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Biomedical subjects

D Durand

Publications and source records attributed to D Durand.

At least 325 records · Page 18Linked to original sources

Ethanol in low doses augments calcium-mediated mechanisms measured intracellularly in hippocampal neurons.

The electrophysiological effects of ethanol in low doses (5 to 20 millimoles per liter or 23 to 92 milligrams per 100 milliliters) were examined intracellularly in CA1 cells of rat hippocampus in vitro. Inhibitory and excitatory postsynaptic potentials were increased when ethanol was applied to the respective synaptic terminal regions. Postsynaptically, ethanol caused a moderate hyperpolarization with increased membrane conductance, even when synaptic transmission was blocked. Ethanol augmented the hyperpolarization that followed repetitive firing or that followed the eliciting of calcium spikes in the presence of tetrodotoxin, but not the rapid afterhyperpolarization in calcium-free medium. Ethanol appears to augment calcium-mediated mechanisms both pre- and postsynaptically.

Animals↗

The early diagnosis of massive acute intestinal ischaemia.

Intestinal ischaemia with ensuing gangrene has been a serious clinical problem. Delay in diagnosis has inevitably led to either massive gut resection or death. It has been shown that the bowel contains high concentrations of both organic and inorganic phosphate. With gut ischaemia, phosphate is released from the bowel and elevated concentrations may be measured in peripheral blood, peritoneal fluid and urine. Associated leucocytosis and acidosis constitute a diagnostic laboratory triad. The alteration in gut phosphate metabolism has been studied extensively in dogs and humans. Under hypoxic conditions, a time period exists before irretrievable gut necrosis ensues. During this vital interval serum phosphate is elevated. In 20 clinical cases an accurate diagnosis of bowel ischaemia was made utilizing phosphate measurements. Three cases had an early diagnosis which led to embolectomy with no loss of gut. Elevated serum phosphate is an accurate diagnostic finding in early cases of massive gut ischaemia. It is hoped that this simple test may help lower the staggering mortality and morbidity associated with massive intestinal ischaemia.

Acidosis↗

Plasma calcium homeostasis in the guinea pig during the perinatal period.

In pregnant guinea pigs on day 60 of gestation, maternal hypercalcemia induced by calcium infusion (10 mg Ca/kg body weight/h, during 2 h) had no significant effect on the fetal plasma calcium level. By contrast, on day 66 of gestation the same infusion of calcium into the pregnant female induced a significant rise both in maternal and fetal plasma calcium levels. This difference might be related to the variations in the efficiency of placental calcium transfer occurring during the last days of gestation in the guinea pig. Plasma calcium, phosphate and magnesium levels decrease during the 12 h following birth in suckling guinea pigs. Plasma calcium and magnesium concentrations returned to normal values at 24 h while plasma phosphate levels increased during the first week of postnatal life.

Animals↗

Interaction of beta-adrenergic agonists and antagonists with the stimulation of growth hormone release induced by clonidine or by morphine in the rat.

The beta-adrenergic agonist, isoprenaline, and antagonist, propranolol, had no effect on the delayed basal secretion of GH consistently observed in rats treated with the narco-analgesic gamma-hydroxybutyrate. Under the same experimental conditions, GH release was distinctly stimulated by infusion of the alpha-adrenergic agonist, clonidine, and by morphine; both responses were dose-dependent. The effects of beta-adrenergic agonists and antagonists on these GH responses were as follows: in rats pretreated with isoprenaline -the GH release induced by clonidine and morphine was abolished whereas it was enhanced in rats pretreated with propranolol. These data confirmed and extended previous reports from this laboratory on the inhibitory role of beta-adrenergic receptors on GH regulation.

Animals↗

[Long-term treatment with captopril in arterial hypertension complicated by renal failure].

Twenty patients with severe hypertension and chronic renal failure were given Captopril during a one year period. Hypertension was always severe: BP: 193 +/- 11.8 mmHg/120.2 +/- 6.7 mm Hg. Mean glomerular filtration rate (GRF) was 42 +/- 10 ml/mn and renal plasma flow (RPF) was 160 +/- 35 ml/min. Mean plasma renin activity was 1.5 +/- 1.1 ng/ml/h and plasma aldosterone 15.9 +/- 1.9 ng/100 ml. Captopril was given in daily doses from 75 to 300 mg. Furosemide was added in 13 cases, and bêta inhibitions in 10 cases. Blood pressure and renal function were measured eight days, every month end after one year of treatment: the fall in diastolic blood pressure was 13 p. 100 after eight days, 23 p. 100 after one year; a period of at least 6 months was necessary to obtain normal blood pressure values; and after one year blood pressure was normalized (diastolic BP less than 90 mmHg) in 19 patients. Renal function was compared with pretreatment values, after 8 days and one year: --RPF was increased (+18 p. 100 and +10.3 p. 100); --GFR was unchanged (+3,8 p. 100 and -8.8 p. 100); --filtration fraction was significantly decreased: (-12.3 p. 100 and -18.3 p. 100); --sodium excretion rate (+16 p. 100 and +9.9 p. 100) and kaliemia increased (+10 p. 100 and +8 p. 100) but severe hyperkalemia never occurred; --PRA increased (+270 p. 100 and +400 p. 100); --Plasma aldosterone was decreased after eight days --28.9 p. 100 but identical to control after one year -4.4 p. 100. Diuretics were efficient to enhance the antipressor of Captopril, whereas bêta inhibitions appeared less useful, and may be indicated only when tachycardia occurs. These results show that long term use of Captopril alone or associated with Furosemide, can normalise blood pressure in patients with renal insufficiency, without any impairment in GFR, and with an increase in RBF.

Adrenergic beta-Antagonists↗

Effect of low concentrations of ethanol on CA1 hippocampal neurons in vitro.

The effects of ethanol (10, 20, 50, and 100 mM) have been studied on field potentials in the CA1 region of the in vitro hippocampal slice preparation. Ethanol produced depression of the orthodromically evoked CA1 population spike and raised the threshold for orthodromic spike production. The effects of ethanol on the size of the population spike were highly correlated with the amount of the inhibition present in the slice as measure by paired pulse stimulation in control medium. Ethanol increased recurrent inhibition in the slice but had no significant effect on the antidromic response and produced only small changes in the dendritic field potential amplitudes. Adaptation or acute tolerance to the depressing effects of ethanol was observed in many slices. It is suggested that ethanol acts by potentiating the intrinsic inhibitory system in the hippocampus.

Action Potentials↗

[Kidney allograft in familial Mediterranean fever a case report and review of the literature (author's transl)].

Chronic renal insufficiency in an Algerian patient with familial mediterranean fever and amyloidosis was treated by kidney transplantation. Diagnosis of the affection was confirmed by the onset of typical acute episodes during haemodialysis, and a bone marrow biopsy established the presence of amyloidosis. The transplant was unsuccessful at an early stage with infective complications. The incidence of similar complications and deaths (11 cases) was particularly high in the 23 previously reported patients in whom transplants had been performed, and no definite relationship was able to be established between the course of the disease and treatment by haemodialysis or transplantation. The functional prognosis of the transplant was apparently not adversely affected by the recurrence of amyloidosis in 3 cases.

Amyloidosis↗

Effect of streptozotocin diabetes on sialic acid content and glycoprotein binding of isolated hepatocytes.

The possible correlation between sialic acid content of hepatocyte plasma membranes, and their binding capacity was investigated. For that purpose, [3H] asialotransferrin binding was tested with hepatocytes from both normal and streptozotocin treated rats. The observed decrease in binding capacity was parallel to a decrease in the sialic acid content Insulin therapy restored simultaneously normal blood glucose level, hepatic membrane sialic acid content and binding capacity.

Animals↗

Long term effect of captopril in hypertension with chronic renal failure.

We report the use of the orally active converting enzyme inhibitor Captopril in hypertensive patients with mild chronic renal failure. Twenty eight patients were followed for a period of six months. Eleven patients required the addition of furosemide. Mean arterial pressure (MAP) decreased in all but two at six months (MAP: 102 +/- 0.8 vs 133 +/- 2.2mmHg, p less than 0.001). Untoward effects were frequent: the commonest reactions are loss of taste (four patients), skin rashes (11 patients), proteinuria (2 patients), tachycardia (2 cases). These side effects disappeared after reduction of dose (10 cases) or withdrawal (8 cases). Patients on 300mg daily or less were free of any untoward effect. In summary (i) Captopril alone or in combination with furosemide has an antihypertensive effect in patients with chronic renal failure and hypertension; (ii) side effects seem to be dose dependant and a reduced dosage should be used in these patients.

Blood Pressure↗