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J Björnson

Publications and source records attributed to J Björnson.

8 recordsLinked to original sources

The haemostatic effect of 51CR-labelled blood platelets. An experimental study in the rabbit.

The haemostatic effect of 51Cr-labelled platelets was studied in 5 rabbits made thrombocytopenic (35,000/micronl blood) by whole body ionizing irradiation. Bleeding times were recorded after standardized cuts on the inner side of the rabbit's ear, a method with an acceptable reproducibility. The animals were then each transfused with concentrates of labelled platelets from 2 healthy donor rabbits. This increased the platelet counts to about 2 x 10(5)/micronl blood. Bleeding time values were markably prolonged before transfusion and became normalized when tested 1 and 4 h after transfusion. In 3 control experiments, where unlabelled platelet rich plasma was transfused to thrombocytopenic recipients, a similar shortening of the bleeding time was observed. It is concluded that 51Cr-labelled platelets retain haemostatic ability comparable to non-labelled platelets, when circulating in a recipient animal.

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Impaired anticoagulant effect of heparin in the artificial kidney. An experimental study.

Dialysis of blood and plasma was performed in vitro, in a 'mini-Kill' dialyser as well as in dialysis bags. A marked shortening of the thrombin-clotting time was observed, indicating fall in heparin anticoagulant effect. The concentration of heparin, however, as measured by polybrene titration, was substantially less reduced. Fibrin formation, as evidenced by the ethanol gelation test, occurred more often in the dialysed than in the control plasma. In conclusion, the discrepancy between concentration and anticoagulant effect of heparin could be partly explained by influx from the dialysate of calcium, magnesium, and acetate ions. The fibrin-polymerizing effect of these ions was confirmed by a shortening of the clotting time with Reptilase, a proteolytic enzyme not influenced by thrombin inhibitors such as heparin. In addition, liberation of platelet factor 4 may be responsible for some reduction in antithrombin activity of heparin. No evidence of heparin being dialysed or adhering to the dialysis membrane was found.

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