Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.2.2.7 (heparinase)
 1,270 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of heparin on platelet aggregation was systematically examined on platelets in plasma (PRP), as well as on gel-filtered, washed, and formaldehyde-fixed platelets. Results indicate that, although heparin causes a mild potentiation of platelet aggregation in the PRP systems, a significant inhibitory activity is observed when heparin is added to isolated platelets. This inhibitory activity appears to be specific and not related to the impurities in the heparin preparations, as heparinase, as well as protamine, effectively neutralizes the heparin-mediated inhibitory activity on platelet aggregation. Although heparin-mediated inhibitory activity can be demonstrated in the presence of a number of different agonists (ADP, arachidonic acid, thrombin, Ionophore A23187, epinephrine, and ristocetin), the most pronounced inhibition is seen in the presence of ristocetin. Further studies show that heparin enhances thromboxane generation in isolated platelets. Platelets pretreated with heparin, however, fail to respond to preformed thromboxane. These findings suggest that, in addition to the potentiation of thromboxane production in platelets, heparin may also attribute some change(s) to the platelet(s)/platelet membrane, which interferes with their ability to respond to the agonists of platelet aggregation. This antiaggregatory activity of heparin was found to be inhibited by a factor(s) present in plasma but not in serum.
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PMID:Effect of heparin on platelet aggregation. 647 40

Platelet dysfunction and loss of procoagulants and platelets leads to impaired hemostasis after cardiopulmonary bypass (CPB). Preoperative platelet sequestration delays surgery, and the large volume shifts, necessary to harvest therapeutically effective components, may be associated with hemodynamic instability. We performed platelet and plasma sequestration after the initiation of CPB during the cooling period in patients undergoing surgery in deep hypothermic cardiac arrest. Five patients who underwent major vascular surgery in deep hypothermia were enrolled in this pilot study. Platelet and plasma sequestration was performed during cooling with the CATS cell saver using the plasma sequestration set. Before processing, 2 x 1,000 ml of blood were concentrated by means of hemofiltration to reduce dilution effects of CPB. The autologous platelet concentrates were rotated at 24 degrees C, and the plasma was stored at room temperature. The harvested plasma and platelets were re-transfused during modified ultrafiltration after CPB. Platelet count, 20 mmol/L ADP stimulated platelet aggregation, and fibrinogen levels were measured preoperatively in the harvested material and in patient blood before and after transfusion. A heparinase thromboelastogram (TEG) was performed preoperatively before and after re-transfusion. There was a significant increase in the ADP stimulated platelet aggregation, platelet count, fibrinogen level, and maximum amplitude of the TEG after re-transfusion of the harvested material. No patient needed transfusion of fresh frozen plasma or random donor platelet concentrates. No patient needed re-exploration due to hemorrhage. The data presented provide evidence that autologous plasma and platelet sequestration during CPB initiation is effective. The harvested material reveals a high platelet count and fibrinogen level and preserves functional integrity.
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PMID:Autologous plasma and platelet sequestration at the beginning of cardiopulmonary bypass: a pilot investigation in five patients undergoing extended vascular surgery in deep hypothermia. 1181 86