth muscle cells, these results altogether suggest a selective defect of primary hemostasis in DMD, likely to be due to impaired vessel reactivity.

Adolescent↗
PubMed2005

Short-term effects of estrogen, tamoxifen and raloxifene on hemostasis: a randomized-controlled study and review of the literature.

INTRODUCTION: Estrogen therapy (ET), tamoxifen and raloxifene are associated with a two- to three-fold increased risk of venous thrombosis (VT); however, the mechanisms by which each drug increases venous thrombosis propensity are not fully understood. The objectives of this investigation were to compare the effects of these three treatments on hemostasis in a head to head randomized placebo-controlled trial. PATIENTS/METHODS: Ninety-four postmenopausal women were assigned to receive oral estrogen (conjugated equine estrogen [CEE] 0.625 mg, n=23), tamoxifen 20 mg (n=24), raloxifene 60 mg (n=24) or placebo (n=23) daily for 6 months. Blood samples were analyzed for procoagulant factors (prothrombin, factors VII [fVII], VIII [fVIII], IX [fIX] and XI [fXI], D-dimer and von Willebrand factor [vWf]), anticoagulant factors (antithrombin [AT], total and free protein S, protein C and activated protein C [APC] resistance) and fibrinolytic factors (thrombin activatable fibrinolysis inhibitor [TAFI] and plasminogen activator inhibitor-1 [PAI-1]), at baseline and at 6 months of treatment. RESULTS: Estrogen increased factor VII and D-dimer, and decreased antithrombin, total and free protein S and PAI-1. Changes with tamoxifen were distinct from estrogen with increases in factors VIII, IX, vWf and free protein S, and decreases in AT, total protein S, protein C and plasminogen activator inhibitor-1. Raloxifene produced similar effects as tamoxifen, but did not increase factor IX or decrease protein C. CONCLUSIONS: Estrogen, tamoxifen and raloxifene affected hemostasis favoring procoagulation and impairing anticoagulation. The biochemical effects of the selective estrogen receptor modulators (SERMs) were distinct from those of estrogen and differed only subtly from each other.

Biomarkers↗
PubMed1994

Autologous fibrin glue: the last step in operative hemostasis.

BACKGROUND: Fibrin glue may be the perfect hemostatic agent for operative use as it seals in minutes, has no tissue toxicity, reabsorbs, and promotes local tissue growth and repair. Use in the United States has been limited because of lack of Food and Drug Administration approval of the commercial homologous products, lack of a concentrated source of fibrinogen, and because of the potential for viral transmission, particularly hepatitis, with pooled homologous plasma and cryoprecipitate-based methods. Autologous fibrin glue (AFG) obviates these problems. METHODS: During the past year, we obtained AFG through the same routine predonation procedure as with red blood cells before major elective surgery. Intraoperatively, we made AFG from the platelet-rich plasma derived from the Plasma-Saver. Our experience has been with 36 patients undergoing aortic, thoracoabdominal, and thoracic surgery, as well as patch graft angioplasty cases. RESULTS: Fibrin glue formation mimics the final stage in the coagulation cascade. The AFG from predonation acts more like an epoxy glue, while the AFG made during surgery is less viscous and acts more like a sealant because of the lesser concentration of fibrinogen in platelet-rich plasma. In emergencies, however, the intraoperative method is obviously the only choice available, and it is a useful adjunct to hemostasis at the end of the procedure. The technique will be described. CONCLUSION: This relatively new approach to hemostasis should gain popularity because it is easy and fairly inexpensive to produce, and because the patient's own blood is used.

Aneurysm↗
PubMed1998

A randomized controlled double-blind study of the effects on hemostasis of two progestogen-only pills containing 75 microgram desogestrel or 30 microgram levonorgestrel.

The effects of two progestogen-only pills containing either 75 microgram desogestrel (DSG) or 30 microgram levonorgestrel (LNG) on hemostasis were investigated in a double-blind, randomized, controlled study of seven treatment cycles in 78 healthy women. DSG reduced factor VII activity (p < 0.05) and prothrombin fragment 1+2 (p < 0.05) and increased protein S (p < 0.001). LNG reduced factor VII activity (p < 0.01) and plasminogen activity (p < 0.01) and increased tissue-plasminogen activator (t-PA) (p < 0.05). At the end of the post-treatment cycle with DSG, protein S (p < 0.01) and t-PA (p < 0.05) were increased and plasminogen activity was decreased (p < 0.05), whereas with LNG, t-PA was increased (p < 0.001) and prothrombin fragment 1+2 (p < 0.05) and plasminogen activity (p < 0.001) were decreased. Between-group comparisons revealed higher values for DSG regarding the anticoagulatory parameter protein S at cycle 7 (p < 0.01) and post-treatment assessments (p < 0.05), and the fibrinolytic parameter plasmin-antiplasmin complex was higher with DSG at cycle 7 (p < 0.05) and at post-treatment (p < 0.05). Both preparations had comparable and potentially favorable effects of hemostasis, and may offer suitable hormonal contraception to women with a personal or family history of venous thromboembolic diseases.

Adult↗
PubMed2002

Effects of vaginally administered high estradiol doses on hormonal pharmacokinetics and hemostasis in postmenopausal women.

OBJECTIVE: To study the effect of high doses of estradiol released from vaginal rings on the pharmacokinetics of hormones, and the long-term effect on hormones and hemostasis in postmenopausal women. DESIGN: A pilot, nonrandomized study. SETTING: Healthy volunteers in an academic research environment. PATIENTS: Postmenopausal women. Eight women were treated with 17 beta-estradiol from three vaginal rings, releasing 7.5 micro g per ring for a total of 22.5 micro g over 24 hours. The rings were changed every morning for 14 days. MAIN OUTCOME MEASURE(S): Hemostatic changes were recorded. RESULT(S): Estradiol was rapidly absorbed, and statistically significant increases in the levels were found after 15 minutes; C(max) was obtained after 1 hour and a steady state after 24 hours. No statistically significant changes were found in the levels of coagulation factors V, von Willebrand factor, and activated factor VII; nor were any changes observed for activated protein C resistance, coagulation inhibitors protein C, protein S, or plasminogen activator inhibitor-1. No indication of increased thrombin formation was demonstrated by analyses of prothrombin fragment 1+2, fibrin D-dimer, and soluble fibrin. CONCLUSION(S)No statistically significant changes in hemostasis were observed from the vaginal administration of estradiol using a dose equivalent to transdermal administration with a release rate of 100 micro g per 24 hours.

Administration, Intravaginal↗
PubMed1980

A microscopic and ultrastructural study hemostasis after laser photocoagulation.

Fiberoptic-coupled, Neodymium-Yag laser beams were directed at induced bleeding mucosal lesions in the stomachs of 13 dogs. Hemostasis was achieved in all cases. The lesions induced by photocoagulation were examined by light microscopy and transmission electron microscopy. Phototherapy induces an endothelial reaction followed by the formation of a platelet thrombus in the damaged vessels. Hemostasis starts shortly after coagulation therapy has been performed.

Acute Disease↗
PubMed2000

Markers of activated hemostasis and fibrinolysis in patients with pulmonary malignancies: comparison of plasma levels in central venous and pulmonary venous blood.

Malignancy frequently is accompanied by activated coagulation and fibrinolysis indicating a hypercoagulable state. The purpose of our study was to estimate the contribution of local tumor-induced mechanisms to the activation of hemostasis and fibrinolysis. In a prospective study, we compared the plasma levels of thrombin-antithrombin complexes, prothrombin fragment 1+2, and D-dimers in blood samples that simultaneously were drawn from the superior vena cava and the pulmonary vein of a tumor-bearing pulmonary lobe. Samples from the superior vena cava were drawn before operation and served as controls. After thoracotomy, a second group of samples was simultaneously taken from the pulmonary veins of the tumor-bearing lobe and the superior vena cava. Forty-five patients with pulmonary malignancies were included (25 adenocarcinomas and 20 squamous cell carcinomas). There were no significant differences of thrombin-antithrombin complexes, prothrombin fragment 1+2, and D-dimers levels in patients suffering from adenocarcinoma and from squamous cell carcinoma. Intraoperatively, prothrombin fragment 1+2 and D-dimers levels were markedly increased when compared with the preoperative values (p<0.0001). There was no increase of thrombin-antithrombin complexes levels due to the operative traumatization. Prothrombin fragment 1+2, thrombin-antithrombin complexes, and D-dimers plasma levels were significantly higher in the pulmonary venous blood than in the blood simultaneously drawn from the superior vena cava (p<0.0001). Our findings indicate that malignant lung tumors directly contribute to the activation of hemostasis and fibrinolysis in these clinical settings.

Aged↗
PubMed1979

Disorders of hemostasis in malignancy.

Disorders of hemostasis are frequent in malignant disease and their cause is often multifactorial and complex. Both primary (platelets and vessel walls) and secondary (coagulation factors) hemostasis are impaired, often concurrently. Therapy is most often directed toward the underlying disease; however, a knowledge of the complications and treatment of each malignancy will often prevent a number of the problems cited in this chapter. The hypercoagulable states are still poorly understood and need better definition, but their recognition, treatment and prevention may decrease morbidity significantly.

Blood Coagulation Disorders↗
PubMed2000

Snake venom proteases affecting hemostasis and thrombosis.

The structure and function of snake venom proteases are briefly reviewed by putting the focus on their effects on hemostasis and thrombosis and comparing with their mammalian counterparts. Up to date, more than 150 different proteases have been isolated and about one third of them structurally characterized. Those proteases are classified into serine proteases and metalloproteinases. A number of the serine proteases show fibrin(ogen)olytic (thrombin-like) activities, which are not susceptible to hirudin or heparin and perhaps to most endogenous serine protease inhibitors, and form abnormal fibrin clots. Some of them have kininogenase (kallikrein-like) activity releasing hypotensive bradykinin. A few venom serine proteases specifically activate coagulation factor V, protein C, plasminogen or platelets. The venom metalloproteinases, belonging to the metzincin family, generally show fibrin(ogen)olytic and extracellular matrix-degrading (hemorrhagic) activities. A few venom metalloproteinases show a unique substrate specificity toward coagulation factor X, platelet membrane receptors or von Willebrand factor. A number of the metalloproteinases have chimeric structures composed of several domains such as proteinase, disintegrin-like, Cys-rich and lectin-like domains. The disintegrin-like domain seems to facilitate the action of those metalloproteinases by interacting with platelet receptors. A more detailed analysis of snake venom proteases should find their usefulness for the medical and pharmacological applications in the field of thrombosis and hemostasis.

Amino Acid Sequence↗