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PubMedDate not supplied

Genetic analysis of hemostasis and thrombosis using vascular occlusion.

The zebrafish is an excellent model for mammalian hemostasis and thrombosis since it possesses coagulation factors, thrombocyte receptors and responds to anti-coagulant and anti-platelet drugs commonly used in clinical treatment. In this study, exposure of larvae to FeCl(3) or laser irradiation produced a vessel injury that caused a visible vascular occlusion as a result of thrombus formation. Using the time to vascular occlusion as an assay, two screening strategies were tested for their utility in identifying novel genes involved in thrombosis. Morpholino knockdown studies of zebrafish factor VII showed a prolongation of the time to occlusion of the vessel whereas knockdown of the recently discovered factor VIIi resulted in a shortening of the time. Genetic screening of a population of zebrafish identified mutants that showed a prolongation of the time to occlusion. Bulk segregant analysis showed linkage of one mutant to a locus, victoria, on linkage group 7. Thus, the vascular occlusion assay developed in this report measures in vivo thrombus formation and is a powerful tool for identifying novel genes involved in thrombosis.

Animals↗
PubMed1991

A comparative study on changes in hemostasis in orthotopic and auxiliary liver transplantation in pigs.

We compared blood loss and hemostasis in pigs which had undergone either orthotopic liver transplantation (OLT) (group A, n = 12) or auxiliary heterotopic partial liver transplantation (APLT) (group B, n = 11). Blood samples were taken at regular intervals during and after the operations. In both groups, nine animals survived longer than 24 h and data from these animals were used for analysis. Median (range) intraoperative blood loss was 825 ml (250-1500 ml) in OLT and 425 ml (300-750) in APLT (P less than 0.01). Routine clotting times, as the activated partial thromboplastin time, prothrombin time and thrombin time, showed no major intraoperative changes in either group. Fibrinogen levels decreased in both groups, but no significant difference was found between the two groups. The only significant difference between group A and B was a more sustained increase in fibrinolytic activity after graft recirculation in group A. Postoperatively, restoration of fibrinogen, antithrombin-III and alpha 2-antiplasmin levels was slightly faster in group B, resulting in significantly higher levels during the first day. We conclude that, in this animal model, APLT is associated with significantly lower blood loss and less severe fibrinolytic activity, than OLT. This difference might result from the lack of an anhepatic period and the reduced surgical trauma in auxiliary heterotopic liver transplantation.

Animals↗
PubMed1995

Effects of beraprost sodium, a new prostaglandin I2 analog, on parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina.

The purpose of this study was to investigate the effects of beraprost sodium, a stable prostacyclin analog, on the parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina. Thirty-one patients with exertional angina who had significant organic coronary artery stenosis in at least one of the three major coronary arteries were selected. All patients underwent quantitative exercise thallium-201 emission computed tomography before and 1 month after 120 micrograms per day of beraprost sodium administration. Before exercise, blood samples were collected from 8:30 a.m. to 9:30 a.m. after the patients had been lying in bed undisturbed for at least 10 minutes. Plasma platelet factor 4 (PF4), fibrinopeptide A (FPA), tissue plasminogen activator antigen (t-PA), and plasminogen activator inhibitor-1 activity (PAI-1) were measured. There were no significant differences in exercise parameters on both exercise tests. However, both the extent and severity scores of ischemia were significantly aggravated (p < 0.05 for both) during beraprost sodium administration. Plasma FPA levels decreased significantly during beraprost sodium administration (p < 0.01). Likewise, plasma PF4 levels decreased significantly during beraprost sodium administration (p < 0.05). As for plasma t-PA antigen levels, there was no significant difference before versus during beraprost sodium administration. Plasma PAI-1 activity levels decreased significantly during beraprost sodium administration (p < 0.05). The results indicate that beraprost sodium has strong antithrombogenic properties. However, its aggravation of myocardial ischemia may limit clinical usage.

Angina Pectoris↗
PubMed1993

Influences of lipid-modifying agents on hemostasis.

Drugs affecting lipid metabolism may influence, to a variable extent, the hemostatic system, that is, platelet activation, fibrinogen, and fibrinolysis. These effects may or may not be linked to the activity of these compounds on the lipid/lipoprotein profile. For this reason it may be important to consider the effects of hypolipidemic drugs on the different aspects of hemostasis, because this may allow a better understanding of their clinical use, as well as, eventually, a more proper selection in individual patients. Among the major lipid-lowering agents, fibric acids belong to a multifaceted series of abnormal fatty acids known to interact with a liver nuclear receptor, in turn activating fatty acid catabolism. A similar activity may be exerted by n-3 fatty acids from fish, as well as by other chemically related or unrelated compounds. Among fibric acids all but gemfibrozil can reduce fibrinogen levels; this last drug can, however, apparently activate fibrinolysis. Among the selective cholesterol-lowering medications, both resins and HMG CoA reductase inhibitors may reduce, in some patients, over prolonged periods of treatment, platelet sensitivity to major aggregants. This effect may be seen best with non-liver-selective agents (e.g., simvastatin), although recent data cast doubt on its constancy. A direct comparative evaluation of different HMG CoA reductase inhibitors on platelet aggregability has never been carried out. These last drugs may also reduce the circulating levels of the tissue factor pathway inhibitor (TFPI), transported by LDL in plasma, which is a potentially negative effect. A lipid-lowering molecule with antioxidant activity, for example, probucol, may also possibly play a role in controlling platelet activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗
PubMed1987

Hemostasis in patients with normal and impaired renal function under treatment with cefodizime.

Ten patients (two with normal, eight with impaired renal function) on their usual diet were treated with cefodizime (HR 221) for seven days. The dosage was 4 g/day, adapted to renal function as appropriate. Platelet function, plasma coagulation and vitamin K metabolism were investigated before and on day 7 of therapy. Platelet function and plasma coagulation remained unchanged, regardless of the size of the serum antibiotic trough levels, in both normal and impaired renal function. Vitamin K1 metabolism remained unaffected, since no increase in vitamin K1 2,3 epoxide in the circulation was observed during the therapy. Cefodizime (HR 221), a parenteral aminothiazole cephalosporin, does not affect hemostasis.

Adult↗
PubMed1979

The effect of normovolemic hemodilution on microvascular hemostasis in the rabbit.

Hemostatic plug formation has been studied in the rabbit mesenteric microcirculation during normovolemic hemodilution. A hemodilution method has been developed which maintains a constant platelet count. Using this method the primary hemostatic plug formation time (PHT) and the total hemostatic plug formation time (THT) has been assessed for different degrees of hemodilutions. Both PHT and THT are significantly prolonged for arterioles perfused with low hematocrits (10.6 and 14.2). At a hematocrit of 19.0 the hemostasis is most effective with the shortest hemostatic plug formation times.

Animals↗
PubMed1996

Differences in hemostasis among sclerosing agents in endoscopic injection sclerotherapy.

Endoscopic injection sclerotherapy is useful in stopping bleeding from esophageal varices. We compared the in vivo effects of sclerosants on thrombogenesis, hemostasis, and endothelial injury. We injected aethoxysclerol (AS) of ethanolamine oleate (EO) into the small veins of the rat intestine. The maximum thrombogenic index with AS was 30.7 and with EO was 9.2. The venous flow stopped sooner with EO than with AS. The thrombi caused by EO were mixed with red blood cells. Heparin pretreatment decreased the thrombogenic index with AS by 96.7%, but not that with EO. The area of the fluorescein-albumin conjugate that permeated from veins with AS was larger than that with EO. The fluorescent intensity with AS was lower than that with EO. We thus conclude that: (1) the size of thrombi is not necessarily proportional to the hemostatic efficacy; (2) change in a patient's coagulation may affect the potential of sclerosants; (3) the excellent hemostatic efficacy of EO is based on localized injury to the endothelium and the involvement of red blood cells aggregation; and (4) in vivo microscopy is useful in determining the rational selection of sclerosants.

Animals↗
PubMed1991

Risk of thromboembolic complications in patients with inflammatory bowel disease. Study of hemostasis measurements.

A large number of hemostasis measurements complications were performed in 20 patients with inflammatory bowel disease; whose changes have been associated with an increased risk of thromboembolic. Of the 20 patients, 9 (45%) had one or more changes suggestive of activation of the hemostatic system. Such changes were more frequently observed in patients with active disease. Two patients had changes in the fibrinolytic system (high plasminogen activator inhibitor-1 levels) and 2 in the natural anticoagulants (low antithrombin III activity). Nine patients had increased plasma fibrinogen levels and 6 patients had slightly increased levels of anticardiolipin antibodies. Most of the changes observed were not related to the type, location or activity of the disease. These data show that various biochemical abnormalities may be found in patients with inflammatory bowel disease, which may account for their increased risk of thrombosis, and suggest that multiple mechanisms may interact in determining such complications.

Adult↗
PubMed2004

Hemostasis and thyroid diseases revisited.

Several papers have reported various hemostatic abnormalities in patients with thyroid diseases. In this concise review, the traditional associations between hypercoagulable state and hyperthyroidism and between hypocoagulative state and hypothyroidism are critically revised on the basis of more recent literature data. In particular, we analyze the hemostatic balance (primary hemostasis, coagulation factors and fibrinolytic system) in different thyroid disorders. Although most of the studies published so far include limited numbers of patients and their results are sometimes contradictory, we can conclude that hyperthyroidism is generally accompanied by a hypercoagulable state, whereas the hemostatic profile in hypothyroidism and thyroid cancer depends on the severity of the disease.

Hemostasis↗
PubMed2001

[Gene polymorphisms of hemostasis and coronary risk].

Hemostatic disorders are substantially involved in the pathogenesis of coronary heart disease and acute coronary syndromes. In addition to biochemical markers, gene polymorphisms of hemostasis have been intensively studied in terms of their association with coronary risk. These include polymorphisms of the genes of platelet glycoproteins, fibrinogen, prothrombin, factors V, VIII and XIII, plasminogen activator inhibitor-1 and tissue-type plasminogen activator. An association of a certain gene polymorphism with an increased coronary risk has usually been demonstrated in retrospective case-control studies. However, numerous clinical studies have not yet been able to identify any of these polymorphisms as unequivocal risk factors of coronary heart disease or acute coronary syndromes. These inconsistencies are mainly due to the complexity of the pathogenesis of coronary heart disease and the minor contribution of a single polymorphism to total coronary risk. This review reports on essential requirements of future studies as a prerequisite to improve our understanding of the genetic basis of coronary heart disease.

Blood Coagulation Factors↗
PubMed2000

Endothelial function and hemostasis.

The vascular endothelium influences not only the three classically interacting components of hemostasis: the vessel, the blood platelets and the clotting and fibrinolytic systems of plasma, but also the natural sequelae: inflammation and tissue repair. Two principal modes of endothelial behaviour may be differentiated, best defined as an anti- and a prothrombotic state. Under physiological conditions endothelium mediates vascular dilatation (formation of NO, PGI2, adenosine, hyperpolarizing factor), prevents platelet adhesion and activation (production of adenosine, NO and PGI2, removal of ADP), blocks thrombin formation (tissue factor pathway inhibitor, activation of protein C via thrombomodulin, activation of antithrombin III) and mitigates fibrin deposition (t- and scuplasminogen activator production). Adhesion and transmigration of inflammatory leukocytes are attenuated, e.g. by NO and IL-10, and oxygen radicals are efficiently scavenged (urate, NO, glutathione, SOD). When the endothelium is physically disrupted or functionally perturbed by postischemic reperfusion, acute and chronic inflammation, atherosclerosis, diabetes and chronic arterial hypertension, then completely opposing actions pertain. This prothrombotic, proinflammatory state is characterised by vaso-constriction, platelet and leukocyte activation and adhesion (externalization, expression and upregulation of von Willebrand factor, platelet activating factor, P-selectin, ICAM-1, IL-8, MCP-1, TNF alpha, etc.), promotion of thrombin formation, coagulation and fibrin deposition at the vascular wall (expression of tissue factor, PAI-1, phosphatidyl serine, etc.) and, in platelet-leukocyte coaggregates, additional inflammatory interactions via attachment of platelet CD40-ligand to endothelial, monocyte and B-cell CD40. Since thrombin formation and inflammatory stimulation set the stage for later tissue repair, complete abolition of such endothelial responses cannot be the goal of clinical interventions aimed at limiting procoagulatory, prothrombotic actions of a dysfunctional vascular endothelium.

Arteriosclerosis↗
PubMed2007

[Perioperative hemostasis management].

Hemostasis management plays an important role in surgery. Anti-platelet drugs and oral anticoagulants are taken by an increasing number of patients. Perioperative management must take into account bleeding as well as thromboembolic risks when withholding these medications. Patients with inherited or acquired hemostatic disorders should receive interdisciplinary care in order to optimise perioperative substitution therapy. For the diagnosis of acquired coagulopathy secondary to massive bleeding, point of care tests have been introduced that should help focus substitution therapy in emergency situations. However, physicians should be aware of the limitations of these methods, and a full diagnostic workup should be done in order to uncover hemorrhagic diatheses not detected by point of care testing.

Anticoagulants↗
PubMed2003

Comparison of ultrasonic energy, bipolar thermal energy, and vascular clips for the hemostasis of small-, medium-, and large-sized arteries.

BACKGROUND: Advanced laparoscopic procedures have necessitated the development of new technology for vascular control. Suture ligation can be time-consuming and cumbersome during laparoscopic dissection. Titanium clips have been used for hemostasis, and recently plastic clips and energy sources such as ultrasonic coagulating shears and bipolar thermal energy devices have become popular. The purpose of this study was to compare the bursting pressure of arteries sealed with ultrasonic coagulating shears (UCS), electrothermal bipolar vessel sealer (EBVS), titanium laparoscopic clips (LCs), and plastic laparoscopic clips (PCs). In addition, the spread of thermal injury from the UCS and the EBVS was compared. METHODS: Arteries in three size groups (2-3, 4-5 and 6-7 mm) were harvested from freshly euthanized pigs. Each of the four devices was used to seal 16 specimens from each size group for burst testing. A 5-Fr catheter was placed into the open end of the specimen and secured with a purse-string suture. The catheter was connected to a pressure monitor and saline was infused until there was leakage from the sealed end. This defined the bursting pressure in mmHg. The ultrasonic shears and bipolar thermal device were used to seal an additional 8 vessels in each size group, which were sent for histologic examination. These were examined with hematoxylin and eosin stains, and the extent of thermal injury, defined by coagulation necrosis, was measured in millimeters. Analysis of variance was performed and, where appropriate, a Tukey's test was also performed. RESULTS: The EBVS's mean burst pressure was statistically higher than that of the UCS at 4 or 5 mm (601 vs 205 mmHg) and 6 or 7 mm (442 vs 175 mmHg). EBVS had higher burst pressures for the 4 or 5-mm group (601 mmHg) and 6 or 7-mm group (442 mmHg) compared with its pressure at 2 or 3 mm (128 mmHg) ( p = 0.0001). The burst pressures of the UCS and EBVS at 2 or 3 mm were not significantly different. Both clips were statistically stronger than the thermal devices except at 4 or 5 mm, in which case the EBVS was as strong as the LC (601 vs 593 mmHg). The PC and LC were similar except at 4 or 5 mm, where the PC was superior (854 vs 593 mmHg). The PC burst pressure for 4 or 5 mm (854 mmHg) was statistically higher than that for vessels 2 or 3 mm (737 mmHg) but not different from the 6 or 7 mm pressure (767 mmHg). Thermal spread was not statistically different when comparing EBVS and UCS at any size (EBVS mean = 2.57 mm vs UCS mean = 2.18 mm). CONCLUSIONS: Both the PC and LC secured all vessel sizes to well above physiologic levels. The EBVS can be used confidently in vessels up to 7 mm. There is no difference in the thermal spread of the LigaSure vessel sealer and the UCS.

Animals↗
PubMed1999

Changes in hemostasis after laparoscopic cholecystectomy.

BACKGROUND: The aim of this work was to study hemostasis in laparoscopic cholecystectomy in order to determine if there are any changes that indicate a greater risk of thrombosis. METHODS: The study was carried out in 20 patients who underwent laparoscopic surgery for noncomplicated cholelithiasis. The average age was 59.4 years (range, 34-77). A total of 75% were female. Mean operation time was 70 min (ranges 35-120). Pneumoperitoneum at 14 mmHg was performed on all patients, who were positioned in the 30 degrees reverse Trendelenburg position. Postoperative mobilization was acheived in 24 hs and patients were discharged 48 hs after the operation. The control group was composed of 12 patients, who were evenly distributed by age, sex, and length of surgery. These patients underwent Bassini herniorraphy for inguinal hernia without any complications or relapse. The following hemostatic parameters were studied: prothrombin activity (PA), activated partial thromboplastin time (APTT), fibrinogen (Fg), anti-thrombin III (ATIII), plasma fibrinolytic activity (PFA), euglobulin fibrinolytic activity (EFA), and D-dimer (D-D). Samples were obtained at the following times: (a) under basal conditions the day before surgery, (b) preoperatively, (c) at the end of the operation, (d) 24 hs after the operation, and (e) On the 7th day following the operation. RESULTS: No patient showed any clinical manifestations of thromboembolic disease immediately after surgery or during a medium follow-up period of 16 months (range, 15-18 months). All hemostatic parameters values were within normal range in the basal samples of both groups. In both groups, the mean value of PA showed a significant decrease (p < 0.05) in the second, third, and fourth basal samples, returning to normal levels by the fifth determination. The mean value of fibrinogen decreased slightly in the second and third samples, increasing significantly with respect to the fourth and fifth determinations in both groups (p < 0.05). The mean value of APTT in both groups was slightly enhanced in the second and third determinations in relation to the first and fifth. The global activity of fibrinolysis (PFA and EFA) increased significantly in the third sample with respect to the other determinations in the group who had laparoscopic surgery (p < 0.005). Only EFA increased in the control group (p < 0.05). D-D decreased in the preoperative second determination followed by a significant enhancement immediate postoperatively (third), and 24 hs (fourth) (p < 0.05); it returned to normal basal values on the seventh day. No significant differences were found between the two groups. CONCLUSIONS: These results indicate that laparoscopic cholecystectomy leads to no greater activation of plasma coagulation than low-risk surgery. On the contrary, the increase of fibrinolytic activity in plasma would extend a certain degree of hypocoagulability during surgery, maintaining it for 24 hs and thus possibly reducing thromboembolic risk in patients undergoing this type of surgery.

Adult↗
PubMed1999

Hemostasis with the ultrasonically activated scalpel. Effective substitute for electrocautery in surgical patients with pacemakers.

In patients with implanted pacemaker/cardioverter defibrillator (ICD), the use of electrocautery can lead to serious pacemaker dysfunction. The ultrasonically activated scalpel, however, which has been introduced mainly for the use in laparoscopic surgery, could potentially avoid the outlined problem, since no electrical current flows while in use. This hypothesis was tested in a pacemaker patient undergoing laparoscopic cholecystectomy. During the procedure, no abnormal rhythms or ECG interferences were detected while working in close vicinity to the device. Thus, the ultrasonically activated scalpel provides adequate hemostasis and does not bear the risk of pacemaker dysfunction.

Cholecystectomy, Laparoscopic↗
PubMed2004

Using the angio-seal to achieve hemostasis in prosthetic endovascular surgery: report of three cases.

At least 10% of patients who undergo bilateral aortofemoral bypass are at risk of needing a reoperation for late prosthetic thrombosis because of reduced outflow as the disease progresses. To prevent occlusion of the prostheses, we performed endovascular surgery with transprosthetic access for distal stenosis. We report our experience of using the Angio-Seal with transprosthetic access after angioplasty in three patients who had undergone bilateral aortofemoral bypass. Hemostasis was achieved in all three patients. There were no complications, such as hemorrhage, hematoma, or prosthetic infection, and all three patients were discharged within 24 h. At the 12-, 15-, and 24-month follow-up, none of the patients had any sign of recurrent claudication. Using the Angio-Seal in bilateral aortofemoral bypass provided the means of treating distal stenosis by endovascular surgery with transprosthetic access. This method is both rapid and safe, and may broaden the indications for the endovascular treatment of distal arteriopathies in patients with vascular prostheses.

Aged↗
PubMed2005

Pharmacological correction of hemostasis-regulating function of the lungs in rats with uncomplicated pregnancy and experimental gestosis.

Fetal growth retardation, hypercoagulation, and changes in pulmonary fibrinolytic activity were observed during experimental gestosis induced by long-term feeding of a high-sodium diet. The course of fraxiparine treatment to correct gestosis improved hemostasis-regulating lung function, decreased coagulation activity of the arterial blood, and increased the weights of the placenta and fetus.

Animals↗
PubMed1990

Effects of long-term gestodene-containing oral contraceptive administration on hemostasis.

The purpose of this study was to evaluate the behavior of the hemostatic system during treatment with gestodene-containing oral contraceptives in monophasic (SHD 356, n = 15) and triphasic (SHD 415, n = 15) formulations. No changes in platelet (beta-thromboglobulin, platelet aggregate ratio, and megathrombocyte) and routine clotting assays were observed. Factor VIIc/factor VIIag ratio and fibrinopeptide A values showed a significant (p less than 0.005) increase after three cycles of both treatments. A slight, significant increase (p less than 0.01) in antithrombin III activity was observed during triphasic treatment. Protein C was unchanged. Fibrinolytic activity and plasminogen levels were significantly increased (p less than 0.05 and p less than 0.001). After 6 and 9 months, the factor VIIc/factor VIIag ratio was still significantly enhanced, whereas fibrinopeptide A values significantly (p less than 0.05) decreased, even if they were higher (p less than 0.05) than basal values. The persistence of factor VII activation without enhanced thrombin formation after long-term use of oral contraceptives suggests that at that time the activity of antithrombotic mechanisms counteracts the prothrombotic tendency, thus helping to minimize unwanted side effects on hemostasis during long-term drug administration.

Adolescent↗