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Biomedical subjects

M Morosetti

Publications and source records attributed to M Morosetti.

At least 37 records · Page 2Linked to original sources
PubMed1990

Oxygen tension monitoring in uremic patients during hemodialysis treatment.

The aim of this study was to evaluate the influence on cerebral and cutaneous vascular regions of PaO2 reduction during acetate dialysis, by monitoring conjunctival oxygen tension (PcjO2) and transcutaneous oxygen tension (PtcO2) during hemodialysis (HD) treatment. The study was performed on 23 patients with end-stage renal disease in chronic HD. All patients underwent dialytic treatment with cuprophan membranes and acetate containing dialysate. PcjO2 and PtcO2 were recorded and PaO2 and arterial carbon dioxide tension (PaCO2) were also measured. Results of the study show that hypoxemia during acetate dialysis with cuprophan membranes is not accompanied by changes of PcjO2 and therefore by changes in cerebral oxygenation. Moreover, PtcO2 remains constant during dialysis treatment. Furthermore, maintenance of normal oxygen tension at the conjunctival level is not obtained at the expense of the peripheral region of the skin.

Adult↗
PubMed1989

Platelet lipid peroxidation in haemodialysis patients: effects of vitamin E supplementation.

In haemodialysis patients, increased concentrations of malonyldialdehyde and decreased vitamin E content indicate lipid peroxidation in the platelets from oxidative damage. The same process has been described in red blood cells and in mononuclear cells in peripheral blood. However, platelet aggregation is within normal limits and does not change after treatment with vitamin E. On the other hand vitamin E supplementation reverts completely the biochemical abnormality of the platelets.

Blood Platelets↗
PubMed1989

Lack of oxidative damage in serum polyunsaturated fatty acids before and after dialysis in chronic uremic patients.

We described previously that in the erythrocytes and mononuclear blood cells from uremic patients on chronic hemodialysis, the membrane concentrations of malonyldialdehyde (MDA), resulting from peroxidation of polyunsaturated fatty acids (PUFA) in the membrane itself increased, and the concentrations of vitamin E (VIT E), the major antioxidizing agent, were lower. In the present study we analysed whether similar oxidative damage is seen in the serum from hemodialysis patients and whether the serum fatty acid pattern is affected. No evidence was found of oxidative damage in the serum during hemodialysis, serum concentrations of MDA and VIT E remaining constant before and after dialysis. No change was observed in serum pattern of PUFA, particularly linoleic acid. We therefore assume that the oxidative damage described in uremic patients is mainly intracellular.

Adult↗
PubMed1988

Discrepancies between serum and erythrocyte concentrations of vitamin E in hemodialysis patients: role of HDL-bound fraction of vitamin E.

Recently, we have demonstrated that hemodialysis (HD) patients have higher serum and lower erythrocyte concentrations of vitamin E than controls. It is known that transfer of vitamin E from serum to erythrocyte is mostly due to high-density lipoproteins (HDL). For a better definition of the pattern of distribution of vitamin E in HD patients, we have dosed the amount of vitamin bound to serum HDL fraction. In 8 patients and in 8 healthy controls, we have determined the concentration of serum erythrocyte and HDL-bound vitamin E. The latest was obtained on an ultracentrifuged HDL fraction. HDL fractions from HD patients have been found to contain larger amounts of vitamin E than controls. The previously described higher serum and lower erythrocyte concentrations of vitamin E in HD patients have been confirmed in the study. The deficit of vitamin E in the membranes of erythrocytes from HD patients has been shown to be the result of increased consumption of the vitamin in the erythrocyte membranes, where it represents the major antioxidant agent. However, the finding of increased amounts of vitamin bound to HDL in HD patients suggests that the transfer of the vitamin to the erythrocyte membranes may also be defective.

Adult↗
PubMed1987

Red blood cell lipid peroxidation in predialysis chronic renal failure.

In hemodialysis patients the pentose-phosphate shunt activity is deficient. As a consequence, the lipid peroxidation of the erythrocyte membranes is increased as shown by the increase in malonyldialdehyde concentrations and is accompanied by a decrease of the level of vitamin E in RBC. In the present study we have found that increased lipid peroxidation of the erythrocyte membranes is present also in chronic renal failure patients in the predialysis state, provided that the serum creatinine levels are higher than 5 mg/dl.

Erythrocyte Membrane↗
PubMed1986

Correction of uremic acid-base imbalance in biofiltration: standardization of the amount of bicarbonate infused.

Beneficial effects of biofiltration on acid-base balance have been described, especially in patients showing poor tolerance to standard hemodialysis. This study was designed to standardize the amounts of bicarbonate to be infused for optimal control of the acid-base balance, without the adverse reactions of symptomatic metabolic alkalosis. In three adult patients (body weight greater than 55 kg) a 300 mEq. bicarbonate infusion achieved normal pre- and post-dialysis plasma levels of bicarbonate and normal pre- dialysis pH. Conversely, in three adolescent patients (body weight less than 40 kg) pre- dialysis plasma bicarbonate levels and pre- dialysis pH could not be adequately corrected in spite of increasingly high doses of bicarbonate infused up to a maximum of 240 mEq per treatment. Larger amounts brought on symptoms of metabolic alkalosis.

Acid-Base Imbalance↗
PubMed1986

Clinical evaluation of biofiltration in uremic patients undergoing chronic hemodialysis.

The clinical efficiency of biofiltration (BF) was evaluated in six hemodialysis patients with poor clinical tolerance for standard hemodialysis. Three were adults (mean age 34 years, mean body weight 67 kg) and three adolescents (mean age 17 years, mean body weight 38 kg). Mean maintenance hemodialysis time was 90.5 months (range 49-132). BF treatments lasted three hours in all cases, for a total of nine hours weekly, with AN69 S membranes and infusion of 3 liters of HCO3 solution (100 mEq/l for the adults, 80 mEq/l for the adolescents). We recorded intra- and inter-dialytic symptoms daily, hematological values and acid-base status monthly. Multimodality evoked potentials were recorded after 3 and 9 months. Biochemical values reached a steady state 9 months from the beginning of the study, metabolic acidosis was corrected more efficiently in both groups at the end of dialysis, but only in the adult patients, were pre-dialysis plasma bicarbonates within normal limits. A clear drop in the number of episodes of intradialytic hypotension was noticed in both groups, but the adolescent patients' tolerance for dialysis did not improve. In conclusion our data show that in adult patients with poor tolerance BF offers a dependable alternative to standard hemodialysis, and the length of treatment can be reduced.

Acid-Base Equilibrium↗
PubMed1985

Red blood cell membrane lipid peroxidation and chronic haemolysis in haemodialysis patients.

Pre dialysis concentrations of malonyldialdehyde (MDA) in the red blood cell membranes and pre and post dialysis percent variation of plasma haemoglobin levels are studied in a group of uraemic patients on maintenance haemodialysis both before and after a therapeutic trial with vitamin E. The findings show a significant correlation between MDA levels and percent variation of plasma haemoglobin during dialysis, thus indicating that reducing the amount of lipid peroxidation can help to reduce intradialytic chronic haemolysis.

Adolescent↗
PubMed1984

Leukopenia, hypoxemia, and complement activation during a single hemoperfusion.

White blood cell count, acid-base balance, PO2, and complement function in five uremic patients undergoing a single hemoperfusion employing activated charcoal coated with methacrylate were studied. After 20 min on hemoperfusion, a marked leukopenia [ranging from 6,080 +/- 526 to 3,740 +/- 1,124 (p less than 0.02)] and hypoxemia [ranging from 106 +/- 13.8 to 80.2 +/- 11.9 mm Hg (p less than 0.02)] were observed. At the same time, total hemolytic complement decreased from 135 +/- 15.7 to 123 +/- 14.7 U/ml (p less than 0.001) and alternative pathway activity from 38.1 +/- 5.1 to 33.1 +/- 6.7 U/ml (p less than 0.005). C3 and B cleavage fragments were detected in the samples tested, thus demonstrating the activation of the complement alternative pathway. After 60 min, the different parameters tended to increase but did not reach the baseline levels. A direct correlation between the degree of leukopenia and the reduction of PO2 throughout the hemoperfusion period was found. pH PCO2, and HCO-3 did not change throughout the hemoperfusion period. The results demonstrate that complement activation, leukopenia, and hypoxemia occur during hemoperfusion.

Acid-Base Equilibrium↗
PubMed1982

Evaluation of acid-base balance and pO2 with acetate dialysis in non-uremic patients.

The aim of our work was to evaluate the immediate effects of acetate-dialysis in patients with normal renal and respiratory function. For this purpose pH, pO2, pCO2 and HCO3- were monitored in arterial blood before dialysis, after 60, 120, 180 mns and at the end of each treatment in two groups of patients on chronic hemodialysis, a first group of schizophrenic patients and a second group of uremic patients. In the first group of patients the predialytic values were in the normal range. After hemodialysis HCO3- and pCO2 significantly decreased, both these changes were associated with a stable pH. The pO2 significantly decreased after 60 mns of dialysis. At the end of dialysis the pO2 increased without significant variation compared to predialytic values. In conclusion in non-uremic hemodialysis patients metabolic acidosis due to the loss of bicarbonate through the membrane is compensated by respiratory alkalosis. This respiratory alkalosis is not due to hypoventilation secondary to respiratory centre inhibition, but is mainly due to the pCO2 loss through the dialysis membranes.

Acetates↗