The Lysis of Artificial Thrombi

1980 ◽  
Vol 43 (01) ◽  
pp. 034-037 ◽  
Author(s):  
Michael J Metcalf
Keyword(s):  
Human Blood ◽  
Final Concentration ◽  
Rabbit Blood ◽  
Factors Influencing ◽  
Dextran 70 ◽  
Chandler Loop ◽  
Loop Technique

SummaryThe susceptibility to lysis of artificial thrombi formed from native rabbit blood in the presence or absence of dextran was determined using the Chandler loop technique. Thrombi of identical weight were formed in the presence of saline or dextran and when spontaneous thrombolysis was allowed to take place, thrombi formed in the presence of dextran 70 were lysed to a greater extent than those formed under control conditions.The possible factors influencing this observation were studied. Increasing concentrations of streptokinase increased the extent of thrombolysis in both control and dextran treated thrombi. Maximal streptokinase induced thrombolysis occurred in the presence of a 2 per cent final concentration of dextran Mw 40,000 and 500,000 and dextran 70 at a final concentration of 1.2 per cent.Increased thrombolysis was not observed when albumin was substituted for dextran.Finally, similar observations were recorded for streptokinase induced thrombolysis using human blood.

Effects of ketorolac and dextran-70 alone and in combination on haemostasis

1998 ◽  
Vol 42 (8) ◽  
pp. 982-986 ◽  
Author(s):  
I. Power ◽  
D. W. Noble ◽  
A. Winter ◽  
I. A. Greer
Keyword(s):  
Dextran 70

Noncardiogenic pulmonary edema secondary to intrauterine instillation of 32% dextran 70

1985 ◽  
Vol 43 (3) ◽  
pp. 479-480 ◽  
Author(s):  
Edward A. Zbella ◽  
Jacob Moise ◽  
Sandra A. Carson
Keyword(s):  
Pulmonary Edema ◽  
Dextran 70

Dextran and postoperative thromboembolism

1975 ◽  
Vol 13 (11) ◽  
pp. 41-43
Keyword(s):  
Platelet Aggregation ◽  
Coagulation Factors ◽  
Venous Thromboembolic Disease ◽  
Vein Thrombosis ◽  
Dextran 70 ◽  
Lower Blood ◽  
Venous Thromboembolic ◽  
Reduce Platelet Aggregation ◽  
Increase Platelet Aggregation ◽  
Deep Vein

Two preparations of dextran have been tried for prevention of venous thromboembolic disease, dextran-40 (average m. w. 40,000) and dextran-70 (average m.w. 70,000). Dextrans reduce platelet aggregation and lower blood viscosity.1 Dextran may also reduce the peri-operative rise in the coagulation factors V and VIII.2 However, in some tests dextrans increase platelet aggregation3 and accelerate fibrin formation,4 so that only clinical trial can show whether dextran reduces the incidence of either deep-vein thrombosis or of pulmonary embolism.

COMPARISON OF POST-BURN FLUID AND ELECTROLYTE BALANCE FOLLOWING RESUSCITATION WITH LACTATED RINGERʼS. HYPERTONIC SALINE OR DEXTRAN 70

1983 ◽  
Vol 23 (7) ◽  
pp. 640
Author(s):  
Robert A. Cunther ◽  
George C. Kramer ◽  
Sanford S. Zweifach ◽  
Michael E. Nerlich ◽  
Richard E. Ward
Keyword(s):  
Hypertonic Saline ◽  
Electrolyte Balance ◽  
Dextran 70

VEGF increases endothelial permeability by separate signaling pathways involving ERK-1/2 and nitric oxide

2003 ◽  
Vol 284 (1) ◽  
pp. H92-H100 ◽  
Author(s):  
Jerome W. Breslin ◽  
Peter J. Pappas ◽  
Joaquim J. Cerveira ◽  
Robert W. Hobson ◽  
Walter N. Durán
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathways ◽  
Mapk Pathway ◽  
Umbilical Vein ◽  
Endothelial Permeability ◽  
Western Blots ◽  
Cell Monolayers ◽  
Dna Oligonucleotides ◽  
Dextran 70 ◽  
Nos Inhibitor

We tested the hypothesis that VEGF regulates endothelial hyperpermeability to macromolecules by activating the ERK-1/2 MAPK pathway. We also tested whether PKC and nitric oxide (NO) mediate VEGF-induced increases in permeability via the ERK-1/2 pathway. FITC-Dextran 70 flux across human umbilical vein endothelial cell monolayers served as an index of permeability, whereas Western blots assessed the phosphorylation of ERK-1/2. VEGF-induced hyperpermeability was inhibited by antisense DNA oligonucleotides directed against ERK-1/2 and by blockade of MEK and Raf-1 activities (20 μM PD-98059 and 5 μM GW-5074). These blocking agents also reduced ERK-1/2 phosphorylation. The PKC inhibitor bisindolylmaleimide I (10 μM) blocked both VEGF-induced ERK-1/2 activation and hyperpermeability. The NO synthase (NOS) inhibitor N G-nitro-l-arginine methyl ester (200 μM) and the NO scavenger 2-phenyl-4,4,5,5-tetramethylimidiazoline-1-oxyl-3-oxide (100 μM) abolished VEGF-induced hyperpermeability but did not block ERK-1/2 phosphorylation. These observations demonstrate VEGF-induced hyperpermeability involves activation of PKC and NOS as well as Raf-1, MEK, and ERK-1/2. Furthermore, our data suggest that ERK-1/2 and NOS are elements of different signaling pathways in VEGF-induced hyperpermeability.

Dextran 70

1991 ◽  
Vol &NA; (343) ◽  
pp. 5
Author(s):  
&NA;
Keyword(s):  
Dextran 70
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