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Biomedical subjects

G Nassuato

Publications and source records attributed to G Nassuato.

27 records · Page 2Linked to original sources
PubMed1981

Biliary excretion of simulateously administered bilirubin and chenodeoxycholic acid in rats with porta-caval shunt.

Portacaval shunting influences several metabolic processes of the liver. The aim of this work was to investigate whether bile salts and bilirubin reciprocally interfere with their biliary excretion in this experimental condition. 12 male Sprague-Dawley porta-caval shunted rats received simultaneously crystalline bilirubin (intravenously) and chenodeoxycholic acid (intraduodenally) 20-26 days after intervention. The biliary excretion of these two compounds was then studied. The results seem to indicate that there exists a mutual interference between bile salt and bilirubin excretion in the bile; moreover it is suggested that porta-caval shunting plays a secondary role in determining the observed interaction between bilirubin and bile salts metabolism in the liver.

Animals↗
PubMed1980

Influence of rifamycin SV on bile acid metabolism in rats.

Sodium cholate was infused with or without Rifamycin SV in rats in order to determine the site of interference of the drug on hepatic bile salt metabolism. Both compounds were administered at rates such as to saturate their respective maximal excretory capacities. When Rifamycin SV was given, bile acid uptake and excretion significantly decreased, with a significant reduction of the percent of conjugated bile salts in bile. Rifamycin SV neither modified bile flow nor affected the correlation between bile flow and bile salt excretion. These data suggest that the antibiotic interferes with the three main steps of hepatic bile acid metabolism. The cholestatic effect and the modification of biliary bile salt output produced by Ryfamycin SV in rats, could be of clinical relevance.

Animals↗
PubMed1978

Platelet aggregation following electrical stimulation.

It was demonstrated that the previous in vitro electrical stimulation of human and rat platelet-rich plasma does not modify the subsequent response of platelets to the aggregating activity of ADP, thrombin, thrombofax or adrenaline. This is interesting in view of the fact that the electrical stimulation can induce clot retraction.

Adenosine Diphosphate↗
PubMed1976

Reptilase clot retraction induced by electrical stimulation.

Retraction of platelet rich plasma clotted by reptilase is induced by electrical stimulation. Optimal retraction is obtained by stimuli, applied for more than 4 min, with the following characteristics: intensity = 150 volts, duration = 50 msec each, frequency = 10/sec. Electrically induced reptilase clot retraction is shown to be inhibited by EDTA, EGTA, methyl-xanthines, PGE1, acetylsalicylic acid, indomethacin, but not by apyrase or by phosphoenolpyruvate-pyruvate kinase and MgCl2. The results indicate that electrical stimulation induces retraction of PRP clotted by reptilase by triggering off an increased availability of Ca2+ in the intracellular space.

Apyrase↗
PubMed1976

Ionophore a 23187: some effects on platelet aggregation and clot retraction.

The ionophore for divalent cations, A 23187, induces plate aggregation and clot retraction. Acetylsalicyclic acid has a potentiating effect on the aggregation induced by A 23187 in platelet-rich plasma, while it inhibits the aggregation of washed platelets. Acetylation of plasma proteins could be the reason of the increased platelet aggregation induced by A 23187 in the presence of acetylsalicyclic acid. Platelet aggregation by A 23187 is probably activated by the passage of Ca2+ through the platelet membrane(s); the aggation, clot retraction by A 23187 requires increased availability in the intracellular space of both Ca2+ and Mg2+.

Animals↗