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Biomedical subjects

P Cernácek

Publications and source records attributed to P Cernácek.

12 recordsLinked to original sources

Influence of inhibitor of glucose utilization on the blood platelet function.

The inhibition of glycolysis by an inhibitor of glucose utilization isolated from urine of the uremic subjects reflects in: (1) decreased platelet aggregation induced by adenosine diphosphate, adrenaline, or collagen, respectively; (2) decreased platelet factor 4 release induced by the same inductors; (3) decreased availability of platelet factor 3, and (4) inhibition of retraction of reptilase clot. It is concluded that the inhibition of glycolysis by 'inhibitor of glucose utilization' contributes to the functional changes of platelets and thus to the alteration of hemostasis in uremic patients.

Blood Coagulation↗

Uremic 'toxins' and blood platelet carbohydrate metabolism.

The effect of various small and middle molecular substances on blood platelet glycolysis was studied in vitro. Creatinine inhibited glucose utilization only at a concentration of 30 mg/dl; no effect of urea was found. o-Hydroxyphenolic acid and guanidinosuccinic acid, which were supposed to interfere with platelet function, inhibited glucose utilization at concentrations found in plasma of patients with chronic renal failure (CRF). Inhibitor of glucose utilization (IGU) peptide of middle molecular weight was found to inhibit glucose utilization without affecting glycogenolysis or lactate production. No additive or potentiating effects were found when interaction of different substances was tested. The only exception was a potentiation of IGU action on platelet glucose utilization by creatinine at a concentration of 15 mg/dl. Impaired glucose metabolism caused by 'uremic toxins' may contribute to the pathogenesis of bleeding in CRF by affecting platelet function.

Blood Platelets↗

Plasma tryptophan level in chronic renal failure.

Total (Trp), free (fTrp) and bound (bTrp) tryptophan concentrations were measured in the plasma of hemodialyzed (HD), peritoneally dialyzed (CAPD) and conservatively treated (ND) patients in chronic renal failure (CRF). 1) A marked decrease of Trp and bTrp was found in all three groups of patients. 2) fTrp concentration was unaltered in the HD and CAPD groups but decreased in the ND patients. 3) No relationship between a fall of bTrp and plasma albumin and transferrin levels was found. 4) Decreased body weight was not reflected in changes in Trp, bTrp and fTrp. 5) An inverse correlation between the serum creatinine and the bTrp/albumin ratio was found. Two alterations of Trp metabolism in CRF may be outlined: Trp deficiency and an alteration of Trp binding to plasma albumin. They affect Trp availability and seem to correlate with the degree of kidney function impairment.

Humans↗

[Metabolic changes in renal insufficiency].

In the chronic renal insufficiency is shown a decrease as well as an accumulation of some metabolites in the organism. There appear dietarily conditioned insufficiency states and also decreased rates of synthesis of 1,25-OH cholecalciferol , of the renal erythropoietic factor and of histidin. Apart from nitrogenous metabolic end products also the molecules with a middle molecular weight (300-1.500 Dalton) are accumulated. From this, among others, the trade-off hypothesis may be derived, which characterizes the biochemical distrubances in renal insufficiency as a sequel of the accumulation of metabolic regulators. In the analysis of the middle molecule fraction by means of combined chromatographic techniques we succeeded in isolating an inhibitor of glucose utilisation and in defining of some of its biochemical qualities. With the help of this survey the authors demonstrate a new way of thinking and a promising direction for the solution of still unclear probelms of renal insufficiency.

Amino Acids↗

[Glycide metabolism disorder in renal failure, therapeutic sequelae].

The in vitro effects of increased concentration of urea, creatinine, phosphate, glucose and of decreased concentration of potassium and calcium on the inhibitory effects of IGU was studied. The following results were obtained: 1. Urea, creatinine and increased concentration of phosphate in the degrees significant clinically did not influence the effect of IGU. 2. Decreased concentration of potassium did not influence utilization of glucose, but abolished completely the inhibitory effect of IGU. 3. Increased concentration of glucose increased its utilization, but did not abolish the inhibitory effect of IGU. The therapeutic implications of these findings for glycid metabolism in renal insufficiency are analysed.

Acute Kidney Injury↗