SummaryThe influence of p-CMB, iodoacetamide, iodoacetic acid, N-ethylmaleimide, glycerinederivatives and of EDTA on thrombingeneration on fibrinpolymeriza- tion and on the physical strength of clots as expressed by spectrophotometrical and thrombelastographic measurements respectively has been examined.P-CMB and N-ethylmaleimide significantly inhibit the thrombin generation.EDTA retards the initial steps of the fibrinpolymerization and it increases the final turbidity. Its effect is neutralized by calcium and magnesium. The sulfhydrylinhibitors do not inhibit the polymerization neither do the glycinederivatives.To judge from these results does FSF not influence the polymerization but calcium and magnesium do. This statement is verified using FSF deficient plasma.The four SH-inhibitors tested inhibit the development of a normal thromb- elastogram, specially in reducing the mA values. Cysteine, having no effect by itself, reverses the effect of p-CMB and iodoacetamide.p-CMB has a similar effect when added to FSF deficient plasma and the main effect of this SH inhibition is suggested to be on platelet enzymes. p-CMB and iodoacetic acid also reduce the m A values of platelet-free normal plasma possibly by inhibiting FSF.

The aggregability of platelets stored in plasma at room‐temperature, pH 7.2–7.4, decreased approximately by a factor ten over a 24 hr period. Storage at pH 6.5 resulted in a more pronounced decrease. In some experiments this was reversible if the platelets were allowed to regenerate by incubation at pH 7.4 one or two hrs before measuring the aggregation. The procedure of concentrating platelets as well as storing the platelets as a concentrate, contributed to a decrease in aggregability. Saline as a medium for storage caused complete loss of aggregability within a few hours. K+, Ca2+ and glucose was shown by dialysis experiments to be vital factors for maintaining platelet aggregability during storage.

Oozing of blood from wound tissues after some time of total body perfusion and the demonstration of microemboli have brought into focus the inevitable disappearance of platelets from the blood during extracorporeal circulation. Recirculation experiments using dog blood are reported. The effect of a bubble oxygenator and a membrane oxygenator is compared. It is concluded that in principle they both contribute to the removal of functionally active platelets.

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Arterial PO2, PCO2 and pH were measured continuously with electrodes placed in a flow cuvette. Comparison between continuous readings and results of single sample analyses showed practically no discrepancy, and the drifts of the electrodes during time of measurements were negligible. During hypothermic perfusion with a Rygg-Kyvsgård bubble oxygenator, autotransplantation of canine hearts was performed. PO2, PCO2 and pH were measured continuously to check the performance of the heart-lung machine, and to evaluate the therapeutic and diagnostic significance of these blood gas values during cardiac surgery. At the start of perfusion, a steep fall in all three parameters was observed. The average fall in PO2 was 313 mmHg; PCO2 fell by 15 mmHg and pH BY 0.15. PCO2 rapidly returned to normal values, while pH and PO2 increased slowly during the perfusion period. PO2 reached its highest value at the lowest temperature and fell during rewarming. PCO was regulated by the carbon dioxide concentration in the heart-lung machine. pH did not return to normal levels within the time of perfusion. In the transistional period from perfusion, PCO2 increased and pH fell. Alterations in the distribution and direction of blood flow and a low systemic blood pressure are possible explanations of the initial fall in PO2 and the post-perfusion changes in PCO2 and pH. The variations in pH and PCO2 at the start of perfusion were caused by an acid priming fluid with low CO2 content. The post-perfusion changes indicated an unstable circulation, but imminent myocardial failure could not alone be diagnosed by continuous measurement.