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Biomedical subjects

A Valenzuela

Publications and source records attributed to A Valenzuela.

At least 127 records · Page 7Linked to original sources
PubMed1985

Therapeutic regimen of septic vascular complications in kidney grafting.

In spite of highly sophisticated tissue matching reducing immunogenicity of a graft a high degree of immunosuppression is mandatory to achieve good graft survival. Septic complications such as a rupture of an anastomosis threaten the recipients life. Thorough donor selection, strict asepsis, as well as repeated bacteriologic examination gives the chance to decrease morbidity and mortality of kidney grafting. In the retrospective analysis of 135 kidney transplantations septic vascular complications occurred in 3.7%. The surgical procedure of choice after graft removal is the ligation of the external iliac artery. Only in one out of four cases ischemia of the lower extremity had to be treated by an extra-anatomic femoro-femoral bypass.

Adult↗
PubMed1985

Differential lipid peroxidative response of rat liver and lung tissues to glutathione depletion induced in vivo by diethyl maleate: effect of the antioxidant flavonoid (+)-cyanidanol-3.

The administration of a single dose of diethyl maleate (DEM) to fed rats elicited a drastic decrease in the content of reduced glutathione (GSH) both in liver and lung tissues after 6 h of treatment. Cellular GSH depletion induced by DEM was accompanied by a marked increase in pulmonary lipid peroxidation which was completely abolished by (+)-cyanidanol-3, without changes in the liver. Superoxide dismutase (SOD) activity remained unchanged in both tissues in this situation. Hepatic and pulmonary GSH depletion induced by a second dose of DEM given 24 h later produced a further increase in lung lipid peroxidation and a diminution of pulmonary SOD activity. In this condition, hepatic lipid peroxidation and SOD activity were not altered. These results indicate that lung and liver tissues exhibit a different lipid peroxidative response to chemically-induced GSH depletion.

Animals↗
PubMed1984

Content of hepatic reduced glutathione in chronic alcoholic patients: influence of the length of abstinence and liver necrosis.

The relationship between the content of hepatic reduced glutathione (GSH) and the length of abstinence was investigated in 45 chronic alcoholic patients. Hepatic GSH levels were significantly correlated (r = 0.58; P less than 0.001) with the length of alcohol withdrawal in the whole group. According to liver histology patients were divided into two groups, with and without hepatic necrosis. Subjects without necrosis showed a significant positive correlation (r = 0.71; P less than 0.001) between GSH values and the length of abstinence; no correlation (r = -0.22; P less than 0.40) was observed in the group with necrosis. According to the period of abstinence patients were separated into two groups, with a short (less than or equal to 5 days) and a prolonged (greater than 5 days) alcohol withdrawal. Patients with and without necrosis exhibited comparable mean levels of liver GSH (2.04 +/- SEM 0.21 and 1.74 +/- 0.23 mumol/g respectively; P less than 0.30) when studied after short periods of abstinence. Alcoholics without liver necrosis showed significantly higher hepatic GSH levels than those with necrosis (3.23 +/- 0.30 and 1.60 +/- 0.33 respectively; P less than 0.01) after prolonged periods of alcohol withdrawal. Similar results were obtained when liver GSH levels were expressed as a function of the mean surface area of hepatocytes, which was not significantly different between patients with and without hepatic necrosis. Parameters assessing the nutritional status of patients with and without necrosis were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Time course study of the changes in blood glutathione induced by acute ethanol intoxication in the rat.

Acute ethanol treatment of rats (5 g/kg) has a biphasic effect on the glutathione content of the erythrocyte. After 3 h of intoxication there is a diminution in total GSH equivalents, followed by a recovery to basal values 6 h after treatment. The decrease of total GSH equivalents is mainly due to a diminution of the oxidized form of the tripeptide. Concomitantly a marked increase in the plasma level of glutathione was found at 3 h, followed by a diminution to values obtained at time zero.

Animals↗
PubMed1983

Hepatic and biliary levels of glutathione and lipid peroxides following iron overload in the rat: effect of simultaneous ethanol administration.

The administration of 125 mg of iron/kg (iron-dextran-Imferon) to fed rats was followed by an increase in the non-hem iron content in plasma and liver over a period of 22 hr, reaching a peak value after 6 hr. Plasma and hepatic iron levels were not modified by ethanol ingestion (5 g/kg). Iron and ethanol treatments enhanced liver lipid peroxidation (malondialdehyde (MDA) formation) by 70 and 35%, respectively, at 6 hr. Since the hepatic MDA formation increased by 92% after the joint iron-ethanol treatment, an additive effect in lipid peroxidation was suggested to occur in this condition. Both iron and ethanol treatments increased biliary levels and release of MDA, in the absence of changes in bile flow. These parameters were further enhanced by the joint iron-ethanol exposure, in that hepatic MDA levels and biliary MDA release were significantly correlated (r = 0.86; p less than 0.05). Plasma MDA levels also increased after iron, ethanol, and iron-ethanol treatments, but they did not reflect the changes in MDA levels in liver. Iron exposure resulted in 26 to 33% decreases in hepatic GSH content at the 6-hr treatment, associated with the peak effect on lipid peroxidation. In this situation, glutathione disulfide (GSSG) levels in liver were not changed, but its biliary release increased by 76%. Hepatic reduced glutathione (GSH) levels were recovered by 18 hr and increased by 23% after 22 hr of iron ingestion. Acute ethanol intake diminished liver GSH content by 30% and enhanced that of GSSG by 73%, thus eliciting a net decrease of 20% in total GSH equivalents (GSH + 2GSSG). Biliary release of total GSH was reduced in this condition. The combined administration of iron and ethanol further influenced the decrease in hepatic GSH and the increase in GSSG levels elicited by the separate treatments, but no alterations in the biliary content and release of total GSH were observed in this situation. These data indicate that iron exposure accentuates the changes in lipid peroxidation and in the glutathione status of the liver cell induced by acute ethanol intoxication.

Animals↗
PubMed1983

Controlled trial of copper supplementation during the recovery from marasmus.

To evaluate copper nutritional status and the effect of a Cu supplement during recuperation, 27 marasmic infants were selected on admission to the nutrition recovery center at the Instituto de Nutrición y Tecnología de los Alimentos. Thirteen infants received 80 micrograms/kg/day of copper supplement as sulphate and the remaining a placebo. They were paired by birth weight, age, and sex. Anthropometric indices, complete blood count, ceruloplasmin, and Cu were measured on admission and at monthly intervals. Superoxide dismutase activity was measured in hypocupremic infants and was found to be low. The mean +/- SE Cu levels on admission were 127 +/- 10 micrograms/dl for the supplemented group and 137 +/- 10 micrograms/dl for the control. We found an increase in plasma Cu to 159 and 162 micrograms/dl on days 30 and 60 in the supplement group, and a significant decrease after day 30 in the placebo group. The ceruloplasmin levels followed this trend. Hypocupremia was found in 30% of the placebo group and none in the supplement group. The placebo group had a significantly higher prevalence of severe lower respiratory infections. It is concluded that a significant proportion of marasmic infants fed a milk-based diet present, during recovery, biochemical evidence of Cu deficiency. Supplementation with Cu is suggested.

Clinical Trials as Topic↗
PubMed1982

Alcohol ingestion, liver glutathione and lipoperoxidation: metabolic interrelations and pathological implications.

Data reviewed here indicate that acute and chronic ethanol ingestion induce a decrease in the concentration of GSH and an increase in lipoperoxidation in the liver both in experimental animals and in man, changes that are closely interrelated GSH depletion is suggested to be due to an oxidation in the liver tissue and to a translocation into the extrahepatic medium as free glutathione and/or as conjugates with ethanol-derived acetaldehyde. As a result, the hepatic GSH/GSSG ratio is drastically reduced. Lipoperoxidation seems to be related to the metabolism of ethanol and acetaldehyde by secondary pathways that are known to generate oxygen-related free radicals. Being lipoperoxidation a process associated with cell damage and death, its stimulation by ethanol ingestion could play a role in the production of alcoholic liver damage in man. The involvement of several contributory factors in the development of a high lipoperoxidative index in the liver in this situation is discussed.

Animals↗
PubMed1981

Effect of (+)-cyanidanol-3 on the changes in liver glutathione content and lipoperoxidation induced by acute ethanol administration in the rat.

Acute ethanol administration to rats fasted overnight resulted in a significant decrease in the content of glutathione (GSH) of the liver concomitantly with a partial increase in oxidized glutathione levels, representing a net 38% decrease in total GSH equivalents. In these conditions, liver lipoperoxidation is significantly enhanced. Treatment with (+)-cyanidanol-3 prior to ethanol ingestion was able to reduce by 80% the ethanol-induced depletion in total GSH equivalents and to completely abolish lipoperoxidation. These results indicate that (+)-cyanidanol-3 has a protective effect on the changes in liver GSH levels and lipoperoxidation induced by ethanol, probably related to its scavenging action exerted on free radicals.

Animals↗