What question did this study set out to answer?

To investigate the effects of activated plasmin on platelet aggregation, the platelet release reaction, and overall hemostatic function in vitro and in vivo.

July 1, 1973Journal of Clinical InvestigationOpen Access

Plasmin-Induced Platelet Aggregation and Platelet Release Reaction. EFFECTS ON HEMOSTASIS

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Authors

SNStefan NiewiarowskiThe Wistar Institute ASAndrew F. SenyiCanadian Red Cross Society PGPeter J. GilliesRutgers, The State University of New Jersey

Discussion

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Implication

Experimental study demonstrates plasmin-induced platelet aggregation and release reaction in animal models, suggesting mechanisms for bleeding defects during thrombolytic therapy.

Key Points

To investigate the effects of activated plasmin on platelet aggregation, the platelet release reaction, and overall hemostatic function in vitro and in vivo.
Treated washed human, rabbit, and pig platelets in vitro with trypsin-activated pig plasmin or streptokinase-activated human plasmin in the presence or absence of inhibitors (soybean trypsin inhibitor, epsilon aminocaproic acid, Persantin, prostaglandin E1, phenylbutazone).
Injected streptokinase (10,000 U/kg) into rabbits with or without pretreatment using Persantin (dipyridamole) or epsilon aminocaproic acid to assess platelet count, serotonin release, fibrinogen depletion, and bleeding time.
Plasmin caused reversible platelet aggregation accompanied by the release of adenine nucleotides, serotonin, and eventual digestion of platelet fibrinogen, with short exposures transiently increasing ADP sensitivity but prolonged exposure impairing thrombin and collagen reactivity.
In vivo streptokinase administration caused a transient drop in platelet counts, depletion of platelet serotonin and fibrinogen, and prolonged primary bleeding time.
Pretreatment with Persantin or epsilon aminocaproic acid protected against serotonin loss and fibrinogen depletion, while Persantin prevented the prolongation of primary bleeding time and preserved collagen responsiveness.

Cite This Study

Niewiarowski et al. (1973) studied this question.

synapsesocial.com/papers/6a18ea8f985da83d5491ebd4 https://doi.org/10.1172/jci107345

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July 1, 1973Journal of Clinical InvestigationOpen Access

Plasmin-Induced Platelet Aggregation and Platelet Release Reaction. EFFECTS ON HEMOSTASIS

View Full Paper

Ask AI

Bookmark

Authors

SNStefan NiewiarowskiThe Wistar Institute ASAndrew F. SenyiCanadian Red Cross Society PGPeter J. GilliesRutgers, The State University of New Jersey

Discussion

Member takes

Implication

Experimental study demonstrates plasmin-induced platelet aggregation and release reaction in animal models, suggesting mechanisms for bleeding defects during thrombolytic therapy.

Key Points

To investigate the effects of activated plasmin on platelet aggregation, the platelet release reaction, and overall hemostatic function in vitro and in vivo.
Treated washed human, rabbit, and pig platelets in vitro with trypsin-activated pig plasmin or streptokinase-activated human plasmin in the presence or absence of inhibitors (soybean trypsin inhibitor, epsilon aminocaproic acid, Persantin, prostaglandin E1, phenylbutazone).
Injected streptokinase (10,000 U/kg) into rabbits with or without pretreatment using Persantin (dipyridamole) or epsilon aminocaproic acid to assess platelet count, serotonin release, fibrinogen depletion, and bleeding time.
Plasmin caused reversible platelet aggregation accompanied by the release of adenine nucleotides, serotonin, and eventual digestion of platelet fibrinogen, with short exposures transiently increasing ADP sensitivity but prolonged exposure impairing thrombin and collagen reactivity.
In vivo streptokinase administration caused a transient drop in platelet counts, depletion of platelet serotonin and fibrinogen, and prolonged primary bleeding time.
Pretreatment with Persantin or epsilon aminocaproic acid protected against serotonin loss and fibrinogen depletion, while Persantin prevented the prolongation of primary bleeding time and preserved collagen responsiveness.

Cite This Study

Niewiarowski et al. (1973) studied this question.

synapsesocial.com/papers/6a18ea8f985da83d5491ebd4 https://doi.org/10.1172/jci107345

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