[Drug committee at Ullevål hospital, Rikshospital, Ringerlike hospital, Trondheim region hospital. Work planning and practical experiences].
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Biomedical subjects
Publications and source records attributed to E Myhre.
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The effects of dipyridamole and ASA on platelet functions were studied in patients with aortic ball-valve prostheses. Before ingestion, platelet adhesiveness was markedly reduced and platelet survival time slightly, but insignificantly shortened. ASA prolonged the bleeding time, reduced collagen-induced platelet aggregation, and inhibited secondary aggregation initiated by adrenalin. Similar effects were obtained with 2 Gm. of ASA alone as with 1 Gm. daily in combination with 225 mg. of dipyridamole. Platelet adhesiveness remained low. Depyridamole alone, 375 mg. daily, did not influence any of these parameters. The mean platelet half-life was prolonged from 3.52 to 3.72 days by each drug and to 4 days by the combined treatment. None of the differences was, however, statistically significant. A clinical study with ASA has been started in a larger series of patients to evaluate the effect on arterial thromboembolism.
A young male patient with Goodpasture's syndrome was treated with bilateral nephrectomy and when antiglomerular basement membrane antibodies could no longer be detected he received a cadaveric renal homograft. Fifteen months later he is in good health and without signs of pulmonary disease. Renal function is satisfactory, and there are no findings indicating recurrence of the nephritis. Serial complement studies during the entire course revealed varying degrees of activity in the sequence in the different phases: a high degree of in vivo activation of complement was found in the period before the nephrectomy, there was a moderate degree of activation in the period between the nephrectomy and transplantation and, finally, there were no signs of activity in the system after transplantation. This investigation strongly suggests that the complement system is of definite pathogenetic significance in this human equivalent to experimental nephrotoxic nephritis.
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