Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Thrombin Time”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources
PubMed1994

Variable and circadian response to a fixed high-dose (12 500 IU twice daily) subcutaneous heparin regimen after thrombolytic therapy for acute myocardial infarction.

AIM: To determine the effect of a fixed high-dose (12 500 IU twice daily) subcutaneous heparin regimen on coagulation parameters after thrombolysis with streptokinase. BACKGROUND AND METHODS: A number of large thrombolytic trials have allocated patients to fixed high-dose (12 500 IU twice daily) subcutaneous heparin with no monitoring of coagulation parameters. We hypothesized that heparin's apparent lack of benefit and increased haemorrhagic complications in these trials may be the result of inappropriate anticoagulation. We therefore studied 11 patients who received intravenous streptokinase and oral aspirin for acute myocardial infarction and were subsequently started on the above heparin regimen. Blood samples were taken for activated partial thromboplastin time (APTT) and thrombin time before streptokinase and then immediately before and 6 h after each heparin injection on days 1,4, and 6, and 3 and 6 h after streptokinase on day 5. Plasma heparin levels were also measured on all post-streptokinase samples. Plasma fibrinogen was measured before the administration of streptokinase and once daily on the other sampling days. RESULTS: Both the median APTT and thrombin time were prolonged above the normal range throughout day 1, when fibrinogen levels were depressed, with a non-significant variation between the sampling points. By day 4, however, when fibrinogen levels had returned to pre-streptokinase levels, the median (range) APTTs at 8 a.m. and 8 p.m. (pre-heparin) were similar, and below the therapeutic range, at 52 (38-76) and 48 (39-79) s (NS). Six hours after each heparin injection the APTTs were elevated, but the median (range) 2 p.m. peak of 63 (46-138) s was lower than that at 2 a.m., 125 (58-178) s (P = 0.003). A similar peak and trough, and apparent circadian, APTT response pattern was seen on days 5 and 6. The thrombin time showed the same variation, which was also mirrored in the plasma heparin levels, although the circadian effect was not as marked. CONCLUSION: There is a marked individual variation in response to fixed-dose (12 500 IU twice daily) subcutaneous heparin, with many patients inadequately anticoagulated and an obvious circadian pattern of response. These findings have important implications when considering the benefits and haemorrhagic complications of subcutaneous heparin therapy in general and following thrombolysis in particular.

Aspirin↗
PubMed1981

[Monitoring of heparin therapy with activated recalcification time].

In in-vivo- and in-vitro-examinations the activated recalcification time, the recalcification time of the plasma, the partial thromboplastin time and the thrombin time were compared concerning their suitability for the control of a heparin therapy. The laboratory methods tested considerably differed in their sensitivity compared with heparin and in the possibility of a quantitative statement. The use of a certain laboratory method depends on the indication for a heparin therapy and on the heparin concentration in the blood to be expected. While thrombin time, recalcification time of the plasma and the partial thromboplastin time are suited only for the proof of lower heparin concentrations, the activated recalcification time allows also the proof of higher heparin concentrations in the blood.

Blood Coagulation Disorders↗
PubMed1986

The release of small amounts of fibrinopeptide-B (FPB) is of critical importance for the thrombin clotting time.

When fibrinogen is clotted with thrombin, mainly fibrinopeptide-A (FPA) is released at gel point, the FPB-release being delayed. The present study present evidence that the small amounts of des-AABB fibrin found at visible gelation improves polymerization, thereby determining the thrombin clotting time. 1. Purified fibrinogen was clotted with thrombin or Reptilase, peptide release monitored radioimmunologically. With thrombin, significantly less fibrin (released FPA) was necessary for gel formation than when Reptilase was used. Furthermore, approximately 10% of the available FPB had been released by thrombin at gel point. 2. Polymerization of monomers prepared by incubation of fibrinogen with Reptilase (des-AA) and thrombin (des-AABB) in urea, were examined by light scattering. Des-AA fibrin monomers polymerised after a lag-phase of 4 minutes. When 20% of these monomers were substituted with des-AABB monomers, the lag was reduced to 1 1/2 minutes. 3. Finally, polymerization of preformed des-AA monomers was studied with and without the addition of small amounts of thrombin, and the FPB-release monitored. The presence of 0.04 NIH U/ml of thrombin reduced the lag from 10 minutes to 3 minutes. At this time approximately 10% of FPB had been released. It is concluded that even small amounts of des-AABB fibrin substantially improves polymerization of des-AA fibrin.

Blood Coagulation Tests↗
PubMed1987

Identification of factor XI deficiency in Holstein-Friesian cattle in Britain.

Blood coagulation tests were performed on dairy cattle in a herd with haemorrhagic problems on a farm in Gloucestershire. The characteristic pattern of prolonged partial thromboplastin time with normal prothrombin time and thrombin time was shown to be associated with a partial factor XI deficiency, a congenital defect previously identified in cattle in North America.

Animals↗
PubMed2005

Prevalence and spectrum of von Willebrand disease from western India.

BACKGROUND AND OBJECTIVE: von Willebrand disease (VWD) is one of the most common inherited bleeding disorders in the west. Limited studies from India showed a prevalence of approximately 10 per cent of VWD among the cases with hereditary bleeding disorders. VWD remains an underdiagnosed entity in India. The prevalence of different subtypes of VWD is also not known which is essential for a proper management of these cases. The present study was thus undertaken to know the prevalence of VWD and its various subtypes in the western part of our country. METHODS: A total of 796 consecutive patients presented with various bleeding manifestations were analysed. The initial screening and confirmation tests for the diagnosis of VWD included bleeding time (BT), screening coagulation tests i.e., prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), factor VIII: C assay, ristocetin-induced platelet aggregation (RIPA) and VWF antigen (VWF:Ag) estimations. VWF multimer analysis, ristocetin cofactor activity (RCOF), VWF collagen binding assay (VWF: CBA), factor VIII : VWF binding assay were also done to classify and subtype these cases. RESULTS: The patients were subtyped as per the International Society of Thrombosis and Haemostasis (ISTH) criteria. Of the 796 patients screened, 58 were diagnosed as VWD. Of the 15 families with a positive family history of bleeding, 26 additional cases were diagnosed as VWD. Majority of the patients were type 3 (59.5%) with severe clinical manifestations, about 18 per cent of type 1 VWD patients were detected in this group while the prevalence of the qualitative variants of VWD i.e., type 2 VWD was found to be 19 per cent and the prevalence of various subtypes were type 2A (9.52%), type 2B (4.76%), type 2M (1.2%), type 2N (3.6%). INTERPRETATION AND CONCLUSION: The high prevalence of type 3 and a low prevalence of type 1 VWD which is in contrast to the western reports, suggests the low awareness of the disease as also the underdiagnosis of the mild cases in our country.

Adult↗
PubMed1994

Intramuscular dermatan sulfate MF701 in patients with hip fracture: relationship between pharmacokinetics and antithrombotic efficacy.

Two groups of 23 and 84 patients with hip fracture received intramuscularly 100 and 300 mg dermatan sulfate (MF701) b.i.d., respectively, for the prophylaxis of deep vein thrombosis. Median duration of treatment was 17 and 16 days, respectively. Four blood samples were collected from each patient while under treatment. Plasma levels of dermatan sulfate were determined by a chromogenic substrate assay. A one-compartment model for multiple doses was employed to estimate the pharmacokinetic parameters. Fitting was applied to mean plasma concentrations calculated for each sampling time and weighted according to the number of samples available at each time. Thrombin clotting time was measured on the same plasma samples. Antithrombotic efficacy was assessed by bilateral venography. Plasma levels of dermatan sulfate increased gradually throughout the treatment, indicating a marked accumulation process. Time to reach steady-state was 14 or 9 days with 100 or 300 mg b.i.d., respectively. This was due to an apparent prolonged terminal half-life (68 or 43 h), which actually reflected slow absorption from the injection sites. The clinical efficacy of MF701 in preventing DVT was found to be dependent on the plasma concentration of the drug and also, but less significantly, on the prolongation of thrombin clotting time. Dermatan sulfate plasma levels greater than 9 micrograms/ml are advisable to optimize efficacy in hip fracture patients.

Aged↗
PubMed1977

The antiheparin effect of alpha1-acid glycoprotein and platelet material, evaluated by the heparin thrombin clotting time.

The effect on the heparin thrombin clotting time (HTCT) of a so-called acute phase protein, alpha1-acid glycoprotein, was studied in test systems consisting of purified fibrinogen, antithrombin III, heparin and thrombin, and compared to the effect of platelet material (crude platelet factor 4). In these test systems a physiological concentration of alpha1-acid glycoprotein (1 g/l) inhibited heparin more effectively than did soluble platelet material from 200 X 10(9) platelets/l. The present observations suggest that alpha1-acid glycoprotein is of great significance for the so-called heparin tolerance, whereas platelet material proved less important.

Blood Coagulation Factors↗
PubMed1986

Hyperfibrinogenemia as a cause of prolonged thrombin clotting time.

Recognized causes of a prolonged thrombin clotting time (TCT) include a decreased plasma fibrinogen level, dysfibrinogenemia, paraproteinemia, heparin contamination, elevated levels of fibrin degradation products, and liver failure. We have frequently seen patients with an isolated prolonged TCT in the absence of any of these conditions and without obvious clinical impact. During a previous evaluation of hyperfibrinogenemia, we noted a surprisingly high incidence of prolonged TCT, prompting this evaluation of hyperfibrinogenemia as a possible cause. In our prospective study nine patients had a TCT more than 3 seconds longer than a matched control subject's TCT, with simultaneously normal prothrombin and activated partial thromboplastin times. Eight patients had fibrinogen levels more than 100 mg/dl above the control level (range 383 to 1,223 mg/dl). Only one patient's prolonged TCT could be explained on the basis of elevated levels of fibrin degradation products. In vitro studies in both a purified fibrinogen system and in plasma confirmed a delay in TCT with increasing initial fibrinogen concentrations. Kinetic measurements demonstrated a slowing of the normal initial increase in turbidity seen upon the addition of thrombin. Possible explanations include binding of thrombin to fibrin, or interference with fibrin assembly by excess fibrinogen. Regardless of the kinetic explanation, isolated prolongations of TCT due to hyperfibrinogenemia appear to be of minimal clinical significance.

Adult↗
PubMed2006

The evaluation of coagulation profiles in calves with suspected septic shock.

The purpose of the study reported here was to evaluate the haemostatic function in calves with suspected septic shock and to reflect the occurrence of disseminated intravascular coagulation (DIC). Twenty-six calves suspected of having septic shock (experimental group) and 10 clinically healthy calves (control group) were used. On admission, the experimental group of calves had been ill for an average of 2 days. Therapy was applied to the experimental group of calves. The packed cell volume (PCV), haemoglobin (Hb), white blood cell (WBC), red blood cell (RBC) and platelet (PLT) counts were determined. Blood smears for toxic neutrophil and schistocyte intensity were evaluated. For the coagulation profile, plasma activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT), fibrinogen and fibrin/fibrinogen degradation products (FDPs) values were determined. Toxic neutrophils in blood smears were observed in 12 calves of the experimental group. APTT was prolonged in the experimental group compared with the control group (p < 0.05). Fibrinogen concentration was found to be higher in the experimental group than in the control group (p < 0.001). Total leukocyte counts were higher in the experimental group compared with the control group (p < 0.01). Platelet counts in the experimental group were lower than the control group (p < 0.001). However, when the individual values of coagulation profiles of each calf were evaluated, 8 calves had at least three abnormal coagulation profiles (APTT >72 s, PT >34.5 s, TT >33.7 s, FDPs >5 microg/ml, PLT < or = 150 x 10(3)/mm(3)) and abnormal erythrocyte morphology (schistocytes > or = 1). The most common abnormal tests in the coagulation profile were APTT and PT (7 cases), FDPs (6 cases), thrombocytopenia (4 cases), and schistocytes in blood smears (8 cases) in these 8 calves. The results of this study indicate that DIC might be a significant risk factor for mortality in calves with suspected septic shock.

Animals↗
PubMed2000

Singlet oxygen inactivates fibrinogen, factor V, factor VIII, factor X, and platelet aggregation of human blood.

Activated polymorphonuclear leukocytes participate in hemostasis. These phagocytes generate up to 5 mmol/l of oxidants of the HOCl- and chloramine-type. The present study shows, for the first time, that physiological concentrations of NaOCl or chloramines act as anticoagulants in human plasma. Prothrombin time, activated partial thromboplastin time, and thrombin time at chloramine concentrations greater than 1 mmol/l are prolonged proportional to the oxidant concentration. Plasmatic coagulation factors sensible to oxidation are fibrinogen, factor V, factor VIII, and factor X with a 50% effective dose of 2-3 mmol/l NaOCl or taurine-chloramine. Chloramines or chloramine-like agents (e.g., chloramine T(R) or vancomycin) also inactivate platelet aggregation (in whole blood or platelet-rich plasma) at an 50% effective dose of about 1.0 mmol. This irreversible oxidation of the hemostasis components is inhibited by addition of methionine, cysteine, ascorbic acid, or azide in 10-fold molar excess prior to oxidation. The oxy-radical inhibitors mannitol, superoxide dismutase, or catalase do not antagonize the action of NaOCl or chloramines. Therefore, the oxidant here involved has reaction characteristics of singlet oxygen (1O(2)), a nonradical, excited (i.e., light-emitting) oxidant. The hemostasis factors sensible to oxidation might dispose of oxidizable, for their function critical, methionine or cysteine residues. In conclusion, blood coagulation factors I, V, VIII, X and thrombocytes are sensible to nonradical oxidants of activated phagocytes. Via 1O(2) generation, polymorphonuclear leukocytes can generate a local pericellular zone of anticoagulation. The data suggest that the cell signal 1O(2) in physiological amounts is an antithrombotic agent.

Animals↗
PubMed1992

Accuracy of coagulation studies performed on blood samples obtained from arterial cannulae.

We have assessed the accuracy of coagulation studies in blood obtained from intra-arterial cannulae. Paired samples were studied in blood from 39 patients receiving intensive care; one sample was obtained by venepuncture and the other from an intra-arterial cannula after the apparatus deadspace plus 5 ml of blood had been discarded. Activated partial thromboplastin time (APTT) (with thromboplastin routinely used in our laboratory), prothrombin time (PT), thrombin time (TT), fibrinogen and heparin assays were measured on each sample. In 37 sample pairs, APTT was measured also using a different thromboplastin. The median difference between the sample pairs was 5.5 s for APTT (P = 0.032) and 1.0 s (P = 0.048) for TT, the times for arterial cannula samples being longer. There was no significant difference between arterial cannula and venepuncture samples for PT or fibrinogen concentration. Heparin assays revealed heparin contamination in samples obtained from arterial cannulae in 15 of 30 patients not receiving heparin. It is concluded that, when coagulation studies are performed using the techniques used routinely in our laboratory, a blood sample from an arterial cannula may give clinically misleading information because of contamination with small amounts of heparin, and that separate venepuncture is recommended.

Blood Coagulation Tests↗
PubMed2002

Comparison of anticoagulation efficacy and clinical safety between imported and domestically manufactured low-molecular-weight heparin during hemodialysis.

OBJECTIVE: To compare the anticoagulation efficacy and clinical safety of domestically manufactured and imported low-molecular-weight-heparin during hemodialysis. METHODS: Sixty patients on hemodialysis were randomly divided into 2 groups, who received intravascular injections of domestically manufactured or imported low-molecular-weight heparin to prevent coagulation. Active partial thromboplastin time (aPTT), prothrombin time (PT), thrombin time (TT) and factor Xa activity were determined during dialysis. RESULTS: No incidence of major bleeding was encountered in all of these patients. Similarly low incidences of clotting in extracorporeal circuit were found in either group. No significant differences in aPTT, PT, TT and plasma levels of factor Xa were observed between the two groups. CONCLUSION: Low-molecular-weight heparin domestically manufactured is safe and efficient for anticoagulation during hemodialysis as compared with the imported heparin.

Adult↗
PubMed2004

[A study of human annexin V derivative: its effects of anticoagulation and antithrombosis].

OBJECTIVE: To investigate the effects of a new anticoagulant, annexin V derivative (AND) on anticoagulation and antithrombosis. METHODS: High and low doses of AND were given to rabbits (groups 1 and 2 respectively) by intravenous (iv) bolus injections followed by half the respective AND doses by iv infusion over 2 hours. Control groups were iv given heparin (group 3) and saline (group 4) of the same volume and procedure as that in group 1 and 2. Blood cell count, activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT) and fibrinogen level were examined before and 15, 30 and 60 min after iv bolus and 2 hours after the end of iv infusion. A 3.0 mm x 15 mm balloon was put into femoral artery to induce endothelial denudation 15 min after IV bolus and the blood pressure of femoral artery was monitored until the pulse pressure recorded 0 mm Hg when the vessel was occluded completely by a thrombus. The femoral arteries were collected and the thrombi were stripped off for measuring their lengths, wet and dry weights. RESULTS: Anticoagulation parameters: APTT at 15 min after iv bolus in AND group was significantly longer than that in group 4 (P < 0.05) but shorter than that in group 3 (P < 0.05); APTT and TT in group 3 were significantly longer than those in groups 1, 2 and 4. Fibrinogen: 0.70 mg/kg AND may decrease fibrinogen. Antithrombosis values: the wet and dry weights in AND groups were significantly lighter than those in group 3 and 4 (P < 0.05). The dry weight in high-dose AND group was remarkably lighter than that in low-dose group (P = 0.029). The length of thrombus in low-dose AND group was remarkably shorter than that in group 4 (P = 0.013), but not for group 3 (P > 0.05). It was remarkably shorter in high-dose AND group than in both group 3 (P < 0.001) and 4 (P = 0.015). The time when pulse pressure equaled to 0 was longer in AND group than in group 4 (P < 0.05), but not in 3. CONCLUSION: AND is an effective anticoagulant and antithrombosis agent, the highest anticoagulation effect occurs at 15 min after IV bolus. Its anticoagulation effect is not more potent than that of standard heparin, while antithrombosis capacity is more effective. AND in treating thrombosis clinically might be promising.

Animals↗
PubMed1988

Time-course of anti-Xa effects of calcium heparin and low-molecular-weight heparin given s.c.: insights for thrombosis prevention.

Thirty healthy volunteers underwent a pharmacokinetic study to control the effect of calcium heparin and low-molecular-weight heparin on coagulation factors. Activated partial thromboplastin time (aPTT), thrombin time (TT) and inhibition of activated factor X (Xa) were checked after a single subcutaneous administration of calcium heparin, 5000 IU (CH group); low-molecular-weight heparin 7500 AXaU (LMWH-LD group); and LMW heparin, 15,000 AXaU (LMWH-MD group). The mean values of aPTT rose significantly only after administration of LMW heparin (15,000 AXaU), while no relevant variations were observed after CH and LMWH-LD administration. The effects on TT were also very small and not relevant to an anticoagulant response. The Xa inhibitory effect exerted by the two LMW heparin doses proved substantially higher and longer-lasting than the effect of unfractioned heparin. A statistically significant Xa inhibition was still present 24 h after LMWH-MD administration and 16-20 h after LMWH-LD administration, while 6 h after CH administration no effect was detectable. The laboratory results confirm the marked antithrombophylic action, without relevant anticoagulant effects, already attributed by other authors to the new LMW heparin under study.

Adult↗
PubMed2005

Perioperative monitoring of primary and secondary hemostasis in coronary artery bypass grafting.

On-pump cardiac surgery is accompanied by complex alterations of hemostasis. The excessive postoperative bleeding has been attributed to acquired platelet dysfunction, impaired plasmatic coagulation, and increased fibrinolysis. The characterization of the hemostatic defects responsible for bleeding is crucial for specific treatment and optimal clinical management of the patient. For rapid determination of platelet-dependent primary hemostatic capacity (PHC), the Platelet Function Analyzer PFA-100 system is available. To evaluate the PFA performance in perioperative monitoring, a study was performed in 49 patients selected for low bleeding risk undergoing selective primary coronary artery bypass grafting (CABG). We compared PHC with Simplate bleeding time (BT) and platelet aggregometry. Furthermore, we analyzed global hemostasis by thromboelastography (TEG) and plasmatic coagulation by standard clotting tests prothrombin time (PT, Quick), activated partial thromboplastin time (aPTT), thrombin time (TT) and clotting factors and fibrinolysis by batroxobin (reptilase) time (RT). In all patients BT was postoperatively increased by 1.5- to 2-fold irrespective of perioperative complications and decreased to mildly prolonged values on the first postoperative day (1st day). In patients without complications, PHC in both collagen-adenosine diphosphate closure time (CADP-CT: 83 seconds preop, 78 seconds postop, and 74 seconds 1st day) and collagen-epinephrine closure time (CEPI-CT: 98 seconds preop, 95 seconds postop, 85 seconds 1st day) remained nearly stable. Apart from a patient with postoperative moderate thrombocytopenia, in bleeding patients no other significant defect of postoperative platelet hemostatic capacity was observed. However, on 1st day, the PHC of those patients was significantly reduced compared with non-bleeding patients. In patients with postoperative myocardial ischemia, increased PHC was identified by significantly shorter postoperative CADP-CT (66 seconds vs. 83 seconds) than in uncomplicated patients. By aggregometry, partial platelet dysfunction was observed in some patients without correlation to bleeding complications. In seven of 9 patients the postoperative bleeding complication was attributed to prolonged heparin anticoagulation and/or mildly enhanced fibrinogenolysis/fibrinolysis by TEG and standard plasmatic coagulation tests (TEG: k time 18 minutes vs. 8 minutes; aPTT: 47 seconds vs. 32 seconds; TT: 18.0 seconds vs. 12.3 seconds) and (RT: 19.5 seconds vs. 17.7 seconds). The impairment of PHC, platelet aggregation, and clotting factors observed on the 1st day in bleeding and in intra-aortic balloon pump (IABP) patients are most likely secondary effects, for example, loss of active platelets and clotting factors, to the primary postoperative bleeding or implantation of the IABP. In conclusion, our data indicate that in standard CABG procedures highly variable alterations of the hemostatic system occur after cardiopulmonary bypass (CPB) even in patients with assumed low operative risks. For identification of post-CPB bleeding complications, thromboelastography, aPTT, and TT and heparin and batroxobin (reptilase) time as fibrinolysis-sensitive assays are useful. Platelet function appears to be rapidly restored in uncomplicated CABG. PHC determination by PFA-100 demonstrates a high specificity for adequate platelet function and, therefore, could be beneficial in improved transfusion of platelet concentrates. PHC testing by PFA-100 may help identify postoperative platelet hyper-reactivity associated with myocardial lesion.

Adult↗
PubMed1990

Circadian variations in blood coagulation parameters, alpha-antitrypsin antigen and platelet aggregation and retention in clinically healthy subjects.

Ten clinically healthy subjects (5 men and 5 women), 31 +/- 11 yrs of age, were studied at six timepoints (0800, 1200, 1600, 2000, 0000, 0400) distributed over a 1-week span. Circadian rhythms in platelet aggregation in response to adenosine diphosphate (ADP) and adrenalin (A), platelet adhesiveness measured as retention in a glass bead column, prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen, Factor VIII activity and alpha-1-antitrypsin antigen showed circadian rhythms. The plasma concentrations of plasminogen, alpha-2-macroglobulin, and antithrombin III (AT III) antigen, Factor V and fibrinogen degradation products showed no circadian rhythm by ANOVA or cosinor analysis. The phase relations of the rhythms of different coagulation parameters are of interest in the physiology and pathobiology of the coagulation-fibrinolytic system. The extent of the circadian rhythm (range of change) described is not of a magnitude to lead to diagnostic problems in the clinical laboratory. The timing of these rhythms, however, may determine transient risk states for thromboembolic phenomena, including myocardial infarction and stroke. Several but not all coagulation parameters suggest a transient state of hypercoagulability during the morning hours. The recognition of these rhythmic, and thus in the time of the occurrence predictable temporary risk states for thromboembolic phenomena, may lead to timed treatment and/or effective prevention.

Adult↗
PubMed2006

[Effects of fusion gene encoding the hVEGF165 and fused hirudin on restenosis of injured carotid artery induced by angioplasty].

OBJECTIVE: To study the effects of fusion gene encoding the hVEGF(165) and fused hirudin on restenosis of injured carotid artery. METHODS: A fusion gene encoding hVEGF(165) and fused hirudin (hVEGF(165)-FH) was constructed and clone into the eukaryotic expression vector pcDNA3.0, thus constructing the plasmid VEGF(165)-FH/pcDNA3.0. Its activities to stimulate endothelial cell proliferation and to inhibit thrombosis were identified. Sixteen New Zealand rabbits underwent ligation of external carotid artery and a balloon was inserted into the common carotid artery for 30 minutes so as to construct model of restenosis of injured carotid artery. Then the rabbits were randomly divided into 4 equal groups. In the one-week and 3-week control groups, 400 microg of DNA of the plasmid pcDNA3.0 were transfused into the arterial lumen at the injured part immediately after the angioplasty, and 400 microg of DNA of the plasmid VEGF(165)-FH/pcDNA3.0 were transfused in the 1-week and 3-week experimental groups. One week and 3 weeks after the treatment peripheral blood samples were collected to detect the activated partial thromboplastin time (APTT), thrombin time (TT), and platelet aggregation rate, and then the rabbits underwent angiography to observe the situation of restenosis. Then the rabbits were killed to take out the injured part of artery to undergo pathological examination and Western blotting. RESULTS: The values of APTT, TT, and platelet aggregation rate were not significantly different among the 4 groups. Angiography conducted 1 and 3 weeks later showed that restenosis was significantly mild in the 2 experimental groups in comparison with the 2 control groups, and severe restenosis was seen in the 3-week control group. Western blotting showed that expression of specific fused protein could be found in the 1-week and 3-week experimental group, the amount of the latter group being less than that of the former group; however, no expression of specific fused protein was found in the 2 control groups. Pathological examination showed that the narrowing of lumen 1-week and 3-week experimental groups were 11.50% and 19.75%, both significantly milder than those of the 1-week and 3-week control groups (33.25% and 52.25% respectively, both f P < 0.05). VB staining showed that the (intima/media (I/M) ratio of the 1-week and 3-week experimental groups were 0.12 and 0.35 respectively, both significantly lower than those of the 2 control groups (0.50 and 1.07 respectively, both P < 0.05). CONCLUSION: Accelerating re-endothelialization and inhibiting thrombosis, the fused gene hVEGF(165)-FH effectively prevents restenosis after angioplasty, On the basis of endothelial repair, construction of fused genes with double even multiple targets may be a novel and potential therapeutic approach for restenosis after percutaneous coronary intervention.

Animals↗
PubMed1988

Blood coagulation studies in guineapigs (Cavia porcellus).

Blood coagulation studies were performed on 45 healthy, adult guinea pigs. Additionally thrombelastograms of 30 animals were recorded. Guineapigs revealed short partial thromboplastin times and euglobulin lysis times, but long prothrombin times and thrombin times. Fibrinogen values were within the range of human normal values. Biphasic ADP-induced aggregation of platelets, as occurs in man, was found in 29% of the animals. Short r (reaction time until the beginning of clot formation) and k times (time from the beginning of clot formation until an amplitude of 20 mm) of their thrombelastograms indicate, that whole blood clotting is enhanced in guineapigs. Higher maximum amplitudes in this species suggest a stronger clot stability than in man.

Adenosine Diphosphate↗