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The chemiluminescence reaction elicited from luminol in the presence of hydroxyl radicals was concentration-dependently suppressed by captopril, indicating efficacious radical scavenging. As to be expected, ACE inhibitors lacking free sulfhydryl groups (ramipril, enalapril) were inactive. However, the endogenous scavenger and anti-oxidant uric acid proved to be far superior to captopril, when concentrations of both were compared that are realized in vivo. A substantial augmentation of endogenous scavenging ability during therapy with captopril thus seems unlikely. In a model of standardized myocardial hypoxia (isolated working heart of the guinea pig with 30 min low flow perfusion) captopril, ramiprilat and uric acid equally improved post-hypoxic heart function. There was no cardioprotective action of captopril in excess of that accountable for by inhibition of ACE. It seems possible that ACE (kininase II) inhibitors exert cardioprotection via elevated tissue levels of kinins: bradykinin also improved heart performance after low flow perfusion and bradykinin-induced coronary dilatation was markedly enhanced in the presence of ramiprilate, reflecting attenuated degradation by endothelial kininase II.

Methylxanthines, such as caffeine and theophylline, show effects increasing the secretion of insulin. Perfusion experiments were intended to find out whether insulin secretion is influenced by uric acid, which is chemically closely related. Besides, it was to be demonstrated that uric acid causes no damages to islet cell structures for it is well established that alloxan, which is chemically related to uric acid, produces necroses in B cells. Isolated rat pancreata were stimulated by glucose at concentrations of 100 mg/100 ml and 300 mg/100 ml. In part of the experiments uric acid was added to the perfusion medium at a concentration of 12 mg/100 ml. We found that uric acid has no influence on insulin secretion if it is stimulated by glucose at a concentration of 100 mg/100 ml. However, if B cells are stimulated by glucose at a concentration of 300 mg/100 ml insulin secretion is enhanced by the addition of uric acid by more than 100%. This indicates that this substance exhibits a glucose-potentiating effect. The characteristic dynamics of insulin secretion demonstrate together with light- and electron-microscopic investigations that uric acid causes a real additional secretion and no leaking of intracellular insulin as a result of destruction of islet cell structures by an effect of uric acid similar to that of alloxan.

A new method of measuring glucose concentrations (Reflotest-Hypoglycemie) was tested on 141 serum samples and 119 capillary blood samples and compared with the hexokinase-glucose-6-phosphate dehydrogenase method. The Reflotest (reflectance meter) compared well with the reference test. Comparison of results with three sera measured by the method in six different laboratories indicated the accuracy of the test. Endogenous bilirubin, uric acid, and haematocrit values did not influence the result. The test is therefore suitable for quantitative measurements.