Heparin-Induced Release of Plasminogen Activator

Markwardt, Fritz; Klöcking, H.-P.

doi:10.1159/000214203

Cited by 54 publications

(35 citation statements)

References 10 publications

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“…The mechanism by which urokinase in duces a systemic lytic state is well known and it was also established that the fibrino lytic response to urokinase is proportional to the dose [1], The mechanism of en hanced fibrinolysis by heparin deserves some discussion. It has been suggested that this effect is attained through the re lease of tissue plasminogen activator [32][33][34][35]. Since it has been observed that tis sue plasminogen activator, unlike previ ous reports [39][40][41][42][43], may induce a systemic lytic state with bleeding [44][45][46], our data may be explained if this mechanism is pos tulated.…”

Section: Discussionmentioning

confidence: 59%

“…Studies in vitro failed to show any influence of heparin on the euglobulin lysis time and on the diluted clot lysis time, suggesting a lack of effect of heparin on the fibrinolytic mechanism [30], I n other studies in vitro, however, hep arin was found to have a dual effect on fi brinolysis: high concentrations inhibited lysis of preformed fibrin while low concen trations enhanced it [31]. Finally, a num ber of authors reported enhancement of fibrinolysis after intravenous administra tion of heparin [32][33][34][35].…”

Section: Discussionmentioning

confidence: 99%

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Fibrinolytic Effects of Urokinase and Heparin in Acute Pulmonary Embolism: A Randomized Clinical Trial

et al. 1988

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Dissolution of pulmonary emboli with heparin and urokinase is ascribed, respectively, to anticoagulation and fibrinolysis. Since truly independent assessment of these effects in man is lacking, we administered each drug alone. Fibrinogen and plasminogen plasma levels and the resolution of pulmonary emboli were measured in three randomized groups of 10 patients each: groups A and C infused with small repeated doses of urokinase and a large single dose of urokinase, respectively, and group B who received heparin. After 6 h of treatment, fibrinogen fell in all the groups, while, after 12 h, remained equally reduced in groups A and B and declined further in group C. Plasminogen behaved similarly. Up to 60 h, statistical analysis showed that these effects were related to timing and amount of urokinase and heparin infusion. These observations suggest that heparin may induce a lytic state. As to signs of pulmonary emboli resolution, no differences between groups were found in lung perfusion and gas exchange recovery at any time (from 1 day to 1 year) and in pulmonary artery pressure reduction at 1 week. The greater angiographic and scintigraphic recovery observed with urokinase, versus heparin alone, after 1 day of treatment in the Urokinase Pulmonary Embolism Trial may be ascribed to a synergistic effect with urokinase of heparin administered during the diagnostic work-out. The indications of heparin and urokinase should be evaluated in the light of these results

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Fibrinolytic Effects of Urokinase and Heparin in Acute Pulmonary Embolism: A Randomized Clinical Trial

et al. 1988

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“…CY 222 also appears to have a profibrinolytic action which might operate through the activation or release of plasmin ogen-activating enzymes contained in the vascular endothelium [2]. This activity, which unfractionated heparins also manifest [12] to a lesser degree, has been demon strated indirectly in the rabbit and in healthy humans by an increase in the area of lysis of Lys-plasminogen-sensitized fibrin plates [14], This sensitization facilitates the estima tion of plasminogen activator concentrations in blood.…”

Section: Discussionmentioning

confidence: 99%

Treatment of Deep Venous Thrombosis with a Very Low Molecular Weight Heparin Fragment (CY 222)

Janvier

Winnock

Dugrais

et al. 1987

Pathophysiol Haemos Thromb

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Thirty patients presenting with phlebographically confirmed deep venous thrombosis were treated with a very low molecular weight heparin fragment (CY 222) in an open and prospective phase-2 trial. A uniform dosage of 750 IC anti-factor Xa units/kg/day was administered subcutaneously for 10 days or more to patients whose thromboses were categorized as postsurgical (17 cases) or medical (13 cases). The clinical symptoms of venous thrombosis diminished in 93% of the patients overall. The extent of vascular clearing was assessed by an original scoring system which compared the pre- and posttreatment phlebo-graphies. The effect of treatment was globally rated ‘very good’ (more than 75 % lysis) in 37% of the patients, ‘good’ (about 50% lysis) in 40% and ‘poor’ (0–25% lysis) in 17%; the phle-bographic thrombosis worsened in 6.6%. Little change occurred in laboratory tests exploring thrombolysis, but a strong anti-factor Xa activity was detected.

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“…A HMW fraction was more active than unfractioned heparin and an LMW fraction had no in vitro effect [27]. In vivo heparin also increases the release of tissue plasminogen activator (TPA) from the vessel wall [28], The experiments with PK showed that there was no in vitro effect on fibrinolysis nor any activation o f factor XII or o f prekallikrein. After injections o f PK, however, a shortening o f the F.I.T was found.…”

Section: Discussionmentioning

confidence: 99%

A New Low Molecular Weight Heparin Fragment (PK 10169): In vitro and in vivo Studies

Vinazzer¹,

Woler²

1986

Pathophysiol Haemos Thromb

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The depolymerized heparin fragment PK 10169 was compared with unfractioned mucosal sodium heparin. The inhibition of factors Xa and IXa by heparin and by PK 10169 was comparable on a weight base, whilst the inhibition of thrombin by PK 10169 was at least 5 times weaker than by heparin. Subcutaneous injection of PK 10169 was not followed by an increase of the thrombin time. The activated partial thromboplastin time was considerably less prolonged after PK 10169 than after heparin. Platelet count and platelet functions were not influenced by PK 10169. In vitro, the euglobulin lysis time (ELT) was shortened after addition of heparin to plasma but not after addition of PK 10169. After injection however, there was an equal shortening of the ELT by both substances. The half-life in circulation of PK 10169 was longer than the half-life of heparin. The advantages of PK 10169 over heparin are therefore the weaker influence on overall coagulation, the missing influence on platelet functions and the longer half-life in circulation.

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Heparin-Induced Release of Plasminogen Activator

Cited by 54 publications

References 10 publications

Fibrinolytic Effects of Urokinase and Heparin in Acute Pulmonary Embolism: A Randomized Clinical Trial

Fibrinolytic Effects of Urokinase and Heparin in Acute Pulmonary Embolism: A Randomized Clinical Trial

Treatment of Deep Venous Thrombosis with a Very Low Molecular Weight Heparin Fragment (CY 222)

A New Low Molecular Weight Heparin Fragment (PK 10169): In vitro and in vivo Studies

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