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Biomedical subjects

J Bariety

Publications and source records attributed to J Bariety.

At least 145 records · Page 8Linked to original sources
PubMed1975

Prostaglandins in neural crest-tumors.

Prostaglandin and catecholamine concentrations were estimated in tumour tissues taken from four phaeochromcytomas and five other neural-crest tumours. Prostaglandins were found to be present in tumours both associated and non-associated with chronic diarrhoea. Prostaglandin F, as well as catecholamine, concentrations were higher in phaeochromocytomas than in other tumours. The hypothesis has been made that while prostaglandins do not reach arterial circulation to give rise to pharmacological effects, such as chronic diarrhoea, prostaglandins F present in phaeochromocytomas may contribute to a higher catecholamine synthesis and/or release, resulting in a higher incidence of hypertension associated with these tumours.

Adult↗
PubMed1975

The release of renal prostaglandins during saline infusion in normal and hypertensive subjects.

1. Renal venous prostaglandin concentrations (PGA, PGE and PGF) were determined, together with renal plasma flow, urinary output and blood pressure changes, before and after infusion of sodium chloride solution (saline) in four normotensive and three hypertensive subjects. 2. No changes in blood pressure and in glomerular filtration rate were observed. 3. Saline infusion induced a significant increase in renal venous PGA and PGE, and also in total and non-cortical renal plasma flow and urinary output. There was an insignificant increase in renal venous PGF. 4. These findings show that prostaglandin release after saline infusion is associated with changes in renal blood flow and suggest that the natriuretic and diuretic effect of saline could be the result of prostaglandin release.

Adult↗
PubMed1975

The effect of indomethacin and prostaglandin (PGE2) on renal failure due to glycerol in saline-loaded rats.

1. Acute renal failure was induced in conscious rate by subcutaneous injection of glycerol. 2. Expansion of the extracellular space by infusion of 150 mmol/l sodium chloride (saline) partly protected the animals against acute renal failure. 3. This protective effect of saline infusion disappeared when the animals were treated with indomethacin. This effect could be reversed by the addition of prostaglandin (PGE2) to the saline infusion. 4. We suggest that prostaglandins may be involved in mediating the protection afforded by saline infusion against acute renal failure due to glycerol.

Acute Kidney Injury↗
PubMed1975

[Origin, nature, role and fate of prostaglandins liberated during the expansion of intravascular space in the anesthetized rat].

In experiments in which blood was cross-circulating in rats, the blood pressure of the recipient dropped while that of the donor rose, following the increase of the circulating blood volume, produced by infusion either of saline or blood. The phenomenon was almost imperceptible when binephrectomized animals were used. In experiments in which the blood-bathed organ technique was used, prostaglandin-like substances were detected, released during the rise of the blood pressure, produced by the same stimulus (the expansion), in anaesthetized rats. A significant difference was found between the prostaglandin-like substances detected using the blood-bathed organ technique, in normal rats (5.387 ng per ml of blood plus or minus 0.288 = SEM) and those detected in binephrectomized rats (3.202 ng per ml of blood plus or minus 0.330, p smaller than 0.025). The biologically active substances detected in 25 ml of blood collected during expansion, while the assay organs showed a prostaglandin-like activity, were found to have the chromatographic behaviour and the bioassay properties of PGA, PGE and PGF series. A great quantity of the biologically active substances, having the chromatographic behaviour and the bioassay properties of PGA, PGS and PGF was detected in the rat renal medulla. Sufficient quantities of the released prostaglandin-like substances could escape the pulmonary vascular bed in this species of animal. It was concluded that a great quantity of the released prostaglandin-like substances came from the kidney and their release by this particular mechanism suggested that they play an important homeostatic role on the blood pressure, blood volume, and sodium and water balance regulation.

Animals↗
PubMed1975

Prostaglandins and hypertension in chronic renal diseases.

The role of prostaglandin A (PG A) in the pathogenesis of renal hypertension has been studied. The concentration of endogenous PG A was measured in the peripheral plasma by radioimmunoassay in patients with chronic renal disease and in control subjects. The mean plasma concentration of PG A1 equivalents was as follows: 1. normotensive healthy volunteers (n=23): 115 +/- 15 pg/ml 2. patients in terminal renal failure on regular hemodialysis a) anephric patients (n=6): 51+/- 21 pg/ml b) patients retaining their own kidneys, all but one with hypertension (n=9): 231 +/- 51 pg/ml (P less than 0.01 versus control) 3. patients with chronic renal disease a) with hypertension (n=7): 204 +/- 60 pg/ml (P less than 0.01 versus control) b) without hypertension (n=11): 136 +/- 30 pg/ml. Renal hypertension was associated with high levels of PG A in peripheral blood. This increase is probably a secondary adaptative mechanism for the excretion of a greater fraction of the glomerular filtrate at a lower blood pressure. PG A may represent a circulating "antihypertensive hormones".

Adult↗
PubMed1975

Striated membranous structures in renal glomerular tufts. An electron microscopy study of 340 human renal biopsies.

Striated membranous structures are membranes 200 plus or minus 20 A thick. They are very common in both normal and pathologic human glomeruli, since they were found in 221 of 340 renal biopsies studied. Their appearance varies according to the plane of the section: on cross-section they resemble a pile of plates or double longitudinal bands. On tangential section they have an areolar appearance. Striated membranous structures are located in the basement membrane, mesangial matrix, or extracellular pathologic deposits such as amyloid or "immune" deposits. These membranes, probably double layered, are of unknown origin. They might derive from the focal or total lysis of cellular elements included within basement membrane-like material or extracellular deposits.

Basement Membrane↗
PubMed1975

Immune complex type glomerulonephritis in cirrhosis of the liver.

Glomerular lesions were detected in 9 of 10 patients with liver cirrhosis: these lesions consisted of a) thickening of basement-membrane-like material, b) electron-dense deposits in mesangial areas and in capillary walls, c) round areas of rarefaction in the membrane-like material and in some deposits, and d) presence of IgA, with IgG and/or IgM and/or C3, in the deposits. The association of these four abnormalities seems to be characteristic of "cirrhotic glomerulonephritis." The deposits could be the result of precipitation in the glomeruli of either aggregated immunoglobulins or circulating immune complexes.

Adult↗