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PubMed1997

Adhesive interactions in hemostasis.

Adhesion molecules and adhesive interactions play a critical role in the process of hemostasis. A vascular rent requires a patch, and this patch must be provided from constituents of the cellular and fluid phases of flowing blood, constituents that must not interfere with this flow under unperturbed conditions. Platelets, the cellular elements of the patch, are inert until they encounter conditions that trigger their activation. In response to injury they undergo a rapid and dramatic change both in shape and in their surface characteristics, a change that allows them to become both the nidus and the stimulus for the precipitation of a meshwork of fibrin. The interactions between platelets and exposed collagen in the damaged vessel wall, plasma and platelet von Willebrand factor, and plasma and platelet fibrinogen can all be considered 'adhesive interactions'.

Animals↗

PubMedDate not supplied

Effects of desmopressin on hemostasis in patients with liver cirrhosis.

The aim of this double-blind, placebo-controlled crossover study was to investigate the effect of 1-deamino-8-D-arginine vasopressin (dDAVP) on hemostasis in patients with chronic liver disease. Nine consecutive patients with biopsy-proven liver cirrhosis and related coagulation abnormalities received in a random order dDAVP, 0.5 microgram/kg, or saline intravenously. Blood samples were taken before dDAVP infusion and 30, 60 and 180 min after its end. dDAVP infusion induced a statistically significant shortening of the bleeding time from 9 min (range 6.5-15.5) to 6 min (range 4.5-9.5) at 1 h after the infusion. The activated partial thromboplastin time was significantly shortened at 30 and 60 min after dDAVP infusion. Plasma levels of factor VIII, XI and XII coagulant activities were significantly increased at all sampling times after dDAVP infusion. The maximum increase over basal values in plasma levels of factor VIII, XI and XII was 63, 22 and 40%, respectively. dDAVP did not induce any significant changes of prothrombin time, thrombin clotting time, fibrinogen, plasma levels of factor II, V, VII, IX, X, factor XII antigen, protein C (activity and antigen), antithrombin III, plasminogen and alpha 2-antiplasmin. Placebo infusion did not produce any significant changes in the evaluated parameters. We conclude that dDAVP can positively influence the hemostatic system in patients with liver cirrhosis. The clinical relevance of this hemostatic improvement deserves further evaluation.

Adult↗

PubMedDate not supplied

Influence of low molecular weight hydroxyethyl starch (HES 40/0.5-0.55) on hemostasis and hemorheology.

Hydroxyethyl starch (HES) with a high or medium molecular weight (MW) and a high degree of substitution is difficult to degrade and leads to an accumulation of large molecules. These molecules have a negative effect on hemostasiological parameters. In 10 patients with cerebrovascular diseases, a hemodilution therapy was carried out with low MW HES for 10 days. Due to the low MW of the HES used (56-61 kD), the rheological parameters erythrocyte aggregation and plasma viscosity were significantly lowered (p < 0.01). No coagulation parameters studied were affected beyond the dilution effect, which was measured using the decline in hematocrit. Low MW starch is a volume substitute that is well-suited for repeated infusion or hemodilution therapy, particularly for patients with increased hemorrhagic diathesis, because it does not affect hemostasis. The disadvantage of a relatively short volume effect can be compensated through a continuous infusion of a larger volume.

Aged↗

PubMed1990

Primary hemostasis in hemodilution--1) Hematocrit.

There are still controversies about the influence of acute preoperative hemodilution on coagulation. Therefore, we examined the platelet function by the In-vitro bleeding test (IVBT) using composed blood samples of different hematocrit but constant platelet concentration. We found an inverse correlation between hematocrit and bleeding time (p less than .05), volume (p less than .001) and flow (p less than .001). These data suggest a considerable impairment of primary hemostasis, due to low hematocrit. The cause may be an alteration of the hemorheology as well as the interaction between red cells and platelets themselves.

Bleeding Time↗

PubMed1990

Primary hemostasis in hemodilution--2) Infusion solutions.

Various infusion solutions are used during preoperative hemodilution or for substituting intraoperative blood loss. We examined the influence of saline 0.9%, albumin 5%, dextran 6% gelatin 3.5% and hydroxyethyl starch 6% (HES, mw 40,000 and 450,000) on primary hemostasis using the In-vitro bleeding test (IVBT) on composed blood samples of different hematocrit but constant platelet concentration. All infusion solutions tested caused longer bleeding times, depending on the volume used. Saline and albumin had the strongest effect, whereas high molecular weight HES or dextran showed hardly any impairment, if used in a quantity of less than 20% of the blood volume. Autologous plasma seems to be the best substitute in hemodiluted patients, at least if more than 20% of the blood volume has to be substituted by infusion solutions.

Bleeding Time↗

PubMed1987

Animal experiments on hemostasis with a collagen-fibrin tissue-adhesive sealant in the nephrostomy tract.

After a median laparatomy, nephrostomy was performed on 22 porcine kidneys: puncture, dilatation and introduction of a 26-French operating sheath through the parenchyma into the renal pelvis. At the end of the operation, an 8-French nephrostomy catheter prepared with a collagen-fibrin tissue-adhesive sealant was introduced through the operating sheath and the sheath was afterwards extracted. The hemostasis in the nephrostomy tract was very good in all 22 cases. There were no complications such as wound infection or stone formation during a post-operative period of between one and 95 days. Experimental investigations showed severe bleeding in nontamponade of the nephrostomy tract, in tamponade with an 8-French nephrostomy catheter and in tamponade of the nephrostomy tract with the collagen fleece wrapped around an 8-French nephrostomy catheter but not coated with the fibrin glue.

Animals↗

PubMed1987

Local hemostasis of nephrostomy tract with fibrin adhesive sealing in percutaneous nephrolithotomy.

In 26 patients percutaneous nephrolithotomy was carried out under local anesthesia with systemic sedation. Instead of the 25-French nephrostomy catheter used so far, a 5- or 10-French nephrostomy catheter prepared with a collagen-fibrin adhesive sealant was introduced into the nephrostomy tract. In all cases, excellent hemostasis was attained with the fibrin glue. In applying a fibrin glue, the danger of protracted venous or arterial hemorrhage from the parenchymal canal can be markedly reduced; the large-lumen nephrostomy catheter can also be dispensed with.

Aprotinin↗

PubMed1995

Association of hormone replacement therapy with hemostatic and other cardiovascular risk factors. The FINRISK Hemostasis Study.

The risk of cardiovascular diseases in women is small until menopause but increases considerably afterwards. When all age groups are considered, cardiovascular diseases are responsible for approximately half of the total mortality in women. It has been suggested that hormone replacement therapy (HRT) in perimenopausal and postmenopausal women could be useful in the prevention of cardiovascular diseases, but its effects are insufficiently known. We performed a cross-sectional study on the associations of menopause and HRT with cardiovascular risk factors, in particular with hemostatic factors, on female participants of the FINRISK Hemostasis Study. The participants, aged 45 to 64 years, were recruited from the Finnish population register by random sampling from three geographically defined areas. The participation rate of women was 83.2%. Of the 1202 women included in the study, 29.2% were current users of HRT. Differences in cardiovascular risk factors by menopausal status and by HRT use were examined after adjustment for age, study area, current smoking, body mass index, self-reported diabetes, and years of education. Postmenopausal women not using exogenous sex hormones had on average a total cholesterol level 0.5 mmol/L (8.9%) higher and an LDL cholesterol level 0.4 mmol/L (11.4%) higher than premenopausal women. Women reporting irregular menstruation (presumably due to perimenopause) had higher adjusted plasma fibrinogen, factor VII coagulant activity, and factor VII antigen than women with regular menstruation or no menstrual periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation↗

PubMed1999

Deficient platelet-derived nitric oxide and enhanced hemostasis in mice lacking the NOSIII gene.

Endothelial nitric oxide synthase (eNOS) has been identified in human platelets. Although platelet-derived nitric oxide (NO) has been shown to inhibit platelet recruitment in vitro, its role in the regulation of the hemostatic response in vivo has not been characterized. To define the role of platelet-derived NO in vivo, we studied mice that lacked a functional eNOS gene (NOSIII). Surface P-selectin expression in platelets from eNOS-deficient mice was not significantly altered; however, bleeding times were markedly decreased in eNOS-deficient versus wild-type mice (77.2+/-3 versus 133.4+/-3 seconds, P<0.00005). To determine the contribution of endothelium- versus platelet-derived NO to the bleeding time, isolated platelets from either eNOS-deficient or wild-type mice were transfused into a thrombocytopenic eNOS-deficient mouse and the bleeding time was measured. The bleeding times in mice transfused with eNOS-deficient platelets were significantly decreased compared with mice transfused with wild-type platelets (Deltableeding time, -24.6+/-9.1 and -3.4+/-5.3 seconds, respectively; P<0.04). Platelet recruitment was studied by measuring serotonin release from a second recruitable population of platelets that were added to stimulated platelets at the peak of NO production. There was 40.3+/-3.7% and 52. 0+/-2.1% serotonin release for platelets added to wild-type or eNOS-deficient platelets, respectively (P<0.05). In summary, mice that lacked eNOS had markedly decreased bleeding times even after endothelial NO production was controlled. These data suggest that the lack of platelet-derived NO alters in vivo hemostatic response by increasing platelet recruitment. Thus, these data support a role for platelet-derived NO production in the regulation of hemostasis.

Animals↗

PubMed2002

The influence of platelet collagen receptor polymorphisms in hemostasis and thrombotic disease.

Extracellular collagens modulate the rate of platelet activation and thereby markedly influence hemostasis and thrombosis. Platelet receptors for collagens, such as the integrin alpha(2)beta(1), platelet glycoprotein (GP) VI or, indirectly, the GPIb complex, are unexploited targets of pharmacological control, and polymorphisms of these receptors have recently become factored into the genetic risk for thrombosis. Seemingly contradictory findings already exist with regard to the contribution of GPIbalpha and integrin alpha(2) polymorphisms, but these discrepancies will be resolved once there is better standardization of clinical studies. There is already substantial evidence that GPIbalpha VNTR A or B alleles, the GPIbalpha-5C allele, and integrin alpha(2) allele 1 (T(807)) each contribute to increased risk for morbidity in thrombotic disease. However, larger, prospective genetic and epidemiological studies are needed to clarify the role of each of these polymorphisms, the contribution of other platelet receptor polymorphisms, and the synergistic effects of combinations of these factors. In addition, in vitro studies that establish the functional relevance of these polymorphisms will provide sound biological explanations for the results of clinical correlation studies.

Antigens, CD↗

PubMed2003

Normal levels of anticoagulant heparan sulfate are not essential for normal hemostasis.

Endothelial cell production of anticoagulant heparan sulfate (HS(act)) is controlled by the Hs3st1 gene, which encodes the rate-limiting enzyme heparan sulfate 3-O-sulfotransferase-1 (3-OST-1). In vitro, HS(act) dramatically enhances the neutralization of coagulation proteases by antithrombin. The in vivo role of HS(act) was evaluated by generating Hs3st1(-/-) knockout mice. Hs3st1(-/-) animals were devoid of 3-OST-1 enzyme activity in plasma and tissue extracts. Nulls showed dramatic reductions in tissue levels of HS(act) but maintained wild-type levels of tissue fibrin accumulation under both normoxic and hypoxic conditions. Given that vascular HS(act) predominantly occurs in the subendothelial matrix, mice were subjected to a carotid artery injury assay in which ferric chloride administration induces de-endothelialization and occlusive thrombosis. Hs3st1(-/-) and Hs3st1(+/+) mice yielded indistinguishable occlusion times and comparable levels of thrombin.antithrombin complexes. Thus, Hs3st1(-/-) mice did not show an obvious procoagulant phenotype. Instead, Hs3st1(-/-) mice exhibited genetic background-specific lethality and intrauterine growth retardation, without evidence of a gross coagulopathy. Our results demonstrate that the 3-OST-1 enzyme produces the majority of tissue HS(act). Surprisingly, this bulk of HS(act) is not essential for normal hemostasis in mice. Instead, 3-OST-1-deficient mice exhibited unanticipated phenotypes suggesting that HS(act) or additional 3-OST-1-derived structures may serve alternate biologic roles.

Animals↗

PubMed2005

Rap1b is required for normal platelet function and hemostasis in mice.

Rap1b, an abundant small GTPase in platelets, becomes rapidly activated upon stimulation with agonists. Though it has been implicated to act downstream from G protein-coupled receptors (GPCRs) and upstream of integrin alpha IIbbeta3, the precise role of Rap1b in platelet function has been elusive. Here we report the generation of a murine rap1b knockout and show that Rap1b deficiency results in a bleeding defect due to defective platelet function. Aggregation of Rap1b-null platelets is reduced in response to stimulation with both GPCR-linked and GPCR-independent agonists. Underlying the defective Rap1b-null platelet function is decreased activation of integrin alphaIIbbeta3 in response to stimulation with agonists and signaling downstream from the integrin alpha IIbbeta3. In vivo, Rap1b-null mice are protected from arterial thrombosis. These data provide genetic evidence that Rap1b is involved in a common pathway of integrin activation, is required for normal hemostasis in vivo, and may be a clinically relevant antithrombotic therapy target.

Animals↗

PubMed1998

Low levels of tissue factor are compatible with development and hemostasis in mice.

Tissue factor (TF) expression is associated with life-threatening thrombosis in a variety of human diseases, including sepsis, cancer, and atherosclerosis. Recently, it was shown that inactivation of the murine TF (mTF) gene results in embryonic lethality. To date, despite extensive studies on the regulation of the TF promoter in vitro, no studies have examined the cis-acting regulatory elements that control TF gene expression in vivo. Here we report that a human TF (hTF) minigene containing the human TF promoter and human TF cDNA directed a low level (approximately 1% relative to mouse TF) of both constitutive and LPS-inducible human TF expression in transgenic mice. Importantly, the human TF minigene rescued the embryonic lethality of murine TF null embryos, suggesting that human TF substituted for murine TF during embryogenesis. Rescued mice (mTF-/-, hTF+), which expressed low levels (approximately 1%) of TF activity, developed normally with no signs of a bleeding diathesis, suggesting that low TF expression can maintain hemostasis compatible with normal survival. These studies establish a novel mouse model system that can be used to examine the regulation of the human TF gene in vivo and the impact of low TF levels on the hemostatic balance in various thrombotic diseases.

Animals↗

PubMed1993

Interruption of thrombosis and hemostasis by anti-platelet agents.

Blood platelets play a fundamental role in hemostasis and thrombosis. The physiological role of platelets is to preserve the integrity of the cardiovascular system such that upon injury platelets are activated and serve to interrupt a potentially deleterious situation (i.e., hemorrhage). However, platelets are also involved in the pathophysiology of thrombosis in which the normal repair process is grossly exacerbated, resulting in interruption of blood flow to vital tissues. Thus, a critical balance exists between the normal function of blood platelets to preserve tissue function and a pathophysiological function in which tissue is damaged due to thrombosis and subsequent ischemia. Numerous anti-platelet agents have been developed in an attempt to interrupt the thrombotic process without severely compromising the hemostatic state of patients. This article will be devoted to a discussion of a commonly utilized anti-thrombotic agent, aspirin, as well as a class of newer, possibly more effective anti-thrombotic agents referred to collectively as fibrinogen receptor antagonists.

Amino Acid Sequence↗

PubMed1981

Hematology of experimental acute Sarcocystis bovicanis infection in calves. II. Serum biochemistry and hemostasis studies.

Of four Holstein-Friesian calves infected with 200,000 sporocysts of Sarcocystis bovicanis, three become ill and died on days 35, 55, and 59 of a 63-day experiment. No control calves became ill or died. Serum biochemicals and hematologic indicators of hemostasis from both groups were measured throughout the experiment. Creatine phosphokinase values for both groups increased markedly during acute infection. Lactic dehydrogenase and aspartate aminotransferase values were high in infected calves on days 25 to 35 and days 24 to 63, respectively, indicating injury of muscle, liver, or other tissues. Sorbitol dehydrogenase values were significantly higher for infected than for control calves on days 25 and 35, indicating liver injury. Serum bilirubin and blood urea nitrogen values were significantly increased in three anemic infected calves from day 25 or 26 to day 35, probably reflecting destruction of erythrocytes. The fourth infected calf was not anemic and had no hyperbilirubinemia and only minimal azotemia. Serum protein and albumin values decreased in infected calves on days 21 to 30 or 35, when, although hypoalbuminemia persisted, total protein concentration increased. Glucose, calcium, sodium, and chloride values decreased in infected calves slightly before onset of illness and remained low throughout the experiment. Potassium, magnesium, and phosphorus values did not differ between infected and control calves. Activated partial thromboplastin time and Russell's viper venom time were normal; prothrombin time was significantly higher from day 27 to day 49 in infected calves. This pattern was interpreted as evidence for acquired factor VII deficiency. Abnormal retraction of blood clots and enlarged platelets in blood smears, which indicate platelet dysfunction and increased platelet turnover, respectively, were seen on days 27 through 35 in anemic infected calves. Values for thrombin time (three calves) and fibrin degradation product concentration (one calf) increased just before death of the infected calves.

Animals↗

PubMed1986

Water intoxication and death associated with the use of posterior pituitary injection for surgical hemostasis.

Posterior pituitary injection is an extract prepared from the dried posterior lobe of the pituitary gland from domestic animals containing two octapeptide hormones, oxytocin and vasopressin. Posterior pituitary injection carries an approved therapeutic indication as an adjunct measure for achieving surgical hemostasis. We report a case of cerebral edema and death attributed to water intoxication in a child who had received a large volume of free water concurrent with posterior pituitary injection to control bleeding after tonsillectomy and adenoidectomy.

Adenoidectomy↗

PubMed2003

Point of care: diagnostics in hemostasis--the wrong direction?

Point-of-care-testing (POCT) is performance of a laboratory assay outside the laboratory by nontrained personnel. The advantages of POCT are: more rapid medical decisions, avoidance of long sample transports, and small samples. The disadvantages of POCT are: no laboratory personnel, insufficient calibration, quality control and maintenance, poor documentation, high costs, difficult comparability POCT/central laboratory. Therefore, disposing of a 24-hour central laboratory, the POCT spectrum should be limited to the vital parameters: K+, Ca++, Na+, glucose, creatinine, blood gases, hemoglobin or hematocrit, NH3, lactate. POCT offers no advantages, if the hospital has a rapid transport system such as a pneumatic delivery to the central laboratory. The rapid diagnosis of the acute hemostasis state of a patient should be performed in the 24-hour central laboratory that is connected to all hospital wards via a good pneumatic delivery.

Biomarkers↗

PubMed2006

Hemostasis and glycemic control in the cardiac surgical patient.

The Centers for Disease Control and Prevention estimate that 6% of the US population meets diagnostic criteria for diabetes mellitus, with at least one third of this group being undiagnosed. A majority of adult blindness, renal insufficiency, and limb amputation may be directly attributed to diabetes. Although the incidence of type 1, autoimmune-mediated diabetes remains relatively stable, increasing age, physical inactivity, and obesity have produced explosive growth in insulin resistance and type 2 diabetes. A direct association between diabetes and atherothrombotic disease remains indisputable. However, recent data further suggest that even minor elevations of fasting plasma glucose, in "nondiabetic" subjects, increase cardiovascular risk. Alterations in hemostasis may play an important contributory role. Both hyperglycemia and hyperinsulinemia induce prothrombotic characteristics, including overexpression of vascular endothelial plasminogen activator inhibitor-1 (PAI-1), down-regulation of fibrinolysis, elevation of plasma coagulation proteins (ie, fibrinogen, factor VII, factor X), and enhanced platelet activation. Furthermore, endothelial dysfunction-characterized by an inflammatory phenotype-commonly accompanies diabetes. Given data supporting prothrombotic potential of both acute and chronic hyperglycemia, aggressive perioperative glucose control appears imperative.

Blood Glucose↗