Biomedical subjects

C Acevedo

Publications and source records attributed to C Acevedo.

At least 37 records · Page 2Linked to original sources

PubMed1997

[Metalloproteinase activity in arteries and veins. Regulation with doxycycline].

BACKGROUND: Alterations in the synthesis and degradation of extracellular matrix occur during atherogenesis. Metalloproteinases, whose activity may be inhibited with doxycicline in other tissues, play an important role in this process. AIMS: 1. To characterize metalloproteinase activities in internal mammary artery and saphenous vein, and 2. To assess the effect of doxycicline in the activity of metalloproteinases of these vessels and of cultured smooth muscle cells. METHODS: Segments of internal mammary arteries and saphenous veins and cultured smooth muscle cells were incubated with and without doxycicline. Metalloproteinases activity was assessed by zymography and Western Blot. RESULTS: Activity of metalloproteinase-9 in saphenous veins was 217% less than in internal mammary arteries. In these vessels doxycicline decreased metalloproteinase-9 activity by 207% and metalloproteinase-2 by 290%. Western Blot analysis showed that docycicline also inhibited metalloproteinase-1 expression. In cultured smooth muscle cells, the median inhibitory concentration of doxycicline for metalloproteinase-2 was 138 microM (r2 = 0.82). CONCLUSIONS: Internal mammary arteries and saphenous veins have different metalloproteinase activities, that are inhibited by doxycicline.

Animals↗

PubMed1996

[Metalloproteinase in carotid endarterectomy plaques: increased activity in critical stenosis zones].

BACKGROUND: The presence of metalloproteinases in atherosclerotic plaques has been described but their role is not well understood. An increased secretion of these proteolytic enzymes could explain plaque instability and distal embolization. AIM: To measure metalloproteinase activity in atherosclerotic plaques obtained after carotid endarterectomy. MATERIAL AND METHODS: Plaques were divided in one segment with and one segment without stenosis, the latter being used as control. Both segments were incubated in culture media for 48 h or were fixed for histology. The conditioned medium was studied using gelatin zimography and digital densitometry. Metalloproteinases were identified by their molecular weight, inhibition with EDTA or Western Blot. Standard histologic study and immunohistochemistry were done. RESULTS: In stenotic areas, metalloproteinase 9 (92kD) secretion was 260% higher than in regular plaques (191 and 73 Kilopixels/microgram protein respectively p < 0.02). The histological study of stenotic areas showed macrophage infiltration and neoformation of blood vessels. CONCLUSIONS: The increased secretion of cellular matrix degrading enzyme metalloproteinase 9 in stenotic areas of atherosclerotic plaques, could explain plaque instability and subsequent embolization.

Arteriosclerosis↗

PubMed1995

Cholestasis as a liver protective factor in paracetamol acute overdose.

1. The effect of paracetamol overdoses on its disposition was investigated in cholestatic rats. 2. Paracetamol plasma concentration and hepatic accumulation decrease about 70-80% in cholestatic rats. 3. Cholestatic rats intoxicated with paracetamol showed less hepatic damage as concluded from biochemical and histological findings. These data are correlated with liver and plasmatic paracetamol. 4. These results indicate a decrease in paracetamol toxicity related to stagnant bile.

Acetaminophen↗

PubMed1994

Studies of tyramine transfer and metabolism using an in vitro intestinal preparation.

The duodenal transfer and metabolism of [3H]tyramine from sacs and perfused segments of rat intestine were determined. In sacs, a linear relationship between the steady-state transfer rate of total tritium and the initial mucosal tyramine concentration was observed, suggesting that the clearance is the same at different concentrations. In duodenal perfusions, there was no significant difference in the amount of total tritium removed between control and everted tissues, whether the flow was 0.2 or 2.0 mL/min. The percentage of [3H]tyramine extracted from the gut lumen depended on the flow rate. About 30-40% of the extracted drug was metabolized; this value decreased to 20% when the rats were pretreated with pargyline. The data support the idea that the transfer mechanism for tyramine is simple diffusion.

Animals↗

PubMed1994

Liver oxygen uptake dependence and mitochondrial function in septic rats.

Defective oxygen consumption and a pathological dependence of oxygen uptake on O2 supply have been considered important events in sepsis. To relate these features with tissue and mitochondrial metabolism, we studied oxygen uptake in whole isolated and perfused rat liver at two O2 supply levels, in the same liver slices, and in isolated liver mitochondria. Experimental sepsis in rats was induced by cecal ligation and double-gauge puncture. The results showed that liver and tissue slices from septic animals had a 60% greater O2 uptake than that of controls and that, during sepsis, liver O2 uptake was markedly dependent on O2 supply. Concomitantly, mitochondrial O2 uptake was nearly 30% greater with malate-glutamate as substrate, but not with succinate; lowering O2 concentration in the medium did not alter the enhanced function. In submitochondrial, only NADH-dehydrogenase activity was 100% higher in septic samples. At least, in some tissues, O2 dependence is a function of O2 availability, sensitized by increased mitochondrial O2 uptake related to changes in respiratory enzymes.

Adenosine Diphosphate↗

PubMed1993

Metabolism of chlorinated guaiacols by a guaiacol-degrading Acinetobacter junii strain.

The metabolism of chlorinated guaiacols by a pure bacterial strain identified by its ability to use guaiacol as the sole carbon and energy source was studied. This strain, identified as Acinetobacter junii 5ga, was unable to grow on several chlorinated guaiacols and catechols. However, strain 5ga grown on guaiacol degraded 4- and 5-chloroguaiacol and 4,5-dichloroguaiacol. Under the same conditions, these cells did not degrade 6-chloroguaiacol, 4,6-dichloroguaiacol, 4,5,6-trichloroguaiacol, or tetrachloroguaiacol, suggesting that the substitution at the 6 position in the ring prevents metabolism of the compound. Degradation of 4-chloroguaiacol was dependent on the initial ratio between the chlorinated compound and viable cells. Transient formation of chlorocatechols resulting from incubation of cells with 4-chloroguaiacol or 4,5-dichloroguaiacol was suggested by UV spectroscopy. Gas chromatography analyses of samples from cultures of strain 5ga grown on guaiacol and incubated with 4- and 4,5-dichloroguaiacol confirmed the presence of 4-chlorocatechol and 4,5-dichlorocatechol, respectively. The formation of the latter was corroborated by gas chromatography-mass spectrometry. Thus, this strain is able to initiate metabolism of specific chlorinated guaiacols by O-demethylation. The starting chlorinated guaiacols and their O-demethylated metabolites inhibited the growth of A. junii 5ga on guaiacol.

Acinetobacter↗

PubMed1990

Accumulation of 3H-(+/-)-noradrenaline by isolated rat liver cells.

Using hepatocytes isolated by collagenase perfusion, we studied the accumulation of 3H-noradrenaline. Cells incubated during 15 min in the presence of 0.4 mumol/l 3H-noradrenaline (without inhibition of noradrenaline metabolism) accumulated 8.32 +/- 1.77 pmol/10(6) cells (n = 3). The accumulation of 3H-noradrenaline in isolated parenchymal liver cells was sensitive to 10 mumol/l cocaine (inhibition 36.6 +/- 7.9%, n = 3) and 1 mumol/l desipramine (inhibition 27.2 +/- 6.9, n = 3). Accumulation of 3H-noradrenaline was temperature and sodium dependent (inhibition 33.2 +/- 9.4%, n = 9, when Na+ was replaced by Tris+) and was influenced by the inhibition of the membrane Na(+)-K(+)-adenosine triphosphatase (Na(+)-K(+)-ATPase) by 150 mumol/l ouabain (34.7 +/- 6.9% inhibition, n = 3). Accumulation of 3H-noradrenaline in the hepatocytes was not affected by the presence of uptake2 inhibitors, normetanephrine (30 mumol/l) and corticosterone (30 mumol/l), but was reduced by 30 mumol/l isoprenaline (76.3 +/- 5.0% inhibition, n = 6). Thus, the system that takes up and accumulates noradrenaline in the isolated rat liver cells possesses some characteristics of both, uptake1 and uptake2 systems and appears to be different from other extraneuronal cocaine-sensitive systems, such as the one reported for pulmonary endothelial cells.

Animals↗

PubMed1989

[Pharmacokinetic interaction of ketoconazole, isoniazid and rifampicin].

Eight male tuberculous patients, between 20 and 60 years of age, were given Isoniazid 5 mg/kg and Ketoconazole 200 mg, first one at a time and then associated. Plasma concentrations were measured 0, 2 and 5 hs after taking the drugs. Isoniazid was measured by spectrophotometry and Ketoconazole by the microbiologic method with Candida albicans as test microorganism. When both drugs were given simultaneously Ketoconazole plasma concentration decreased 75% at 2 hs (p less than 0.025) and 85% at 5 hs (p less than 0.05), whereas that of Isoniazid remained unchanged (Table 1). Mean half-life of Isoniazid was 3.9 +/- 1.4 hs in 7 slow acetylators and 1.1 hs in one fast acetylator when given one at a time and 4.4 +/- 1.5 hs when given simultaneously. A similar study was conducted on 11 tuberculous patients who were given Rifampicin 10 mg/kg and Ketoconazole 200 mg, one at a time and concurrently. Rifampicin was measured by high pressure liquid chromatography. When Rifampicin and Ketoconazole were given concurrently plasma concentration of both drugs was reduced: Ketoconazole decreased 85% at 2 hs (p less than 0.025) and 98% at 5 hs (p less than 0.025) whereas Rifampicin decreased 45% at 2 hs (p less than 0.005) and 40% at 5 hs (p less than 0.005) (Table 2). Mean half-life of Rifampicin was 3.5 +/- 0.8 and 4.2 +/- 1.1 hs, respectively, when it was given alone and concurrently. Studies on chemical interactions between Isoniazid and Ketoconazole and between Rifampicin and Ketoconazole yielded negative results.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

Uptake and metabolism of 3H-(+/-)-noradrenaline in the isolated perfused rat liver.

The influence of inhibitors of metabolism and uptake of noradrenaline on the 3H-noradrenaline removal from the perfusion fluid by the isolated rat liver was studied. Livers were perfused with 3 nmol/l 3H-noradrenaline and 3H-noradrenaline and 3H-metabolites were determined in effluent, liver and bile. After the perfusion with 14,900 +/- 920 dpm.g-1.min-1 during 90 min, cumulative removal of tritium was 323,574 +/- 63,103 dpm/g. 3H-metabolites recovered from the liver after 90 min perfusion represented 71.1 +/- 9.0% of total metabolite formation. Only the OMDA-fraction appeared in the perfusate; its approach to steady state of efflux was slow. The inhibition either of MAO or COMT changed neither the total removal of tritium nor the 3H-metabolites recovered from the liver. Cocaine (10 mumol/l) reduced the accumulation of 3H-noradrenaline in the liver. The uptake2 inhibitor corticosterone (30 mumol/l) diminished total removal of tritium and the 3H-metabolites recovered from the liver without changing the accumulation of 3H-noradrenaline. The hypothesis of two different compartments, one responsible for the metabolism and the other for the accumulation of the amine is discussed.

Animals↗

PubMed1985

[Vitamin D3 poisoning and irreversible sequela].

Twenty-four children with vitamin D intoxication and a follow-up of one to thirteen years old (means: four years and seven months) are reviewed. Over-dosage was prescribed by medical order in 66.6% of patients and by the mother herself in 16.6%. Intensity of clinical symptoms (renal, neurologic, digestive) were related with daily dose administered whilst final secuelae depends on duration of overdosage. Hipercalcemia was easily corrected by association of low calcium diet, corticoesteroids and/or furosemide in least than a month in 81% of cases. Two patients died during the acute fase and 22.7% remain with permanent damage (five in chronic renal failure, one in haemodialysis and three with low IC).

Bone Diseases, Metabolic↗

PubMed1972