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Rheology of blood.

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Afibrinogenemia↗

Coagulation studies for severe liver disease detection in a gastroenterologic department.

15 patients with clinical, histological and laboratory findings of cirrhosis were investigated. When the results of routine hemostasis tests--thrombin time, reptilase time and fibrinogen quantitation by clotting methods--were prolonged, further immunological determinations were done. Normal results in the immunological determinations together with prolonged ones obtained by clotting methods are suggestive of dysfibrinogenemic states. A possible survey of the treatment with the help of these determinations is proposed.

Afibrinogenemia↗

Severe congenital dysfibrinogenemia (fibrinogen-Riyadh): a family study.

Congenital severe dysfibrinogenemia was discovered in a small Saudi family. Their single child exhibited abnormal severe bleeding tendency since birth and his coagulation profile revealed evidence of severe dysfibrinogenemia. The parents who were first-degree cousins and completely asymptomatic showed evidence of dysfibrinogenemia but to lesser degree than in their son. The child presented with large cephalohematoma and evidence of intracranial hemorrhage and left hemiparesis. He was treated with cryoprecipitate and his hematoma resolved, but his neurological deficit remained.

Acute Disease↗

Interference on the haemostasis in dogs with induced coagulopathies by drugs affecting the platelet function.

Acetylsalicylic acid and phenylbutazone increased the bleeding significantly from standardized wounds in dogs defibrinogenated with Defibrase. Administration of dipyridamole and Xylocain had no effect. The results were the same in dogs treated with warfarin sodium. The results demonstrate the value of using laboratory animals with an induced coagulopathy when establishing the effect on the haemostasis exerted by drugs known in vitro to interfere with platelet functions. Acetylsalicylic acid and dipyridamole did not alter the activity of the K-vitamin-dependent coagulation factors, factors V, VIII, platelet count or fibrinogen concentration.

Afibrinogenemia↗

Adhesion of human blood platelets to glass polymer surfaces. II. Demonstration of the presence of a natural platelet adhesion inhibitor in plasma and serum.

Adhesiveness of washed platelets resuspended in citrated plasma, serum, or several different media has been investigated. A method specific for quanititation of adhesion was used. Platelets suspended in saline of Tyrode's solution were found to be highly adhesive to glass, polyethylene, polyvinyl chloride, or Cuprophane. This adhesiveness of platelets to test surfaces decreased by nearly 50% when plasma was the suspension medium. When the suspension medium was serum, the decrease in adhesion was nearly 75%. Cohn fraction V also decreased the adhesiveness of platelets significantly, but highly purfied albumin had only a small effect. Several pharmacologic agents decreased platelet adhesiveness when added to platelets suspended in plasma or serum, but had negligible effect on the adhesiveness of platelets suspended in artificial media devoid of proteins. Normal washed platelets, when suspended in citrated plasma obtained from an afibrinogenemic donor or in normal serum, showed a significant decrease in adhesion compared to the same platelets suspended in normal citrated plasma. Addition of fibrinogen to afibrinogenemic plasma or normal serum restored the adhesiveness of platelets to normal levels. Normal platelets resuspended in plasma obtained from a thrombasthenic donor exhibited normal adhesiveness. These observations suggested that while fibrinogen promotes platelet adhesion, plasma or serum possess also an adhesion-inhibiting activity.

Afibrinogenemia↗