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PubMed1975

Physiological role of an endoperoxide in human platelets: hemostatic defect due to platelet cyclo-oxygenase deficiency.

The endoperoxide prostaglandin G2 (PGG2) induced platelet aggregation as well as the platelet release reaction (release of ADP and serotonin) when added to human platelet-rich plasma. Formation of a metabolite of PGG2 [8-(l-hydroxy-3-oxopropyl)-9,12L-dihydroxy-5,10-heptadecadienoic acid] and a lipoxygenase product [12L-hydroxy-5,8,10,14-eicosatetraenoic acid] accompanied the release reaction caused by aggregating agents such as collagen, ADP, epinephrine, and thrombin. Indomethacin inhibited the release reaction and PGG2 formation induced by these agents but had no effect on PGG2-induced release reaction. The aggregating effect of PGG2 was abolished by furosemide, which is a competitive inhibitor of ADP-induced primary aggregation. These data indicate that the aggregating effect of PGG2 is due to release of ADP and that PGG2 synthesis is required for induction of the release reaction by various aggregating agents. A subject with a hemostatic defect due to abnormal release mechanism [decreased aggregation with epinephrine (second wave) and collagen and normal platelet ADP] had a deficiency of the cyclo-oxygenase that catalyzes formation of PGG2. Normal aggregation and release reaction were obtained with added PGG2. Ii is concluded that the endoperoxide (PGG2) is essential in normal hemostasis because of its role in initiating the release reaction required for aggregation by collagen and the second wave of aggregation caused by, e.g., ADP.

Adenosine Diphosphate↗
PubMed1985

Purified human factor VIII procoagulant protein: comparative hemostatic response after infusions into hemophilic and von Willebrand disease dogs.

The procoagulant protein F.VIII:C is noncovalently bound to von Willebrand factor (vWF) to give the factor VIII macromolecular complex. New highly purified preparations of isolated human F.VIII:C, devoid of vWF and about 500,000-fold purified, were administered to hemophilia A and von Willebrand disease (vWD) dogs to determine their hemostatic effectiveness and survival in the circulation. Two preparations of F.VIII:C were used: peak 1, with active components of Mr 185,000-280,000, and peak 2, with a single component of Mr 170,000. In hemophilic dogs, with no plasma F.VIII:C but normal vWF, both preparations immediately elevated plasma F.VIII:C to expected levels, promptly stopped induced and spontaneous hemorrhages, and gave sustained plasma levels of F.VIII:C. The isolated F.VIII:C immediately complexed with endogenous vWF in hemophilic plasma and was eliminated exponentially, with a half-life (t1/2) of about 9 hr. Survival of peak 2 F.VIII:C was longer than that of peak 1 material. In contrast, F.VIII:C complexed to vWF in a therapeutic concentrate administered to hemophilic dogs was eliminated biexponentially with first-phase t1/2 of 3.2 hr and second-phase t1/2 of 9 hr. In vWD dogs with no vWF and reduced F.VIII:C levels, the isolated F.VIII:C produced supernormal levels of F.VIII:C without effect on induced bleeding. It was rapidly eliminated from plasma with a t1/2 of about 1 hr, as was the complexed F.VIII:C in the concentrate. These data indicate that isolated F.VIII:C promptly complexes with vWF and in this form is highly effective in controlling hemophilic hemorrhages with good survival in plasma. Without endogenous vWF with which to complex, the F.VIII:C is promptly eliminated.

Animals↗
PubMed2006

Effect of a combined oral contraceptive containing 20 microg ethinyl estradiol and 75 microg gestodene on hemostatic parameters.

The effects of a combined oral contraceptive (COC) containing 20 microg ethinyl estradiol (EE) and 75 microg gestodene (GSD) on prothrombin activity (PA), activated partial thromboplastin time (APTT), thrombin time (TT), platelet number, fibrinogen, antithrombin III (ATIII), protein C, protein S and D-dimer were evaluated over 6 months in 23 young, healthy women. Laboratory assessments were performed prior to initiation of COC use (pretreatment) and after 3 and 6 months of use. Results showed no significant changes in fibrinogen, protein C, ATIII or D-dimer during COC use, compared with pretreatment values. The increase in platelet count, decreases in protein S level, PA and APTT, and the prolongation of TT were significant. In conclusion, the use of a COC containing 20 microg EE and 75 microg GSD did not cause any significant changes in the hemostatic parameters studied that could be suggestive of a higher prothrombotic risk. Further studies with a larger sample size are necessary in order to obtain conclusive data.

Adolescent↗
PubMed2001

Impact of plasmapheresis on platelet hemostatic capacity in healthy voluntary blood donors detected by the platelet function analyzer PFA-100.

Previous flow cytometry studies showed that platelet activation may occur during cytapheresis, cardiopulmonary bypass and hemodialysis. The aim of this pilot study was to determine if the impact of plasmapheresis leads to alterations in platelet hemostatic capacity. Plasmapheresis was carried out in 30 volunteers using an Autopherese C (Baxter) and an MCS3p (Haemonetics). Blood samples were collected and analyzed immediately before and after plasmapheresis. As a result of the plasmapheresis on the Autopherese C, the mean closure time (CT) for collagen/epinephrine (Col/Epi) increased from 118.2 +/- 25.1 to 149.9 +/- 35.0 s and from 88.7 +/- 16.9 to 98.5 +/- 26.3 s for collagen/ADP (Col/ADP), respectively. Seven subjects showed impaired CTs after plasmapheresis for Col/Epi. For Col/ADP, five subjects showed impaired CTs after apheresis. Statistical analysis (McNemar test) showed a significant difference before and after apheresis for Col/Epi (P = 0.024) but not for Col/ADP (P = 0.088). Similar results were shown for plasmapheresis carried out with the MCS3p. These findings show that plasmapheresis can cause an impairment of platelet function in healthy volunteers as measured by the PFA-100, an effect of so far unknown clinical significance.

Adult↗
PubMed2003

Detection of hepatitis C virus antibody and RNA in hemostatic gauze used for dentistry.

We investigated whether the presence of hepatitis C virus (HCV) infection can be detected in hemostatic gauze used during oral treatments. We were able to detect both antibody to HCV and HCV RNA in samples from patients serologically proven to have HCV and also in gauze used for these patients that was left at room temperature even for as long as 24 hours. Thus, this method is useful for the screening of HCV infection in situations in which blood sampling is not feasible.

Cross Infection↗
PubMed1991

Lipid, lipoprotein, and hemostatic effects of fish vs fish-oil n-3 fatty acids in mildly hyperlipidemic males.

The effects of fish and fish oil on lipids, hemostasis, and blood pressure were compared in 25 mildly hyperlipidemic men who received 4.5 g eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) daily for 5 wk. Six additional subjects served as controls. Fish and fish oil lowered plasma triglycerides 20% and 28% and very-low-density-lipoprotein (VLDL) triglycerides 42% and 52%, respectively (all P less than 0.05 compared with control). High-density-lipoprotein (HDL) cholesterol increased by 10% and 9%, with 34% and 32% increases in the proportion of HDL2 particles for fish and fish oil, respectively. Changes in total cholesterol, LDL cholesterol, apolipoprotein B, and blood pressure with fish and fish oil were not significantly different from changes for the control diet. The fish lowered fibrinogen (15.7%) and thromboxane (10.5%) and increased bleeding time (10.8%) (P less than 0.05 compared with control). Eating fatty fish and fish oil produced comparable lipid and lipoprotein changes, but only the fish improved hemostatic factors.

Adult↗
PubMed1999

Hemostatic changes in Rocky Mountain spotted fever and Mediterranean spotted fever.

Rocky Mountain spotted fever and Mediterranean spotted fever are rickettsial infections primarily of endothelial cells that normally have a potent anticoagulant function. As a result of endothelial cell infection and injury, the hemostatic system is perturbed and shows changes that vary widely from a minor reduction in the platelet count (frequently) to severe coagulopathies, such as deep venous thrombosis and disseminated intravascular coagulation (rarely). Changes favoring a hypercoagulable state include endothelial injury and release of procoagulant components, activation of the coagulation cascade with thrombin generation, platelet activation, increased antifibrinolytic factors, consumption of natural anticoagulants, and possibly high levels of coagulation-promoting cytokines. Yet, most studies have been performed on endothelial cell cultures that provide nonphysiologic, reductionistic, experimental conditions. The lack of flow, platelets, and WBCs makes these experiments far from simulating the response of endothelial cells in the human body. Coagulopathies and thrombotic events should be considered as potential complications of severe Rocky Mountain spotted fever and Mediterranean spotted fever.

Blood Coagulation↗
PubMed1990

Lack of increased bleeding after liver biopsy in patients with mild hemostatic abnormalities.

Prophylactic transfusions of fresh frozen plasma and platelets are sometimes given to patients with mild elevations in prothrombin time (PT) and partial thromboplastin time (PTT) and mild thrombocytopenia before percutaneous liver biopsy. To determine whether PTs and PTTs 1.1-1.5 times midrange normal levels and platelet counts 50-99 x 10(9)/L are associated with increased bleeding complications, hospital records of all patients who underwent percutaneous liver biopsy during 56 consecutive months (n = 291) were reviewed. Complete information was available for 177 inpatient procedures (155 standard, 22 fine needle). Overall, the frequency of bleeding complications in patients with platelet counts greater than or equal to 50 X 10(9)/L was 3.4% (6 of 175), with no significant difference between patients with mild hemostatic abnormalities and patients with normal parameters. These data suggest that prophylactic transfusions may not be necessary. One factor was highly associated with bleeding complications: a patient diagnosis of malignancy, 14% (7 of 50) compared with 0.8% (1 of 127) among other patients (P less than 0.001). These patients should be monitored closely after biopsy.

Adult↗
PubMed1991

Laboratory hemostatic abnormalities in massively transfused patients given red blood cells and crystalloid.

Most of the literature on massive transfusion concerns whole blood replacement, whereas clinically, packed red blood cells are commonly given. To determine when hemostatic abnormalities occur in patients resuscitated primarily with packed red blood cells and crystalloid, the cases of 39 consecutive patients who were transfused with 10 or more red blood cell units of any kind within 24 hours were reviewed. After transfusion with 20 or more units of red blood cell products of any kind (packed red blood cells, cell-saver units, or whole blood), 75% (3 of 4) of patients had platelet counts less than 50 x 10(9)/L, compared to 0 of 29 patients given less than 20 units (P less than 0.001). After transfusion of 12 units of relatively plasma-free red blood cell products (packed red blood cells or cell-saver units), 100% (8 of 8) of patients had prothrombin time prolonged by more than 1.5 times mid-range of normal, compared to 36% (5 of 14) of patients given less than 12 units (P = 0.012). These data confirm that patients massively transfused with red blood cells of any kind develop significant thrombocytopenia after 20 units. Importantly, probably clinically significant prothrombin time and partial thromboplastin time prolongations occurred consistently after transfusion of 12 units of relatively plasma-free red blood cells in unselected patients at an urban trauma hospital. These data suggest that coagulation factor replacement is necessary in patients who receive 12 or more units of packed red blood cells or cell-saver blood, and platelet replacement is necessary in patients who receive 20 or more units of any red blood cell product. A prospective study is needed to determine whether the expected abnormal clinical bleeding indeed occurs in patients with such laboratory coagulation abnormalities and to determine when plasma transfusion is indicated in patients massively transfused with red blood cells.

Adult↗
PubMedDate not supplied

Hemostatic derangement produced by Rift Valley fever virus in rhesus monkeys.

Rift Valley fever (RVF) is an important cause of disease in animals and humans in sub-Saharan Africa. In a small percentage of human cases, the disease is complicated by hemorrhage, which often is associated with a fatal outcome. Inoculation of rhesus monkeys with the Zagazig Hospital strain of RVF virus produced a clinical picture similar to illness in humans. Ten of 17 monkeys developed clinical evidence of hemostatic impairment. When coagulation tests were performed, this group of monkeys had significant abnormalities, including evidence for disseminated intravascular coagulation. These abnormalities were much less pronounced in the remaining seven monkeys-whose only sign of illness was transient fever-and, in general, they paralleled the level of viremia and the degree of elevation in levels of serum hepatic enzymes. Autopsy of the three monkeys with severe disease revealed hepatic necrosis.

Animals↗
PubMedDate not supplied

The minor problem of hemostatic impairment in nephropathia epidemica, the mild Scandinavian form of hemorrhagic fever with renal syndrome.

Nephropathia epidemica (NE) is the mild Scandinavian form of hemorrhagic fever with renal syndrome (HFRS). Its hemorrhagic manifestations are so mild that initially--as its name implies--it was not considered a hemorrhagic fever. It is, however, clinically, histologically, and epidemiologically similar to Korean hemorrhagic fever (KHF) except that hemorrhagic manifestations are fewer and mortality is lower. The etiologic agents of the two disorders, Puumala virus (NE) and Hantaan virus (KHF), are closely related. NE is the most benign of the hemorrhagic fevers. Hemostatic impairment is not a significant clinical problem in this disease and therefore has not been thoroughly studied, although abnormalities in hemostasis have been noted. Further investigations of this disease might provide insights concerning the treatment of other, more severe, hemorrhagic fevers.

Hemorrhagic Fever with Renal Syndrome↗
PubMedDate not supplied

Activated leukocytes and the hemostatic system.

Activated leukocytes are capable of activating the blood-clotting system. Upon adequate stimulation (e.g., by endotoxin, by lectins, in the course of immune reactions, and in response to lymphokines of T cell origin), macrophages and monocytes synthesize tissue thromboplastin and expose it on their surface. Leukocyte proteases may interfere with blood coagulation by degrading clotting factors, in particular factors V, VIII, and XIII. Furthermore, these enzymes act as fibrinolytic agents, which also cleave fibrinogen. Leukocyte elastase attacks the platelet glycoproteins Ib (the receptor for von Willebrand factor) and V (a thrombin substrate) and at the same time exposes the platelet fibrinogen receptor. Platelet-activating factor of leukocyte origin may induce platelet aggregation and is a powerful potentiator of other inducers of platelet activity. The last-mentioned property has also been reported for leukotrienes. Activated leukocytes and their products play an important role in the pathogenesis of important disorders of the hemostatic system, with disseminated intravascular coagulation as the most prominent example.

Animals↗
PubMedDate not supplied

Delayed hemostatic changes following cardiopulmonary bypass.

A variety of hemostatic abnormalities has been reported in patients following open-heart surgery. Since surgery itself may induce changes in the coagulation system, the analyses of postoperative coagulation assays in the bleeding patients may be extremely difficult to interpret without an understanding of the coagulation dynamics in the nonhemorrhagic postoperative patients. Thus, we studied the pattern of change in several coagulation assays performed on 36 consecutive patients before and during the first two postoperative weeks. Approximately one third of the patients has some clotting abnormality before surgery. Shortened prothrombin time (PT) and activated partial thromboplastin time (APTT) were observed within the first three postoperative days. Only following warfarin therapy (initiated on the third postoperative day) was significant prolongation of PT and APTT observed. During the 14 postoperative days, fibrinogen levels and fibrinogen degradation products progressively increased without prolongation of the thrombin time or decrease in the euglobulin clot lysis time. On the first postoperative day, the platelet count and platelet adhesiveness values were significantly less than before surgery (p less than 0.01 and p less than 0.05). Over the following two weeks, the platelet count and platelet adhesiveness returned to normal. Although there was slight lengthening of the Ivy bleeding time on the first postoperative day, this assay was never abnormal. Thus, we conclude that the following cardiopulmonary bypass there is (1) probably activation of circulating procoagulants, (2) progressive increase in fibrinogen levels, (3) activation to the fibrinolytic system, and (4) transient thrombocytopenia with a superimposed platelet defect.

Adolescent↗
PubMed1996

Factors associated with excessive postoperative blood loss and hemostatic transfusion requirements: a multivariate analysis in cardiac surgical patients.

The purpose of this study was to prospectively evaluate whether heparin and protamine doses administered using a standardized protocol based on body weight and activated clotting time values are associated with either transfusion of hemostatic blood products (HBPs) or excessive postoperative bleeding. Analysis using 10 multiple logistic or linear regression models in 487 cardiac surgical patients included perioperative variables that may have an association with either transfusion of HBP and/or excessive postoperative chest tube drainage (CTD). Prolonged duration of cardiopulmonary bypass (CPB), lower pre-CPB heparin dose, lower core body temperature in the intensive care unit, combined procedures, older age, repeat procedures, a larger volume of salvaged red cells reinfused intraoperatively and abnormal laboratory coagulation results (prothrombin time, activated partial thromboplastin time, and platelet count) after CPB were associated with both transfusion of HBP and increased CTD. Female gender, lower total heparin dose, preoperative aspirin use and the number of HBPs administered intraoperatively were associated only with increased CTD, whereas a larger total protamine dose was associated only with perioperative transfusion of HBPs. Preoperative use of warfarin or heparin was not associated with excessive blood loss of perioperative transfusion of HBPs. In contrast to previous studies using bovine heparin, data from the present study do not support the use of reduced doses of porcine heparin during CPB.

Age Factors↗
PubMed1996

Profound normovolemic hemodilution: hemostatic effects in patients and in a porcine model.

Previous systematic investigations of the hemostatic effects of normovolemic hemodilution (NHD) have not explored the influence of hematocrits less than 20% in humans or animals. However, clinical interest in maximizing the perioperative conservation of erythrocytes may involve profound NHD beyond traditionally accepted empiric end points. We report here on coagulation data in eight healthy adolescent patients undergoing profound NHD in concert with surgical correction of idiopathic scoliosis, and in 29 swine undergoing experimental stepwise NHD until death. Blood was replaced with 5% albumin in 0.9% saline in our patients, and with 5% albumin in lactated Ringer's solution in our pigs. A 75% blood volume exchange in our patients yielded a platelet count (PLT) of 158 +/- 26 x 10(3)/microL, fibrinogen concentration (FIB), 50 +/- 7 mg/dL, prothrombin time (PT), 25.4 +/- 2.6 s, activated partial thromboplastin time (aPTT), 87 +/- 15s, and a nadir hemoglobin of 2.8 +/- 0.2 g/dL; however, global oxygen delivery as assessed by body oxygen consumption remained adequate. Coagulation during the experimental porcine hemodilution was assessed by measuring PLT, FIB, PT, and aPTT, as well as by measurement of coagulation factor activities. In neither species did clinically significant thrombocytopenia (PLT < 100 x 10(3)/ microL) become manifest prior to clinical or other laboratory evidence of coagulopathy. Rather, a combined deficiency of coagulation factors explains the coagulopathy developing during NHD in both patients and swine. Abnormal hemostasis develops prior to compromise of global tissue oxygenation, assessed by mixed venous oxygen saturation and total body oxygen consumption, during NHD in healthy patients anesthetized as described. Therefore, NHD may be more limited by preservation of normal coagulation than of global oxygen delivery and consumption.

Adolescent↗
PubMed1984

Value of the preoperative history as an indicator of hemostatic disorders.

Eighty-three general surgical patients completed the standardized bleeding history questionnaire, and screening tests of platelet counts, prothrombin times, partial thromboplastin times, and Ivy bleeding times were done on these patients. Fifty-two per cent had undergone previous operation; 25% described symptoms of potential hemostatic disorders and seven per cent had positive family histories. Laboratory results indicated abnormalities in five patients (6%). The bleeding history is an important part of the preoperative evaluation of a patient, but it can have serious false-negative results. This history should guide the selection of laboratory tests. Such testing can yield an unexpectedly high rate of abnormalities. When identified, these abnormalities require further investigation.

Adolescent↗
PubMed1995

Hemostatic abnormalities in patients with pulmonary embolism compared with that in deep vein thrombosis.

We investigated hemostatic abnormalities in 37 patients with deep vein thrombosis (DVT) and pulmonary embolism (PE) (PE patients) and in 40 patients with DVT without PE (DVT patients). Plasma fibrinogen, thrombin-antithrombin complex (TAT), plasmin-plasmin inhibitor complex, fibrin-D-dimer, activated protein C (APC)-protein C inhibitor (PCI) complex, von Willebrand factor (vWf), tissue plasminogen activator (t-PA), PA inhibitor-I (PAI-1), and thrombomodulin levels in both PE and DVT patients were significantly increased compared with normal volunteers. Plasma APC-PCI complex, PAI-1, and vWf levels in PE patients were significantly higher than those in DVT patients without PE. These findings indicate that PE patients are more hypercoagulable and hypofibrinolytic than DVT patients. Plasma TAT, APC-PCI complex, PAI-1, and vWf levels were the most sensitive indicators for PE. In these patients, increases in TAT and APC-PCI complex suggest DVT and increased PAI-1 and vWf suggest the risk of onset of PE.

Aged↗
PubMed1999

Invertebrate compounds acting on the hemostatic mechanism.

Physiological secretions from some invertebrates have toxic effects on mammalian blood coagulation and fibrinolytic systems. Some of these effects occur because the substances contained in the secretions resemble the components of the hemostatic system. Some of the substances have been characterized, and have been found to have similar molecular weights or sequences, which may indicate a common ancestry. The components can be divided into five groups: antithrombic agents (group I); inhibitors and activators of the prothrombinase complex (group II); substances that affect platelet function (group III); substances that affect the fibrinolytic mechanism (group IV); and a group of miscellaneous agents whose activities are difficult to group together (group V). In group I special mention of the antithrombin agents in Hirudo medicinalis should be made. In group II, the agents affecting the prothrombinase complex are antistasin from Haementeria officinalis, ghilanten from Haementeria Ghiliani and the tick anticoagulant protein from Ornithodoros moubata, a factor V activator/inhibitor from Lonomia achelous and factor II and factor X activators from L. achelous and Lonomia obliqua. Examples of factors which affect platelet function (group III) are glossina from the black fly Glossina morsitans, calin from H. medicinalis, decorsin (a desintegrin) from Macrobdella decorsa, and FAGA from Stichopus japonicus selenka. The first three of these are inhibitors of platelet aggregation, and the last is an inducer. The plasminogen activators (group IV) from the L. achelous caterpillar and Eutriatoma maculata trigger the fibrinolytic system, whereas hementin from H. officinalis and hementerin from Haementeria depressa are directly fibrinolytic. The last group of substances (group V) include those with factor-XIIa-like activity from D. farinae, kallikrein-like activity and a factor XIII degrading enzyme from L. achelous, destabilase from H. medicinalis and prolixin S (nitroforin 2, or anti-factor-IXa) from Rhodnius prolixus. Some of these components have been well characterized, cloned and prepared in recombinant form, and seem to be very promising from the therapeutic point of view.

Animals↗