No abstract available.
Blood Coagulation* ; Pulmonary Embolism* ; Tissue Plasminogen Activator*

OBJECTIVETo explore the relationship between phlegm-stasis syndrome (PSS) and the fibrinolytic status in patients with non-alcoholic fatty liver (NAFL).

METHODSSeventy patients with NAFL were divided into the PSS group and non-PSS group according to TCM Syndrome typing, and a control group consisted of 28 healthy subjects was set up. Levels of plasminogen (PLG), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and D-dimer were determined and compared.

RESULTSThe activity of t-PA in NAFL patients was significantly lower than that in the control group (P<0.05), and PLG and PAI-1 were significantly higher than those in the control group (P<0.05). In respect to the TCM Syndrome typing, in patients of PSS, t-PA was significantly lower and PLG, PAI-1 were significantly higher than those in patients of non-PSS (P<0.05 or P<0.01), while D-dimer was insignificantly different between patients of the two Syndrome types (P>0.05).

CONCLUSIONNAFL patients of PSS type shows significant lower of fibrinolytic activity, indicating that there is certain degree of microcirculatory disturbance and hyper viscosity state, so the application of dissolving phlegm and dispelling stasis principle in treating NAFL is significant.

Adult ; Aged ; Diagnosis, Differential ; Fatty Liver ; blood ; diagnosis ; Female ; Fibrinolysis ; Humans ; Male ; Medicine, Chinese Traditional ; Middle Aged ; Plasminogen ; metabolism ; Plasminogen Activator Inhibitor 1 ; blood ; Tissue Plasminogen Activator ; blood

BACKGROUND: After multiple trauma, blood coagulation activity is enhanced and fibrinolytic activity is suppressed. Due to high tissue thromboplastin concentration in cerebral tissue, more serious coagulation and fibrinolytic abnormalities may occur when concomitant head trauma is present. The aim of this study was to determine the changes in coagulation and fibrinolysis after trauma and the effects of head trauma on coagulation and fibrinolysis. METHODS: This study includes 35 trauma patients: 16 patients with head trauma (group A) and 19 patients without head trauma (group B). We measured the plasma levels of functional protein C, antithrombin III (AT III), thrombin antithrombin III complex (TAT), plasmin alpha 2 plasmin inhibitor complex (PIC), tissue plasminogen activator antigen (t-PA), and plasminogen activator inhibitor-1 antigen (PAI-1) on admission and on days 1, 2, 4, and 6 after the trauma. RESULTS: The TAT and the TAT/PIC were significantly higher in group A than in group B on all days. PIC was significantly lower in group A than in group B on all days except the day of admission. Over the course of time, the TAT and the TAT/PIC decreased in both groups and PIC increased. On admission, the PAI-1 of both groups was increased, but it decreased over the course of time. The t-PA was increased on admission, was suppressed on the 1st day, and then increased again. The PAI-1 and the t-PA showed no significant difference between the two groups. CONCLUSIONS: After multiple trauma, coagulation was enhanced and fibrinolysis was suppressed. Enhanced coagulation and suppressed fibrinolysis were significantly greater in group A than in group B.
alpha-2-Antiplasmin ; Antithrombin III ; Blood Coagulation ; Craniocerebral Trauma ; Fibrinolysin ; Fibrinolysis* ; Humans ; Multiple Trauma* ; Plasma ; Plasminogen Activator Inhibitor 1 ; Plasminogen Activators ; Protein C ; Thrombin ; Thromboplastin ; Tissue Plasminogen Activator

BACKGROUND: After multiple trauma, blood coagulation activity is enhanced and fibrinolytic activity is suppressed by overproduction of plasminogen activator inhibitor-1 (PAI-1). Intermittent sequential pneumatic compression (ISPC) is an effective method to prevent deep vein thrombosis. Its action is explained by the mechanical effect on blood flow, as well as by the enhancement of fibrinolysis by the reduction of PAI-1. The aim of this study was to determine the effects of ISPC on coagulation and fibrinolysis after multiple trauma. METHODS: Thirty-nine trauma patients were either treated with ISPC (ISPC group, 20 patients) or without ISPC (control group, 19 patients). We measured the plasma levels of the thrombin antithrombin III complex (TAT), the plasmin alpha 2 plasmin inhibitor complex (PIC), the tissue plasminogen activator (t-PA), and the plasminogen activator inhibitor-1 (PAI-1) on admission and at 1, 2, 3, 6, 12, and 24 hours after admission. RESULTS: The TAT was higher than normal in both groups, with no significant difference between the two groups throughout the study period. The PIC level of ISPC group was significantly higher than that of the control group. In the ISPC group, the PIC level increased gradually, reaching a peak at 3 hours and decreasing thereafter. In the control group, the PIC level increased to a peak level at 2 hours. The TAT/PIC ratio dropped in the first two hours and increased at 3 hours, dropping again thereafter. In the ISPC group, the ratio dropped gradually without an intermittent fluctuation. At 3 and 6 hours, the control group showed a significantly greater ratio compared to the ISPC group. PAI-1 was higher than normal in bothgroups, with a significantly lower level in the ISPC group from 2 hours to 24 hours. For the t-PA level, no difference was noted between the two groups, with the peak level occurring at 1 hour. The PAI-1/t-PA ratio was significantly greater in the control group from 2 hours to 12 hours than in the ISPC group, but the difference was not significant at 24 hours. CONCLUSIONS: In multiple trauma patients, ISPC does not seem to affect coagulation, but enhances fibrinolysis through suppressed PAI-1 production. This effect of ISPC may be maintained for 12 hours.
alpha-2-Antiplasmin ; Antithrombin III ; Blood Coagulation ; Fibrinolysin ; Fibrinolysis* ; Humans ; Multiple Trauma* ; Plasma ; Plasminogen Activator Inhibitor 1 ; Plasminogen Activators ; Thrombin ; Tissue Plasminogen Activator ; Venous Thrombosis

OBJECTIVE: To investigate the correlation of platelet and coagulation function with blood stasis syndrome (BSS) in coronary heart disease (CHD). METHODS: The protocol for this meta-analysis was registered on PROSPERO (CRD42019129452). PubMed, Excerpta Medica Database (Embase), the Cochrane Library, and China National Knowledge Infrastructure (CNKI) were searched from inception to 1st June, 2020. Trials were considered eligible if they enrolled BSS and non-BSS (NBSS) patients with CHD and provided information on platelet and coagulation function. The platelet function, coagulation function, and fibrinolytic activity were compared between the BSS and NBSS groups. Forest plots were generated to show the SMDs or ESs with corresponding 95% CIs for each study. Subgroup analysis and sensitivity analysis were performed to explore potential sources of heterogeneity. RESULTS: The systematic search identified 1,583 articles. Thirty trials involving 10,323 patients were included in the meta-analysis. The results showed that mean platelet volume, platelet distribution width, platelet aggregation rate, platelet P selectin, fibrinogen, plasminogen activator inhibitor-1 (PAI-1), thromboxane B2 (TXB2), 6-keto-prostaglandin F1alpha (6-keto-PGF1 α), and TXB2/6-keto-PGF1 α were higher in the BSS group than in the NBSS group (P<0.05 or P<0.01). Activated partial thromboplastin time was lower in the BSS group than in the NBSS group in the acute phase of CHD (P<0.01). The R and K values in thromboelastography and tissue plasminogen activator (t-PA) and t-PA/PAI-1 were lower in the BSS group than in the NBSS group (all P<0.01). No difference was found in the results of platelet count, plateletcrit, maximum amplitude, von Willebrand factor, prothrombin time, thrombin time, international normalized ratio, etc. between groups. CONCLUSIONS Increased platelet function, hypercoagulability, and decreased fibrinolytic activity were found among CHD patients with BSS.
Blood Coagulation ; Blood Platelets ; Coronary Disease ; Humans ; Platelet Aggregation ; Tissue Plasminogen Activator

OBJECTIVETo study the protective impact of tea polyphenols (TP) on the injury of fibrinolytic functions induced by high-methionine dietary in rats.

METHODS50 male Wistar rats were divided by stratified based on body weight into 5 groups with 10 in each group: namely control group, model group, low-dose TP group, medium-dose TP group and high-dose TP group. The rats in model group and TP groups were fed with 3% methionine dietary, control group rats with routine diet. In addition, rats in low-dose, medium-dose and high-dose TP groups were treated with TP at 50, 100 and 200 mg/kg dosage respectively by gavages every day, control group and model group rats were given with same amount distilled water. The animals were sacrificed after 8 weeks. The levels of tissue-type plasminogen activator (t-PA) and type-1 plasminogen activator inhibitor (PAI-1) in plasma were determined by ELISA assays, mRNA levels of t-PA and PAI-1 in aortic arch were detected by RT-PCR, t-PA and PAI-1 expression in aortic arch were detected by immunohistochemistry strept-avidin-biotin complex (SABC).

RESULTSAfter experiment, the t-PA expression of aortic arch in control group, model group, low-dose TP group, medium-dose TP group and high-dose TP group were 133.03 ± 10.14, 95.46 ± 11.08, 111.97 ± 11.91, 130.23 ± 10.80, 139.39 ± 9.41 (F = 14.15, P < 0.01), respectively, and the PAI-1 expression were 90.91 ± 8.67, 166.76 ± 12.18, 139.63 ± 12.71, 134.66 ± 13.19, 109.49 ± 10.82 (F = 31.44, P < 0.01). The t-PA concentration of plasma were (10.69 ± 1.26), (6.13 ± 0.92), (8.56 ± 1.19), (9.69 ± 0.92), (11.97 ± 1.08) ng/ml, respectively (F = 41.98, P < 0.01), and the PAI-1 concentration of plasma were (6.31 ± 0.81), (16.98 ± 1.27), (11.39 ± 0.82), (8.46 ± 0.67), (8.08 ± 0.91) ng/ml, respectively (F = 207.74, P < 0.01). The mRNA levels of t-PA in aortic arch were 1.12 ± 0.02, 0.75 ± 0.14, 1.01 ± 0.09, 0.95 ± 0.08, 1.05 ± 0.13 (F = 5.77, P < 0.05), and the mRNA levels of PAI-1 in aortic arch were 1.25 ± 0.11, 1.74 ± 0.06, 1.23 ± 0.05, 1.09 ± 0.14, 1.23 ± 0.04 (F = 23.56, P < 0.01).

CONCLUSIONThe results indicate that TP seems to have regulatory function on transcription and protein levels of t-PA and PAI-1, in addition to maintaining the balance between PAI-1 and t-PA and healing the injury of fibrinolytic functions in rats induced by high-methionine dietary.

Animals ; Diet ; Fibrinolysis ; drug effects ; Male ; Methionine ; adverse effects ; Plasminogen Activator Inhibitor 1 ; blood ; Polyphenols ; pharmacology ; Rats ; Rats, Wistar ; Tea ; chemistry ; Tissue Plasminogen Activator ; blood

To date, reperfusion with tissue plasminogen activator (tPA) remains the gold standard treatment for ischemic stroke. However, when tPA is given beyond 4.5 hours of stroke onset, deleterious effects of the drug ensue, especially, hemorrhagic transformation (HT), which causes the most significant morbidity and mortality in stroke patients. An important clinical problem at hand is to develop strategies that will enhance the therapeutic time window for tPA therapy and reduce the adverse effects (especially HT) of delayed tPA treatment. We reviewed the pharmacological agents which reduced the risk of HT associated with delayed (beyond 4.5 hours post-stroke) tPA treatment in preclinical studies, which we classified into those that putatively preserve the blood-brain barrier (e.g., minocycline, cilostazol, fasudil, candesartan, and bryostatin) and/or enhance vascularization and protect the cerebrovasculature (e.g., coumarin derivate IMM-H004 and granulocyte colony-stimulating factor). Recently, other new therapeutic modalities (e.g., oxygen transporters) have been reported which improved delayed tPA-associated outcomes by acting through other mechanisms. While the above-mentioned interventions unequivocally reduced delayed tPA-induced HT in stroke models, the long-term efficacy of these drugs are not yet established. Further optimization is required to expedite their future clinical application. The findings from this review indicate the need to explore the most ideal adjunctive interventions that will not only reduce delayed tPA–induced HT, but also preserve neurovascular functions. While waiting for the next breakthrough drug in acute stroke treatment, it is equally important to allocate considerable effort to find approaches to address the limitations of the only FDA-approved stroke therapy.
Blood-Brain Barrier ; Granulocytes ; Hand ; Hemorrhage ; Humans ; Minocycline ; Mortality ; Oxygen ; Reperfusion ; Stroke* ; Tissue Plasminogen Activator

OBJECTIVE: To investigate the antithrombotic effects of recombinant hirudin and its mechanism. METHODS: Sixty male Kunming mice were randomly divided into 6 group (=10):control group, model group, aspirin (25 mg/kg) group, recombinant hirudinlow, middle and high dose (0.05, 0.1, 0.2 mg/kg) groups.Except mice in control group, 2.5 mg/kg carrageenan was injected intraperitoneallyto mice in the other groups to produce thrombosis on the mice tail. The mice in aspirin group were administrated intraperitoneally 25 mg/kg aspirin, the mice in recombinant hirudinlow, middle and high dose groups were administrated intraperitoneally 0.05, 0.1, 0.2 mg/kg combinanthirudin, the mice in control group and model group were administrated intraperitoneallynormal saline at the same volume respectively at 24 h, 0.5 h before injecting carrageenan and 24 h after injecting carrageenan. The black tail length of mice and the incidence of black tail were observed at 48h after injection of carrageenan; prothrombin time (PT), activated partial thromboplastin time (APTT), tissue plasminogen activator (t-PA), type-1 plasminogen activator inhibitor (PAI-1), 6-keto-PGF1α, and thromboxane B2 (TXB2) level in mice plasma were determined. RESULTS: As compared with control group, the mice in model group presented tail thrombosis; PT level in plasma was significantly shortened (<0.01), PAI-1 and TXB2levels in plasma were significantly increased (<0.01), while the t-PA and 6-keto-PGF1α levels in plasma in model group were significantly decreased (<0.01). As compared with model group, the thrombus length in the tail was significantly shortened (<0.05, <0.01), PT level was obviously prolonged (<0.01), and the plasma levels of PAI-1 and TXB2 were significantly decreased (<0.01), while the plasma levels of t-PA and 6-keto-PGF1α were significantly increased (<0.01)in the mice of recombinant hirudin low dose, middle dose, high dose groups and aspirin group. As compared with aspirin group, the thrombus length in the tail was significantly increased (<0.05), PT level was obviously shortened (<0.01), and the plasma levels of PAI-1 and TXB2 were significantly increased (<0.01)in the mice of recombinant hirudin low dose group; the plasma level of 6-keto-PGF1α was significantly decreased (<0.01, <0.05) in the mice of recombinant hirudin low dose and middle dose groups; the plasma levels of PAI-1 and TXB2 were significantly increased (<0.01, <0.05)in the mice of recombinant hirudin middle dose group. CONCLUSIONS The recombinant hirudin can fight against thrombosis, its antithrombotic mechanisms may be related to its influence on the exogenous coagulation system and the promotion of fibrinolysis function.
Animals ; Blood Coagulation ; Fibrinolytic Agents ; Hirudins ; pharmacology ; Male ; Mice ; Recombinant Proteins ; Thromboxane B2 ; Tissue Plasminogen Activator

OBJECTIVETo investigate the effects of chronic mercury poisoning on blood coagulation and fibrinolysis systems, and the possible mechanism.

METHODSTwenty-seven patients with chronic mercury poisoning were studied with 30 healthy people as control. Thrombomodulin (TM), tissue plasminogen activator (t-PA), plasminogen activator inhibitor (PAI), interleukin-13 (IL-13), interleukin-18 (IL-18), soluble intercellular adhesion molecule-1 (SICAM-1) were examined with ELISA methods, and superoxide dismutase (SOD) and lipid peroxidation (LPO) was examined with chemical catalysis methods. Two to three weeks after treatment with reduced glutathione, tiopronin and daidzein, blood was used for determin the above items again.

RESULTS(1) The concentration of TM in patients [(2.36 +/- 0.16) ng/ml] was significantly lower than in the control [(4.36 +/- 0.24) ng/ml] (P < 0.01), while TM tended to be higher after treatment [(4.82 +/- 0.34) ng/ml] (P < 0.05). (2) The concentration of t-PA in patients [(3.44 +/- 0.34) ng/ml] was significantly lower than in the control [(4.52 +/- 0.16) ng/ml] (P < 0.05), and was higher significantly [(5.63 +/- 0.58) ng/ml] after treatment (P < 0.05); The concentration of PAI in patients [(48.23 +/- 3.59) ng/ml] was significantly higher than in the control [(31.59 +/- 2.13) ng/ml] (P < 0.05), but after treatment no significant change [(50.71 +/- 4.29) ng/ml] was found (P > 0.05). (3) The activity of SOD in patients [(953.85 +/- 9.56) U/g Hb] was significantly lower than in the control [(1,308.75 +/- 10.21) U/g Hb] (P < 0.01), and was higher significantly [(1,217.95 +/- 6.29) U/g Hb] after treatment (P < 0.05); and the concentration of LPO in patients [(9.53 +/- 0.26) nmol/ml] was significantly higher than in the control (P < 0.05), and significantly lower [(7.29 +/- 0.35) nmol/ml] after treatment (P < 0.05). (4) The concentrations of IL-13 [(35.93 +/- 5.28) pg/ml], IL-18 [(28.79 +/- 2.53) pg/ml], SICAM-1 [(603.16 +/- 29.12) ng/ml] were significantly higher than those in the controls (P < 0.05, P < 0.01), but no significant difference was found after treatment.

CONCLUSIONDysfunction of the TM/protein C system and t-PA/PAI system (i.e. the decrease of anti-coagulation activity and the inhibition of the function for the fibrolysis system) may play a key role in the secondary hypercoagulable state induced by chronic mercury poisoning.

Adult ; Blood Coagulation ; physiology ; Case-Control Studies ; Chronic Disease ; Female ; Fibrinolysis ; physiology ; Humans ; Male ; Mercury Poisoning ; blood ; physiopathology ; Plasminogen Inactivators ; blood ; Thrombomodulin ; blood ; Tissue Plasminogen Activator ; blood

OBJECTIVETo measure the concentration of D-dimer (DD), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and plasminogen (PLG) activity in plasma and cerebrospinal fluid in patients with acute cerebral infarction and to investigate their clinical significance.

METHODSThe concentrations of D-dimer, t-PA, and PAI-1 in plasma and cerebrospinal fluid in patients were measured by enzyme-linked immunosorbent assay (ELISA). The PLG biological activity was detected using the chromophore method. The results were compared with those of the controls.

RESULTSThe concentrations of D-dimer, t-PA and PAI-1 in cerebrospinal fluid and plasma in patients with acute cerebral infarction were much higher than those of normal subjects (P < 0.01). Conversely, the level of PLG activity was significantly lower in the patients than in the controls (P < 0.01).

CONCLUSIONHypercoagulability and secondary hyperfibrinolysis exist in patients with acute cerebral infarction.

Acute Disease ; Aged ; Blood Coagulation ; Cerebral Infarction ; blood ; Female ; Fibrin Fibrinogen Degradation Products ; analysis ; cerebrospinal fluid ; Fibrinolysis ; Humans ; Male ; Middle Aged ; Plasminogen ; analysis ; cerebrospinal fluid ; Plasminogen Activator Inhibitor 1 ; blood ; cerebrospinal fluid ; Tissue Plasminogen Activator ; blood ; cerebrospinal fluid