Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hemostatic alterations in two adult patients who were supported by left ventricular assist devices (LVADs) because of postcardiotomy heart failure were evaluated. In both patients, fibrinopeptide A and thrombin-antithrombin III complex increased markedly during the first several days, and thereafter decreased moderately but remained above normal over the entire procedure. Furthermore, fibrinopeptide B beta 15-42 and alpha 2 plasmin inhibitor-plasmin complex were also markedly increased over the entire course of LVAD treatment. These data show that the LVAD system strongly activates both the coagulation and the fibrinolytic system, even when thromboembolic or bleeding complications are not clinically evident. Furthermore, the decrease in physiological coagulation inhibitors, especially protein C, indicates that these factors are activated and consumed during LVAD treatment. Because protein C is important in regulating the coagulation cascade during LVAD treatment, exhaustion of this system might result in thromboembolic complications during LVAD treatment.
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PMID:Hemostatic alterations caused by ventricular assist devices for postcardiotomy heart failure. 199 93

Exercise to exhaustion was associated with the appearance in plasma of plasminogen activator (PA) in several mol wt forms, as identified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) with zymography. A number of active bands, all immunologically identified as tissue-type PA (t-PA), were observed. The major form had an apparent mol wt of approximately 60,000 and is due to free t-PA. The other strong bands had apparent mol wts of approximately 110,000 and 180,000. The 110,000 band, also present in pre-exercise samples, represents t-PA complexed with its major inhibitor (PAI-1), and the 180,000 band is due to t-PA complexed with C1 inhibitor. The released forms of t-PA were cleared rapidly after cessation of exercise at exhaustion. Urokinase-type PA (u-PA) activity was also identified in pre- and postexercise samples at an apparent mol wt of approximately 50,000. This is consistent with its being free u-PA; no complexed forms of u-PA were observed. Qualitatively similar changes in plasma PA were observed after venous occlusion. Small quantities of plasmin were generated after strenuous exercise, as observed by detection of plasmin-alpha 2-antiplasmin complex by two-dimensional immunoelectrophoresis in three of five subjects. This complex was cleared rapidly after cessation of exercise. Plasmin-alpha 2-antiplasmin complex was not detected in any of the subjects after venous occlusion.
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PMID:Plasminogen activator in normal subjects after exercise and venous occlusion: t-PA circulates as complexes with C1-inhibitor and PAI-1. 295 96

12 surgical critically ill patients were studied for a better management of perioperative coagulation dysfunction. Their primary disease, clinical manifestation as well as some coagulation tests before and after therapy were retrospectively analysed. The result showed that secondary disseminated intravascular coagulation (DIC) is the main type of perioperative coagulation disorder, especially in decompensated hepatopathy and severe sepsis patients. It should be emphasized that: control of primary disease, effective drainage of focus, strict indication for 2nd surgical hemostasis and correct operation are required. For those hepatopathy with hypofibrinogenemia, some hemostatic drugs should be prohibited or very carefully used, in order to avoid the activation of plasmin and the exhaustion of fibrin. The early administration of heparin and aprotinin after the supplement of fibrinogen has shown a great potential benifit to stop the cascade of hypercoagulation and hyperplasminogenemia by enhancing the level of AT-III and fibrinogen in plasma.
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PMID:[Management of coagulation dysfunction in critically surgical patient]. 959 75

In the healthy individual intensive physical exercise leads to a minor activation of blood coagulation that appears to be balanced by a concomitant activation of the fibrinolytic system. This study tested the hypothesis that vigorous exercise might give rise to an exaggerated activation of coagulation in subjects with resistance to activated protein C (APC). Molecular markers of thrombin (prothrombin fragment 1 + 2, thrombin-antithrombin III complexes) and fibrin formation (fibrinopeptide A), as well as markers of the fibrinolytic activity (plasmin-antiplasmin complexes, D-dimers), were determined in nine asymptomatic male individuals with APC resistance [age, 18 +/- 3 years; maximal oxygen consumption, 56.7 +/- 2.7 ml/kg per min (mean +/- standard deviation)] and in nine male control subjects (age, 19 +/- 4 years; maximal oxygen consumption, 56.2 +/- 3.2 ml/kg per min) after 1 h of running to exhaustion. Baseline levels of prothrombin fragment 1 + 2 were higher in individuals with APC resistance than in controls [0.67 +/- 0.06 nmol/l (mean +/- standard error) versus 0.48 +/- 0.01 nmol/l; P < 0.05]. In response to exercise, hemostatic variables significantly increased in both groups to a similar small extent. Likewise, exercise-induced changes of fibrinolytic variables in subjects with APC resistance paralleled those observed in controls. In summary, exhaustive running in subjects with APC resistance does not provoke an abnormal hemostatic or fibrinolytic response, suggesting that vigorous exercise does not imply an increased risk for thrombosis in young male subjects with APC resistance.
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PMID:Exercise-induced activation of coagulation in subjects with activated protein C resistance. 1516 17

Stabilized, active plasmin is a novel thrombolytic for direct delivery to clots. Although it is known that protease inhibitors in plasma inhibit plasmin, the amount of plasmin that can be added to plasma/blood before free plasmin is observed is not clear. Determination of free plasmin activity in plasma using chromogenic substrates represents a challenge due to false-positive signals from plasmin entrapped by alpha2-macroglobulin. Size-exclusion chromatography was used to separate the plasmin-alpha2-macroglobulin complex from uninhibited, free plasmin. In this in-vitro study, exogenous plasmin is effectively inhibited up to 2.4 micromol/l after 5-min incubation with plasma at 37 degrees C. Initially, plasmin was consumed predominantly by alpha2-antiplasmin up to 1.2 micromol/l plasmin. Following exhaustion of alpha2-antiplasmin, plasmin was further consumed by alpha2-macroglobulin up to 2.4 micromol/l plasmin added to human plasma. Whole human blood was found to have an increased inhibitory capacity over that of plasma; free plasmin activity could be measured only above 3.8 micromol/l added plasmin. In conclusion, several mechanisms exist that control plasmin activity in human blood; in addition to alpha2-antiplasmin and alpha2-macroglobulin, blood cells contribute to the inhibition of exogenously administered plasmin. These in-vitro results indicate that doses of plasmin up to approximately 12 mg/kg in humans can be completely inactivated by blood.
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PMID:Blood inhibitory capacity toward exogenous plasmin. 1741 60