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Biomedical subjects

D Durand

Publications and source records attributed to D Durand.

At least 289 records · Page 16Linked to original sources
PubMed1986

Electrical stimulation can inhibit synchronized neuronal activity.

The effect of electrical stimulation on abnormal neuronal activity was studied in the hippocampus in vitro. Epileptiform electrical activity was induced by adding penicillin or picrotoxin to the perfusing medium. Orthodromic stimulation generated large repetitive field potentials measured extracellularly. Electrical stimulation was then applied to the neurons with a 50 micron electrode located in the somatic layer. Large decreases in the amplitude of the population spikes were generated when stimulation was synchronized with the electrical activity. The inhibitory effect was charge-dependent and could be obtained with applied electrical charges similar to those used to stimulate nerves in the central nervous system. It is suggested that this method could be useful to prevent the synchronization and propagation of epileptic seizures.

Animals↗
PubMed1986

The Brattleboro rat: normal growth hormone secretion, decreased hepatic growth hormone receptors and low plasma somatomedin activity.

Three-month-old male Brattleboro rats with hereditary diabetes insipidus (DI) present a growth defect; Brattleboro rats were studied together with age-matched Long-Evans (LE) rats. Pituitary growth hormone (GH) content was comparable in both groups of rats. Pulsatile GH release and mean 6 h GH plasma levels did not appear significantly different in chronically catheterized DI and control animals. In parallel with the growth defect, the plasma somatomedin bioactivity was significantly lower in DI than in LE rats. The specific binding of [125I]iodo-hGH to liver microsomal membranes of DI rats was 59.7% that of controls. The number of the GH binding sites rather than the affinity of the binding was decreased. The specific binding of [125I]iodo-insulin was oppositely affected by the DI state: it was 1.5 times higher in liver membranes of DI rats than in membranes of LE rats. These findings make a non-specific effect of the DI state on liver membrane proteins unlikely. The Brattleboro rats present a growth failure without reduction of their GH secretion. The decreased number of the hepatic GH receptors and the subsequent low plasma somatomedin activity could explain the growth retardation of the DI rats.

Animals↗
PubMed1986

Further evidence that thyrotropin-releasing hormone participate in the regulation of growth hormone secretion in the rat.

Effects of thyrotropin-releasing hormone (TRH) on growth hormone (GH) secretion were investigated in vivo (on intact or mediobasal hypothalamic lesioned rats tested under either anesthesia or free moving conditions) as well as in vitro (in incubation or perifusion systems of anterior pituitary tissue). The peptide induced a rapid, dose-dependent increase of plasma GH levels in free moving animals bearing an extensive lesion of the mediobasal hypothalamus including the median eminence. Under comparable conditions, TRH was ineffective in intact animals. After chloral hydrate anesthesia a GH response to TRH was recorded in both groups, but lesioned rats exhibited a better responsiveness to all doses tested. In vitro TRH increased GH release from incubated or perifused pituitaries sampled from both intact and lesioned rats in a transient and concentration-dependent manner. A similar effect was obtained with the (3 Me His2) analogue of TRH. These findings indicate that TRH can affect GH secretion at the pituitary level under specific experimental conditions and support the hypothesis that either peripheral hormones or other, still unidentified hypothalamic neurohormones may modulate this effect.

Anesthesia, General↗
PubMed1986

Plasma and pituitary content of growth hormone luteinizing hormone, and prolactin in uremic rats. Effects of chronic infusion of insulin.

The influence of chronic renal failure on pituitary content and on serum concentrations of growth hormone (GH), prolactin (PRL), and luteinizing hormone (LH) was studied in chronically uremic rats by comparison with control rats fed ad libitum and diet-restricted rats pair-fed with uremic rats. A decrease of pituitary GH content was found in uremic and diet-restricted rats, in association with a normal circulating GH level. A decrease of pituitary PRL and LH content with respectively high and normal serum values was observed in uremic but not in diet-restricted rats. These data strongly suggest that GH disturbances are related to malnutrition, whereas PRL and LH abnormalities are related to the uremic state per se. As hypoinsulinemia was observed in uremic rats, and as insulin is largely implicated in growth, we have investigated the effects of chronic infusion of insulin, using miniosmotic pumps, on pituitary hormone content. In spite of normalization of circulating insulin levels in uremic rats treated with insulin, pituitary GH, LH, and PRL contents were unaffected. Thus, insulin deficiency did not appear to be responsible for the diminished pituitary reserve of these hormones.

Animals↗
PubMed1986

[Predictability of post-captopril acute renal failure in hypertension with renal artery stenosis of a single kidney or bilateral stenosis].

Use of converting-enzyme inhibitors in patients with hypertension and bilateral renal artery stenosis or renal artery stenosis in a single kidney may be complicated by acute renal failure (ARF). The aim of this work was to find a simple test to predict this accident. PAH clearance (CPAH), Inuline clearance (CIn) and Glomerular Filtration Fraction (GFF) were measured before and three hours after a single oral dose of Captopril (50 mg) in 7 hypertensive patients (sodium intake = 6 g/24 h). All these patients presented significant stenosis (greater than 60%) of the artery of a transplanted kidney (5), of a single kidney (1) or a bilateral renal artery stenosis (1). During the following three days, 50 mg captopril was given twice a day. ARF with creatinine serum level higher than 300 mumoles/l was seen in 4 patients (Group II); in 3 patients (Group I) creatinine serum level didn't change. Values measured before the single dose of captopril and variations after three hours are reported in the table: (Table: see text). Before captopril, in Group II CPAH and CIn are lower and GFF is higher, but these is not significant difference between the two groups. After Captopril CIn and GFF are significantly decreased in Group II (29.1 and 36.6% vs 7.8 and 10%). These results allow two conclusions: 1) Basal values of Glomerular Filtration Rate plasma flow and filtration fraction are not predictive parameters for acute renal failure after captopril therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1985

Low haematocrit and prolonged bleeding time in uraemic patients: effect of red cell transfusions.

This study demonstrates that a low haematocrit is the main determining factor of the prolonged bleeding time often encountered in uraemic haemodialysed patients. Thirty-three patients submitted to regular haemodialysis and having a platelet count greater than 100 X 10(9)/l were investigated with the following tests: simplate bleeding time, blood cell count, platelet aggregation induced by ADP, collagen and sodium arachidonate, arachidonate induced MDA synthesis, tests for detection of an acquired storage pool disease, and factor VIII complex level. The results were compared to two other groups; one of uraemic patients not yet subjected to haemodialysis and another of healthy volunteers. The results were basically identical in the two groups of uraemic patients. The only consistent abnormality was a 30-35% reduction in the platelet MDA synthesis in comparison with control subjects. There was a negative correlation between the log bleeding time and the haematocrit (r = 0.78, P less than 0.01). Fourteen uraemic patients having a prolonged bleeding time were submitted to a red cell transfusion programme and were investigated a second time under identical conditions. There was no change in any of the platelet function tests or in the factor VIII complex level, but the bleeding time was normalized when the post-transfusion haematocrit was over 26% (nine patients). This study emphasizes the role of anaemia in the pathogenesis of the prolonged bleeding time in uraemia and suggests that red cell transfusion can be a long-term efficient therapeutic measure to stop bleeding in these patients.

Adolescent↗
PubMed1985

Electrotonic parameters of neurons following chronic ethanol consumption.

The electronic parameters of nerve cells in the dentate gyrus following long-term ingestion of ethanol were studied in vitro. The ethanol was administered in a liquid diet for a period of 20 wk followed by a 3-wk withdrawal period. A control group received a similar diet with the ethanol replaced by maltose-dextrins. Intracellular recordings were obtained from 44 neurons, and the voltage decays following current injections were analyzed with a recent electrical model of granule cells to take into account a somatic shunt already detected in previous studies. The new model accurately accounted for the fast voltage transients and showed that the membrane time constant in the dendrites is, on average, five times larger than the somatic time constant. Injection of horseradish peroxidase into the neurons for the morphological analysis showed that neurons in the ethanol group have a longer dendritic tree than neurons in the control group. Estimation of the membrane surface area showed that the membrane area in the dendrites is at least 60% greater (in both control and ethanol groups) when the membrane foldings and irregularities are taken into account. The results of the modeling analysis showed that the membrane time constant and the input resistance are not affected by ethanol. However, the membrane resistance is significantly increased in the ethanol group (6,632 versus 18,460 omega X cm2), and the capacitance is significantly decreased (4.48 versus 1.71 microF/cm2). The electrotonic length is also increased by chronic ethanol treatment (0.85 versus 0.94). Higher values of membrane specific resistance (Rm) mean larger transmission coefficients. However, since the neurons from the ethanol group are on average longer than neurons in the control group, it is suggested that the change in Rm compensates for the increase in the length of the dendrites, thereby maintaining a value of the electrotonic length under 1.0. The observed changes in the passive parameters are in opposite direction from the recently measured effect of acute doses of ethanol on hippocampal neurons. These results support a model of chronic alcohol intake where homeostatic adaptive changes lead to the development of long-term changes in cellular physiology.

Alcoholism↗
PubMed1985

Thyroidectomy abolishes pulsatile growth hormone secretion without affecting hypothalamic somatostatin.

The effects of thyroid hormone deprivation and of subsequent replacement therapy on growth hormone (GH) secretion were investigated in unrestrained unanesthetized rats. Male rats were thyroparathyroidectomized (TPTX) 5 weeks prior to plasma sampling for GH assay, or to decapitation for evaluation of hypothalamic somatostatin (SRIF) content and in vitro SRIF and GH release. Thyroid hormone deprivation suppressed pulsatile GH secretion as well as GH release induced by clonidine (150 micrograms/kg). Treatment of TPTX rats with small doses of triiodothyronine (T3) restored an episodic pattern of GH secretion, but with lower peak values than controls, as well as the GH response to clonidine. Thyroid deprivation induced a 92-fold decrease in GH release from the pituitary; however, the ratio between GH release and GH content was similar in TPTX and normal rats, and human pancreatic growth hormone-releasing factor (GRF) (3 X 10(-8) M) was still able to stimulate residual GH release by hemipituitaries from TPTX rats in a manner similar to that in euthyroid controls (295 and 254% stimulation, respectively). Thyroid deprivation or T3 replacement did not modify SRIF content in the hypothalamus or other brain structures tested. The capacity of K+ depolarization to release SRIF in vitro from the hypothalamus was not modified by TPTX. These findings indicate that thyroid hormones are necessary to maintain both pulsatile and induced GH secretion in unanesthetized rats. In addition they suggest that impairment of GH secretion in thyroidectomized rats does not depend upon changes in the hypothalamic SRIF regulation of the hormone but could be dependent on a defect in GRF release and/or, most probably, GH synthesis directly at the pituitary level.

Animals↗
PubMed1985

D-galactosamine-induced liver injury: a rat model to study the heterogeneity of the oligosaccharide chains of alpha 1-acid glycoprotein.

The effect of D-galactosamine on the structure of the glycan moiety of alpha 1-acid glycoprotein was studied throughout a nine days experiment. It was shown that: D-galactosamine led to an alteration of the Concanavalin A crossed immunoelectrophoresis pattern and to a decreased sialic acid content of alpha 1-acid glycoprotein. The undersialylation of alpha 1-acid glycoprotein was not linked to a change in the relative ratio of various Concanavalin A forms. At the end of the experiment (9 days after galactosamine injection), the Concanavalin A non-reactive forms of alpha 1-acid glycoprotein remained elevated whereas alanine transaminase activity, total protein and alpha-acid glycoprotein had returned to a control level. D-galactosamine-treated rats seem to be a suitable model for the study of the very fast cyclic modulations of the synthesis of the glycan moiety of glycoproteins.

Animals↗
PubMed1985

[Pregnancy in renal transplant patients].

Renal transplantation is compatible with pregnancy in women under permanent dialysis, and leads to no problems for the mother or the transplant. The seven pregnancies observed in the authors' center over the past fifteen years progressed satisfactorily. There were no rejections, no cases of renal failure. In two cases, however, there was an aggravation of hypertension with acute gravidic toxemia and spontaneous abortion. The effects on the fetus of immunosuppressive drugs are difficult to evaluate; the main risk is prematurity.

Adult↗
PubMed1985

Immunohistochemical evidence for the expression of the carcinoembryonic antigen by human thymic epithelial cells in vitro and in neoplastic conditions.

Thymic epithelial cells (TECs), which are known to influence T-cell differentiation, may undergo phenotypic changes and lose some differentiation antigens (for example, the HLA-DR complex) in neoplastic conditions and when they are grown in culture. Using an indirect immunofluorescence assay, the authors investigated the expression of the carcinoembryonic antigen (CEA) by normal cultured or pathologic human TECs. This antigen, which can be regarded as a marker of undifferentiation, disappears during the normal development of epithelial tissues and reappears in neoplastic conditions. In normal as well as hyperplastic (myasthenia gravis-associated) thymuses, the epithelial network (revealed in double-labeling experiments by an anti-keratin monoclonal antibody) is virtually CEA-negative, except for the specific labeling observed on some cells of Hassall's corpuscles. In thymomatous epithelial cells, however, a strong and specific fluorescent labeling was consistently detected in all thymomas studied. Thymic epithelial cells grown in cultures from fragments of normal thymuses also expressed CEA on their cell membranes. Interestingly, the relative number of CEA-positive cells increased as a function of the age of the primary culture and reached virtually 100% when monolayers became confluent (Days 12-14). Moreover, using an ELISA assay, the authors demonstrated the presence of CEA in supernatants from TEC cultures. Interestingly, the amount of CEA in these supernatants decreased as a function of the age of the culture. In addition, a marked inhibition of TEC proliferation was observed after treating the cultures with an anti-CEA serum. Our results demonstrate that CEA is expressed not only in situ by differentiated neoplastic TECs but also by normal TECs cultured in vitro. In addition, the inhibitory action of the anti-CEA serum on TEC proliferation suggests that CEA may act physiologically as a growth factor for proliferating epithelial cells. In this respect, cultures of human TECs represent a good model for further studies.

Adult↗
PubMed1985

[Reversible renal insufficiency and arterial hypertension after renal transplantation: role of transplant artery stenosis and a captopril-furosemide combination].

Acute renal failure after captopril therapy in patients with transplant artery stenosis is well known. The study of a new observation may stress three particular points: 1) Diagnosis may be difficult just after transplantation in case of initial acute renal failure. 2) Renal function rapidly improved after withdrawing captopril and furosemide; after surgical treatment of the stenosis, a new course of captopril therapy was possible without any decrease of glomerular filtration rate. 3) A critical fall in filtration fraction seems to be the essential mechanism of renal failure, but specific interstitial lesions of the transplant showed on kidney biopsies, might be discussed.

Acute Kidney Injury↗