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Iron catalysis is involved in oxygen-derived free radical generation and subsequent lipid peroxidation, which have been reported to occur during cardiopulmonary bypass in humans. We assessed the effects of the iron chelator deferoxamine on the susceptibility of circulating low density lipoproteins (LDLs) to induced peroxidation in 20 adult patients (10 controls and 10 treated) undergoing cardiopulmonary bypass for coronary or valve procedures. Deferoxamine was given both intravenously (30 mg/kg body wt, starting 30 minutes before bypass and extending for the next 4 hours) and as an additive to the cardioplegic solution (250 mg/l). Blood samples were taken from both atria before and immediately after the end of cardiopulmonary bypass. Plasma lipid peroxidation was assessed by measuring spectrophotometrically the thiobarbituric acid reactive substances (TBARS) content of selectively isolated LDLs after their exposure to a peroxidizing agent. Before cardiopulmonary bypass, the right and left atrial blood values of LDL-TBARS were not significantly different between the two groups. Cardiopulmonary bypass resulted in a lipid peroxidation of significantly greater magnitude in control than in treated patients. Postbypass right atrial values for LDL-TBARS (expressed in mumol/mmol LDL-phospholipids) were 45.7 +/- 17.2 (mean +/- SEM) in control patients and 6.9 +/- 2.9 in treated patients (p less than 0.02), whereas in the left atrial blood, LDL-TBARS yielded values of 62.7 +/- 20.5 and 10.3 +/- 3.9, respectively (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

The present study is concerned with the effects of L-arginine hydrochloride administration on the disturbances of liver glutamine metabolism following acute ammonia intoxication in the rat.Our results show that arginine administration does not suppress the decrease in the hepatic glutamine level and the marked activation of liver glutaminase I induced by ammonia.These alterations do not therefore appear to be related to the limitation of ammonia detoxication through the urea cycle.

The study of blood levels of the principal acids of the tricarboxylic acid cycle as well as pyruvic and lactic acids in patients suffering from chronic renal insufficiency shows that pyruvic acid and citric acid are normal, lactic acid is significantly lowered, while α-ketoglutaric acid, and especially malic acid are elevated. At the same time, the urinary elimination of citric and α-ketoglutaric acids, but not of malic acid, is strongly diminished. The changes in these blood levels are not related to modifications of the metabolic or excretory functions of the kidney. Neither are they explicable by variations in the acid-base equilibrium, nor by the degree of reduction of nicotinamide adenine dinucleotide. The role of enzymatic inhibitors, acting in particular upon malic dehydrogenase, does seem essential in the genesis of these changes.