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Biomedical subjects

G De Fino

Publications and source records attributed to G De Fino.

3 recordsLinked to original sources
PubMed1990

[Permeability of dialysis membranes for endotoxins. Clinical and experimental results].

In the presented investigation in 20 endotoxaemic patients 70 haemodialyses were performed. It was revealed that the prehaemodialyzation LAL positivity in 50 haemodialyses (71%) declined, while no differences were observed in the effectiveness of cuprophan and AN 69 membranes. Research in vitro revealed that LAL positivity of blood which contains endotoxins and is subjected for 300 minutes to haemofiltration remains unaltered; in ultrafiltrates LAL is permanently negative. This is due to a mechanism of endotoxin fragmentation as a result of interaction of blood and membrane. Moreover, the LAL positivity of blood containing lipid A declines gradually when subjected to 80 minutes haemofiltration; the dialyzation permeability for lipid A is then proved by the fact that LAL positivity appears in the ultrafiltrate. From the submitted results ensues that reduction of LAL positivity by haemodialysis occurs as a result of elimination of filtrable endotoxin fragments (lipid A) which are released in the body.

Acute Kidney Injury↗
PubMed1989

The permeability of dialytic membranes to endotoxins: clinical and experimental findings.

This study of 20 endotoxemic patients submitted to 70 hemodialyses (HD) found a reduction of the pre-HD limulus amebocyte lysate (LAL) positivity in 50 HD (71%), without appreciable differences in terms of effectiveness between cuprophan and AN 69 membranes. To define the mechanisms responsible for the reduction in LAL positivity during HD, the membranes were used in two in vitro studies, the first of which showed that the LAL positivity of blood containing lipopolysaccharide (LPS), submitted to hemofiltration (HF) for 300 min, remained unchanged and the ultrafiltrate remained constantly LAL negative. These results suggest that the reduction in LAL positivity observed in HD in vivo, an expression of reduced endotoxemia, cannot be attributed either to the filtration of the LPS as such or to its fragmentation following blood-membrane interaction into theoretically less filtrable molecules or to mechanisms of LPS adsorption on the membrane. The in vivo reduction of LAL positivity is more likely due to removal of the filtrable endotoxin fragments already released in the body, like lipid A, the biologically active component of LPS, known to react to LAL. This hypothesis was borne out by the second in vitro study, where the LAL positivity of blood containing lipid A, treated by HF for 80 min, gradually decreased, and dialytic permeability to lipid A was confirmed by the appearance of LAL positivity in the ultrafiltrate.

Clinical Trials as Topic↗