Changes in organic (labile) phosphate in human trichinellosis.
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Biomedical subjects
Publications and source records attributed to V Marţincu.
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On the bases of the published data and their own experience the authors outline the context of the functional biochemical alterations that give an orientation in the choice of the major objectives of pathogenic therapy in the course of septicemias. Analysis of the frequency and intensity of these alterations make it possible to establish therapeutical priorities. In this sense it is demonstrated that hyperazotemia, hyperalbuminemia, low alkaline reserve, elevated serum lactate and a decrease in the plasma Na+/K+ ratio are characteristic of septicemia with a state of toxiinfectious shock.
Alpha-Lipoic acid associated with xi-aminocaproic acid proves to have a protector effect in the posttreatment of endotoxinic shock in rabbits, produced by the administration of E. coli O111, in doses of 1.5 mg/kg body weight. This effect was observed when administered early in the stage of energy privation, and was manifested by a longer survival, diminution of lactacidemia and protection of labile phosphate reserves.
The complex biologic investigation of thyphoid fever is dictated by the necessity of instituting a pathogenetic therapy, especially in the toxic and complex forms. Performing 178 fuctional-metabolic tests in 50 cases of typhoid fever (of which 10 severe and complicated forms), the authors established the prognostic value energy deficiency (approximately P), lactate, alkaline reserve and GPT. Azotemia is only characteristic in the forms with renal involvement, and the other transaminases may be positive even whe the liver is not enlarged. In one case of repeated digestive hemorrhage no evidence could be found of the mechanism of consumption coagulopathy.
The experiments carried out demonstrate that under the influence of tetanus exotoxin, Gram-negative bacteria endotoxins, staphylococcal infection and infestation with Tr. spiralis, inhibition of the Pasteur effect occurs. Recently published data show that the same manifestation of pathogenicity is induced by diphtheria alpha and delta exotoxin, staphylococcal toxin, Pseudomonas aeruginosa exotoxin, staphylococcal enterotoxin, streptolysin O, infections with Cl. perfringens, Pasteurella and Rickettsia and hepatitis viruses in man. These data confirm a previous hypothesis according to which inhibition of the Pasteur effect represents the expression and metabolic measure of pathogenicity and toxicity. The inhibitory effect was proportional to the amount of pathogenic agent or toxin, just as the respective anatoxin or toxin + endotoxin mixture does not influence the Pasteur effect. The metabolic criteria of the Pasteur effect, i.e. inhibition of hyperlactacidaemia and decrease of the organic P/inorganic P ratio, are thus the direct indices of pathogenicity and toxigenicity. This also accounts for deep alteration of the Pasteur effect in infections generating states of infectious and endotoxinic shock.
Mucoproteinuria, determined by Bugard's semiquantitative method, revealed values of 100-350 mg/24 h in common scarlet fever and of 300-882 mg/24 h in scarlet fever complicated by early nephritis, pseudorheumatism and acute diffuse glomerulonephritis. These alterations appear to lend support to the recent hypothesis concerning the mucoprotein substrate of the autoimmune mechanism in the complications of streptoccal infection.