CHANGES IN PLATELET ACTIVITY, FIBRONECTIN AND TISSUE PLASMINOGEN ACTIVATOR DURING ARTERIOGRAPHY IN PATIENTS WITH ISCHAEMIA EXTREMITIES INFERIES

1987 ◽  
Author(s):  
W Augustyniak ◽  
C S Cierniewski ◽  
V Slawincki ◽  
J H GOCH ◽  
R Polanowaka

Platelets and endothelial cells may be activated to release their contents during arteriography, which is one of the most frequently used examinations of patients with peripheral vascular diseases. This technique involves lumbar aortic puncture and catheterization with administration of contrast medium in arteriosclerosis obliterans (AO) extremities inferies. In this report we have studied 26 patients aged 37 to 73 years with AO who were subjected to arteriography performed according to the Seldinger method. Concentrations of β-thromboglobulin (β-TG), platelet factor 4 (PF4) and plasma fibronectin (Fn) were determined by radioimmunoassay and tissue plasminogen activator (t-PA) activity was measured by a solid-phase fibrinolytic assay using polystyrene test tubes coated with 125I-fibrin. The levels of these parameters were analysed in samples of both the arterial and vein blood which had been taken before and after the injection of contrast medium and obtained results are given in the Table.Our results suggest that after the injection of contrast medium there is a significant increase in the t-PA activity in the arterial blood and the β-TG concentration in the vein blood.

1994 ◽  
Vol 14 (3) ◽  
pp. 472-477 ◽  
Author(s):  
Karsten Overgaard ◽  
Tomas Sereghy ◽  
Hans Pedersen ◽  
Gudrun Boysen

The effect of delayed thrombolysis with recombinant tissue plasminogen activator was tested in an embolic stroke model. The carotid territory was embolized in 103 rats with fibrin-rich clots formed and washed in polyethylene tubes. Hemispheric cerebral blood flow before and after embolization was measured by the intra arterial 133Xe injection method. At five delay times, 15–240 min after embolization, 69 animals were treated with tissue plasminogen activator, 20 mg/kg, and 34 animals with saline. Carotid angiography displayed the grade of occlusion of the cerebral arterial supply before and after treatment. Brains were fixed after 2 days, evaluated neuropathologically, and infarct volume measured. Cerebral blood flow was reduced by 56–71% after embolization. Reperfusion induced by thrombolytic therapy was demonstrated by comparing the posttreatment angiography of the pooled five treatment groups to control animals. Thrombolytic therapy significantly reduced the infarct volume and improved the prekill clinical score by up to 2 h of treatment delay, and treatment might have been beneficial even after 4 h delay. Prolonging the delay of treatment increased the infarct volume ( p < 0.001, Jonckheere–Terpstra test). Only a few hemorrhagic complications were observed. Thus, thrombolytic therapy in embolic stroke induced recanalization. The effect on clinical outcome and infarct volume was dependent on delay time.


1990 ◽  
Vol 64 (02) ◽  
pp. 260-266 ◽  
Author(s):  
Elizabeth E Branscomb ◽  
Marschall S Runge ◽  
Christopher E Savard ◽  
Keith M Adams ◽  
Gary R Matsueda ◽  
...  

SummaryBispecific monoclonal antibodies that bind simultaneously to human fibrin and tissue plasminogen activator (tPA) enhance the fibrinolytic potency of tPA. Two bispecific antibodies (F36.23 and F32.1) were generated by somatic cell fusion. Antibody F36.23 derives its tPA binding from monoclonal anti-tPA antibody TCL8 and its fibrin binding from monoclonal antifibrin antibody 59D8. After purification from cell supernatants and ascites by two steps of affinity chromatography, hybrid-hybridoma bispecific antibody F36.23 simultaneously bound tPA and fibrin in solution and in solid-phase assays. In an assay for the lysis of human fibrin monomer, F36.23 increased the fibrinolytic potency of tPA by 5 to 10 fold, regardless of whether the bispecific antibody had been combined with the tPA before or during the assay. Bispecific F36.23 F(ab′)2 also bound tPA and fibrin simultaneously, and the enhancement in fibrinolysis in the presence of F36.23 F(ab′)2 was identical to that in the presence of intact F36.23. The second bispecific antibody, F32.1, was produced by an alternative strategy that has a wider potential for applicaton in other systems. Hybridoma bispecific antibody F32.1 was derived from the fusion of immune splenocytes (in mice immunized with a synthetic oligopeptide representing the amino terminus of the α-chain of human fibrin) with the anti-tPA cell line TCL8. The properties of hybridoma bispecific antibody F32.1 and its F(ab′)2 were indistinguishable from those of hybrid-hybridoma bispecific antibody F36.23 in solid-phase binding assays and in assays of fibrinolysis. Bispecific antibodies produced by somatic cell fusion, particularly in the form of F(ab′)2, may have potential for use in clinical thrombolysis.


2019 ◽  
Vol 13 (1) ◽  
Author(s):  
Toshiyuki Ohtani ◽  
Ryosuke Sintoku ◽  
Tasuku Yajima ◽  
Naoyuki Kaneko

Abstract Background Idarucizumab is a specific antidote for the anticoagulant dabigatran. Although its efficacy has been recently reported, the drug is still in postmarketing surveillance and requires case data in different emergency settings. A newer intravenous thrombolytic therapy with recombinant tissue plasminogen activator has been proposed after injection of idarucizumab in patients receiving dabigatran; however, the safety and efficacy of this therapy are equivocal because of the limited number of reported cases. We describe a case of a patient with acute lacunar stroke causing dysarthria and hemiparesis successfully treated with intravenous thrombolytic therapy with recombinant tissue plasminogen activator after reversal of dabigatran with idarucizumab. Case presentation A 67-year-old Asian woman was transferred to our emergency center 200 minutes after sudden onset of dysarthria and right-sided hemiparesis. She had been taking dabigatran for prevention of stroke recurrence caused by atrial fibrillation. Diffusion-weighted magnetic resonance imaging revealed a new lacunar infarction near old putamen infarctions. We treated her with intravenous thrombolytic therapy with recombinant tissue plasminogen activator after administering idarucizumab. The time to recombinant tissue plasminogen activator administration was 5 minutes from idarucizumab injection and 269 minutes from symptom onset. The patient’s activated partial thromboplastin times were 68.0 and 43.2 seconds before and after the therapy, respectively. The patient’s neurological symptoms improved significantly after the treatment, and she experienced no adverse events. Conclusions Intravenous thrombolytic therapy with recombinant tissue plasminogen activator after reversal of dabigatran with idarucizumab may be safe and feasible in patients with acute ischemic stroke with lacunar infarct. Furthermore, intravenous thrombolytic therapy with recombinant tissue plasminogen activator could be used in patients in emergency settings until just before the end of the recommended time limit within which it needs to be administered because of the immediate effect of idarucizumab.


1992 ◽  
Vol 65 (4-5) ◽  
pp. 663-665 ◽  
Author(s):  
R. Polanowska ◽  
M. Wilczyńska ◽  
Y. Sławinski ◽  
J.H. Goch ◽  
W. Augustyniak ◽  
...  

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