Search

1. In the molar end concentration of 1 X 10(-6), 1,4-bis-[3-(3,4,5-trimethoxybenzoyloxy)-propyl]-perhydro-1,4-diazepine (dilazep) has no effect on crystalline adenosine desaminase. 2. In the same concentration dilazep does not affect adenosine desaminase activity of human hemolysing erythrocytes. 3. Under the influence of dilazep the methylene blue activated respiration of human erythrocytes is inhibited adenosine serving as substrate. a) The final molar concentration of 1 X 10(-7) leads to minor inhibition of the respiration. b) After transitory activation, final molar concentrations of 1 X 10(-6) and 1 X 10(-5) also lead to inhibition, which is complete after 4 h and in which the concentration of 1 X 10(-6) has the most pronounced effect. 4. Basing on the experimental results obtained it is not yet possible to classify the mode of activity of dilazep.

Hypoxic damages are normally determined by acid-base status as well as lactate and pyruvate levels. Since several other illnesses lead also to raised levels of these parameter, they are not specific for tissue hypoxia. In animal experiments it was shown that purine metabolites, especially hypoxanthine, are a very exact indicator for hypoxia. To test its validity in clinical situations the changes in acid-base status, lactate, pyruvate and purine metabolism were measured in 17 patients undergoing reconstructive aortic surgery. Blood samples were taken just before and after declamping of the aorta systemically and from the femoral vein. After declamping especially the systemic hypoxanthine levels increased 3 fold, due to a 20 times higher hypoxanthine concentration in the femoralis vein. The concentration changes of hypoxanthine in percent correlated very good with the aorta clamping time (R = 0,85). The changes in acid-base status and lactate levels were erratic and showed no correlation with the duration of ischemic period. Systemic hypoxanthine concentrations are a more specific and reliable parameter for hypoxic damages.