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Biomedical subjects

C Marie

Publications and source records attributed to C Marie.

68 records · Page 4Linked to original sources
PubMed1990

Beneficial effect of 1,3-butanediol on cerebral energy metabolism and edema following brain embolization in rats.

We assessed the effect of 1,3-butanediol on cerebral energy metabolism and edema after inducing multifocal brain infarcts in 108 rats by the intracarotid injection of 50-microns carbonized microspheres. An ethanol dimer that induces systemic ketosis, 25 mmol/kg i.p. butanediol was injected every 3 hours to produce a sustained increase in the plasma level of beta-hydroxybutyrate. Treatment significantly attenuated ischemia-induced metabolic changes by increasing the concentrations of phosphocreatine, adenosine triphosphate, and glycogen and by reducing the concentrations of pyruvate and lactate. Lactate concentration 2, 6, and 12 hours after embolization decreased by 13%, 44%, and 46%, respectively. Brain water content increased from 78.63% in six unembolized rats to 80.93% in 12 saline-treated and 79.57% in seven butanediol-treated rats 12 hours after embolization. (p less than 0.05). The decrease in water content was associated with significant decreases in the concentrations of sodium and chloride. The antiedema effect of butanediol could not be explained by an osmotic mechanism since equimolar doses of urea or ethanol were ineffective. Our results support the hypothesis that the beneficial effect of butanediol is mediated through cerebral utilization of ketone bodies arising from butanediol metabolism, reducing the rate of glycolysis and the deleterious accumulation of lactic acid during ischemia.

3-Hydroxybutyric Acid↗
PubMed1989

Increased lipid peroxidation in vulnerable brain regions after transient forebrain ischemia in rats.

We examined cerebral lipid peroxidation, estimated by a thiobarbituric acid test, in rat brain regions after 30 minutes of severe forebrain ischemia and at recirculation periods of up to 72 hours. The lipid peroxide levels remained unaltered in all brain regions during ischemia and during the first hour of recirculation but were selectively increased between 8 and 72 hours of recirculation in the ischemia-sensitive regions of the hippocampus, striatum, and cortex. The most pronounced increases (30-37%) were seen at 48 hours of recirculation. In contrast, lipid peroxide levels were unchanged in infarcted brain regions 24 hours after intracarotid injection of microspheres, indicating that reoxygenation of the ischemic brain is a prerequisite for lipid peroxidation. We assessed the lipid peroxidation capacity of cerebral homogenates obtained from rats subjected to ischemia and recirculation by measuring the production of lipid peroxides after aerobic incubation. The homogenates from rats exposed to 30 minutes of ischemia or to 1 hour of recirculation were not more susceptible to peroxidation. However, the production of lipid peroxides was selectively increased in the hippocampus, striatum, and cortex at 8-48 hours of recirculation, suggesting a loss of efficacy of the antioxidant systems. These results, showing a delayed and long-lasting increase in lipid peroxidation that occurs in ischemia-sensitive brain regions and parallels the development of neuronal necrosis, support the hypothesis that free radical processes participate in postischemic neuronal damage.

Animals↗
PubMed1989

[Effect of bromocriptine and bromocriptine combined with prolactin on the proliferation of thymocytes in young rats].

The effects of bromocriptine and bromocriptine associated to prolactin have been investigated on young rat thymocytes after sensitization with T-cell antigen SRBC using a quantitative nucleus image analysis (Samba 200). Bromocriptine alone induces an inhibition of lymphocyte proliferation, a chromatin condensation and enhances cell differentiation. These effects are reversed by prolactin, which therefore acts on lymphocytes before they leave the thymus.

Animals↗
PubMed1987

Protective action of 1,3-butanediol in cerebral ischemia. A neurologic, histologic, and metabolic study.

1,3-Butanediol (BD) is converted in the body to beta-hydroxybutyrate, and previous studies have shown that hyperketonemia had beneficial effects in experimental models of generalized hypoxia. The aim of this study was to determine if BD would reduce brain damage following cerebral ischemia. A transient forebrain ischemia of 30-min duration was induced by the four-vessel occlusion technique in control and BD-treated rats (25 mmol/kg, i.p.; 30 min prior to ischemia). BD treatment led to significant improvement of neurologic deficit during the 72-h recovery period and reduced neuronal damage in the striatum and cortex but not in the CA1 sector of the hippocampus. Evaluation of cerebral energy metabolism before and at the end of the ischemic period showed that the treatment did not change the preischemic glycolytic and energy metabolite levels but attenuated the ischemia-induced metabolic alterations. It increased energy charge, phosphocreatine, and glucose levels, and reduced lactate accumulation. The decrease in brain lactate concentration might account for the beneficial effects of BD by minimizing the neuropathological consequences of lactic acidosis.

3-Hydroxybutyric Acid↗
PubMed1986

[Abdominal lymph node tuberculosis: diagnostic value of echography and x-ray computed tomography].

The aspects of abdominal ultrasonography and computed tomography (CT) were studied in 4 patients (3 African and 1 Haitian) with abdominal tuberculosis. All were markedly debilitated and three patients had protracted fever. Tuberculosis was documented in all cases by demonstrating Mycobacterium tuberculosis in cultures of lymph nodes taken during laparotomy and/or cultures of products of gastric aspiration. Ultrasonography showed enlarged lymph nodes in the pancreatic and peripancreatic areas and also in the mesenteric, perivascular and hepatic pedicle areas. CT showed hypertrophied lymph nodes with low tissue density ranging from 20 to 35 Hounsfield units. Although non pathognomonic, these aspects were suggestive of tuberculosis. Intravenous contrast medium administration failed to increase the density in the center of lymph nodes but disclosed the existence of a thick hyperdense rim surrounding the hypodense center of the caseous lymph nodes. Repeated ultrasound and CT examination allowed to control the efficacy of antituberculous chemotherapy.

Abdomen↗
PubMed1984

[Evolution of the regional blood deficit and energy metabolism after induction of transient cerebral ischemia by occlusion of the vertebral and carotid arteries in the rat].

A transient brain ischemia of 10 min duration was produced in rats by electrocautery of the vertebral arteries and reversible occlusion of the carotid arteries. Ischemia reduced blood flow to 10-18% of the control values in forebrain structures (cortex, striatum, thalamus) and to 25-50% in the mesencephalon, cerebellum and brain stem. In these last structures, after 30 min of recirculation, the flow rates returned to normal values but a 20-35% reduction of blood flow was present in the forebrain structures, indicating that the development of the postischemic hypoperfusion was related to the severity of the preceding ischemia. After 30 min of recirculation, there was a near complete recovery of the high energy compounds but a residual metabolic dysfunction was evidenced by an increase in lactate/pyruvate ratio and an elevation of the glucose content, suggesting a depression of cerebral metabolism which may account for the brain hypoperfusion.

Animals↗
PubMed1981

Ontogenesis of the adrenal glucocorticoids and of the target function of the enzymatic tyrosine transaminase activity in the chick embryo.

Adrenal and plasma glucocorticoids were determined in developing chick embryos of Gallus domesticus from days 8 to 19 of incubation, using a competitive protein-binding assay. At the same time, tyrosine transaminase activity in the liver was studied as an adrenal-dependent target function. Total amounts of glucocorticoids in the adrenal gland increased from day 11 and reached 7 ng/pair of glands on day 19. This increase was related to growth of the adrenal since concentrations remained constant at about 380 pg/micrograms dry weight from days 9 to 18. Glucocorticoids appeared in the plasma on day 12 and their concentrations rose to 10 ng/ml on day 19, with a marked peak on day 13. This peak was not reflected in the tyrosine transaminase activity which appeared and developed independently of the variations in the circulating glucocorticoids.

Adrenal Glands↗
PubMed1976

[A new synthetic antiparkinsonian drug, tropatepine hydrochloride in extrapyramidal syndromes induced by neuroleptics].

Tropatepine hydrochloride was given per oral route to 184 patients and per injections to 34 patients. Average prescribed doses were about 20 mg (2 tablets). This clinical study has shown that tropatepine hydrochloride has an antiparkinson activity against neuroleptic-induced extra-pyramidal syndrome. In comparison to the activity of the other synthetic antiparkinson drugs, the activity of tropatepine hydrochloride is: -- similar on akineto-hypertonia and on tremor; -- better on akathisia and, though less frequently, on anormal dyskinetic movements due to long term neuroleptic treatment. Tolerance is good ; furthermore clinical and biological performed examinations have shown that the drug seems free of toxic effects In more than 200 treated patients no severe mental aberration and no habituation have been reported.

Adult↗