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Biomedical subjects

M Dupont

Publications and source records attributed to M Dupont.

At least 91 records · Page 5Linked to original sources
PubMed1981

Symptomatic hypopituitarism revealing a primary empty sella turcica.

A 64-year-old nulliparous woman presented with clinical signs of thyroid and adrenocortical insufficiency. Subsequent hormonal investigations demonstrated a failure of all anterior pituitary functions. Pneumotomo-encephalography revealed a large arachnoid herniation, leading to the diagnosis of primary empty sella turcica syndrome with secondary panhypopituitarism. This unusual observation emphasizes the necessity of ruling out an empty sella turcica syndrome in patients with pituitary insufficiency.

Empty Sella Syndrome↗
PubMed1981

[Effect of indomethacin on renin secretion in isolated perfused rat kidney (author's transl)].

In vivo administration of indomethacin (I) is associated with a decrease in basal and stimulated plasma renin activity in man and other animal species including the rat. In order to identify the mechanism(s) underlying the effect of I on renin secretion, studies were carried out using isolated rat kidneys perfused at a constant rate (5 ml/min) with cell-free medium. In this model, the infusion of I into the renal artery at concentrations ranging from 5.5 to 167 mumol/1 induced a dose-dependent and reversible increase in renal renin release. Although these effects were observed without variation in perfusion pressure and kidneys were non-filtering, no definitive conclusion may be drawn concerning their mediation by macula densa or baroreceptors from the present data. Inhibition of renal prostaglandin biosynthesis by I may play a role; however, another possible mechanism could be the inhibition of phosphodiesterase activity by I. Supporting this view was the finding that theophylline, a potent known inhibitor of phosphodiesterase activity mimicked the effect of indomethacin in our model.

Animals↗
PubMed1980

Indirect evidence against a role of the kinin system in the renal hemodynamic effect of captopril in the rat.

The effects of acute saralasin (SAR) and captopril (SQ) administration on arterial pressure (AP), plasma renin activity (PRA), urinary excretion of water and electrolytes, glomerular filtration rate (GFR), renal blood flow (RBF), and glomerular blood flow (GBF) distribution (microsphere technique) were assessed in rats with activation of the renal renin and kallikrein systems (that is, chronic sodium depletion). In both groups AP decreased, and PRA and RBF increased markedly. Blood flow to outermost (C1) glomeruli was (in nl/min/g of kidney wt) 270 +/- 35 in SAR and 219 +/- 20 in the SQ group (NS when compared to 208 +/- 9 in control chronically sodium-depleted rats). Blood flow to innermost glomeruli (C4) strikingly increased from 95 +/- 10 (control) to 216 +/- 21 (SAR) and 180 +/- 13 (SQ group). Hence, preferential vasodilatation of innermost glomeruli occurred (C1/C4 ratio of 2.18 +/- 0.27 in control, 1.26 +/- 0.11 in SAR, and 1.25 +/- 0.07 in SQ rats). Chronic (6 days) administration of SQ was associated with a rapid and marked increase in water and sodium excretion. At the end of the study, RBF was higher than control, and GBF distribution was similar to that observed in acutely treated rats (C1/C4 ratio of 1.16 +/- 0.10). These results suggest that angiotensin plays a significant role in the systemic and renal hemodynamic changes associated with chronic sodium depletion. The similarity of the changes induced by SAR and SQ provides an indirect evidence against an effective role of the renal kallikrein system in the effect of captopril.

Animals↗
PubMed1980

[Stereological analysis of human gingival connective tissues. Clinically healthy gingiva].

The purpose of this study was to analyse stereologically the composition of the human gingival connective tissue after a period to two weeks of intense oral hygiene. Thiry young adults participated in this study. A clinical examination (plaque index and gingival index) was made at day 0 and day 14: on this last day an interdental papilla in the premolar region was sampled. The stereological analysis on point integration field has been made on serial sections of the interdental papillae sectioned in a buccal lingual plane. The gingivodental status of the subjects after the period of intense hygiene was characterized by a total absence of dental plaque and signs of gingival inflammation. The connective tissue was mainly made of by a dense network of collagen fibers. However an infiltrated zone of inflammatory cells (about 25% of the connective tissue) was always present. As a whole the gingival connective tissue was made of 88.4% of collagen, 7.3% of blood and lymph vessels, 4.9% of edema, 8.4% of fibroblasts, 8.2% of inflammatory cells and 2.7% of residual tissue (unidentified cells, nerves...). The infiltrated zone showed a certain number of differences with the non-infiltrated zone (collagen decrease, increase in oedema, vessels and mainly in inflammatory cells, principally monocytes, polymorphonuclear leukocytes and lymphocytes).

Adult↗
PubMed1980

Influence of lipidic plant extracts on carrageenin-induced inflammation of guinea-pig palatal mucosa.

Inflammation was induced in the guinea-pig palatal mucosa by a carrageenin solution injection. The inflammatory process was studied by a stereologic procedure. A determination was made of the volume fraction occupied by collagen, edema and vessels 1, 3, 6, 12, 24 hours and 4 days after the injection. The non-treated animals group presented a maximal collagen volumetric density decrease 6 hours after the carrageenin injection. The volume fraction of collagen then increased to reach approximately a value similar to the healthy mucosa collagen volumetric density 4 days after the injection. Edema was correlatively maximal 6 hours after the carrageenin injection and decreased during the next hours. During the whole course of the experiment, the volumetric density of vessels was higher than in healthy mucosa. The modification of the inflammatory process in the group of animals treated by the lipidic plants extracts (15 mg daily during 60 days before the carrageenin injection) mainly consisted in a stabilization of the vessels volumetric density during the experiment. The lipidic plants extracts would act as an inhibiting factor of the inflammatory vascular neoformation.

Animals↗
PubMed1980

Influence of lipidic plant extracts on cells kinetics during carrageenin-induced inflammation of guinea pig palatal mucosa.

It has been shown that guinea pigs treated during 60 days with vegetal insaponified fractions presented a stabilization of the vessels volumetric density during the 4 days following a carrageenan injection in the palatal mucosa when compared with the vascular increase observed in non-treated animals. This inhibition of the inflammatory vascular neoformation influences the cells kinetics during the carrageenan induced inflammation of the palatal mucosa. The cellular volume fractions were calculated by a stereologic technique based on a morphometric point counting procedure described by Weibel (1969). The principal result consists in a general decrease of the inflammatory cells volume densities, specially concerning the polymorphonuclear leukocytes. This phenomenon must be related to the vascular volume fraction stabilization during the inflammatory process and could explain the drug activity on inflammatory states.

Animals↗
PubMed1975

Effect of a competitive angiotensin antagonist on the renal haemodynamic changes induced by inhibition of prostaglandin synthesis in rats.

1. Inhibition of prostaglandin synthesis by indomethacin induced an increase in blood pressure which did not occur when rats were bilaterally nephrectomized. 2. The blood pressure effect was related to the state of sodium balance and thus to the activity of the renin--angiotensin system. 3. Indomethacin induced a decrease in renal blood flow. 4. Angiotensin receptor blockade with Sar1-Ala8-angiotensin II blunted the blood pressure effect and prevented the renal haemodynamic changes induced by indomethacin.

Angiotensin II↗