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Biomedical subjects

J L Cuche

Publications and source records attributed to J L Cuche.

At least 55 records · Page 3Linked to original sources
PubMed1986

[Plasma catecholamines, free and conjugated, in the hemodialyzed chronic renal failure patient].

Free, sulfo and glucuro-conjugated catecholamines (dopamine, noradrenaline and adrenaline) were measured to study their metabolism in 35 non-selected patients with chronic renal failure, and under hemodialysis for various periods of time. Our data demonstrate a statistically significant increase of free dopamine, and free noradrenaline concentration in these patients, while that of free adrenaline was not different from controls. However a careful scrutiny of 35 individual data suggests that sub-groups of patients with either high normal or low plasma free noradrenaline concentration could exist; this likely heterogeneity could be a good explanation for conflicting conclusions provided by previous reports. Suspecting that conjugated catecholamines might be altered in these patients, plasma sulfo and glucuro-conjugated amines were measured. We have found a predictable and highly significant increase of sulfo-conjugated catecholamines; glucuroconjugated dopamine and noradrenaline were unchanged, while glucuroconjugated adrenaline was significantly increased. The physiological meaning, if any, of these new observations on conjugated catecholamines cannot be assessed at the moment.

Adult↗
PubMed1985

Free and conjugated catecholamines in digestive tissues of rats.

Using a radioenzymatic technique, the highest concentrations of free catecholamines were found in the duodenum, and the lowest in the liver of untreated rats. When compared to the antrum, the concentration of free dopamine was higher, and that of norepinephrine lower in the fundus. As far as conjugated catecholamines are concerned, the tissue concentrations of both sulfo- and glucurono-conjugates were usually low, and often non detectable, with an exception: the concentration of glucurono-conjugated dopamine was very high in the duodenum, ileum, and liver of untreated rats.

Animals↗
PubMed1983

Is dopamine a physiological natriuretic hormone in the dog?

Both plasma and urinary dopamine and noradrenaline were measured as free and sulphate conjugates, by a radioenzymatic method, before and during extracellular volume expansion (ECVE) with hypo-, iso- or hyper-tonic fluid (usually sodium chloride solution) in dogs. During ECVE there was a decrease in plasma catecholamine concentration. For all cases except noradrenaline, this is probably due to a dilution phenomenon since when results were expressed as pg/mg of protein, ECVE had no effect. This change in noradrenaline accounted for the increase in the dopamine/noradrenaline ratio. As expected, there was an increase in the urinary excretion of dopamine during ECVE with both iso- and hyper-tonic fluid. This increase was not observed in the group of dogs given hypotonic fluid, although the increase of fractional excretion of sodium was of a similar order of magnitude. The increase in the urinary excretion of dopamine was apparently not affected by an increase in plasma sodium concentration and/or osmolality. The demonstrated dissociation between sodium and dopamine in urine does not support a physiological role for dopamine in renal handling of sodium during ECVE, and raises the question of its specificity.

Animals↗
PubMed1983

[Natriuretic effect of haloperidol in dogs].

A 0.5 microM/kg/min infusion of haloperidol in the renal artery of 20 sodium-loaded dogs undergoing water diuresis is showed to induce the following net effects: a statistically significant reduction of both clearance of PAH (-18.1 +/- 6.6 ml/min), and glomerular filtration rate (-4.3 +/- 1.5 ml/min), an increase of both fractional excretion of sodium (+ 6.8 +/- 1.1%) and potassium (+ 55.1 +/- 5.5%), a decrease of fractional excretion of phosphate (-5.3 +/- 1.5%), and a lack of change of free water clearance (infused minus controlateral kidney difference).

Aminophylline↗
PubMed1982

[Urinary excretion of catecholamines in the dog: physiopathologic hypotheses in man].

Renal handling of free catecholamines (dopamine, norepinephrine and epinephrine) was studied in 36 hydropenic anesthetized mongrel dogs in accordance with the clearance technique. There was no statistically significant correlation between plasma concentrations and either systemic (mean blood pressure, or cardiac output) or renal (clearance of PAH or glomerular filtration rate) hemodynamics. Net tubular transport (NTT) was calculated as the difference between filtered load and urinary excretion for any catecholamine. The mean NTTs of free catecholamines were as follows: --2,72 ng/min for dopamine, --3,18 for norepinephrine, and --1,36 for epinephrine, showing that they are mostly reabsorbed. However the use of averages is misleading inasmuch as tubular transport of free catecholamines is a heterogeneous phenomenon: a secretion appears to predominate when plasma concentrations are low and a reabsorption predominates when they are high. Whether such a heterogeneity is due to either a genetic heterogeneity in mongrel dogs, or an age-related difference is discussed.

Animals↗
PubMed1982

[Renal effects of chlorpromazine in dogs].

The renal effects of chlorpromazine (CPZ) were studied in sodium-loaded dogs. Intrarenal artery infusion of CPZ at 0.2 microM/kg/min induces a significant decrease of both clearance of PAH and GFR, with no measurable effect on the excretion of electrolytes. This result is interpreted as direct evidence in favor of a physiological role of dopamine, since CPZ is known to be a dopaminergic blocking agent. At 2.0 microM/kg/min, CPZ no longer induces a renal hemodynamic alteration, but has a powerful natriuretic effect associated with an increased kaliuresis, and an increase of the free water clearance; phosphate excretion was unchanged. This effect on the excretion of electrolytes is apparently reversible within the 30 minutes immediately following the discontinuation of the CPZ infusion. The CPZ-induced natriuresis and kaliuresis are not additive to aminophylline's, suggesting a renal cyclic nucleotide phosphodiesterase inhibition. In conclusion, CPZ has a dose-dependent effect on dog kidney: it induces a reduction of the renal hemodynamics at a low dose, and an inhibition of the tubular sodium transport at a high dose.

Aminophylline↗
PubMed1981

[Long term treatment of resistant hypertension with captopril (author's transl)].

The orally active angiotensin converting enzyme inhibitor SQ 14225 (captopril) was administered to 14 hypertensive patients resistant to conventional therapy. A marked antihypertensive effect was observed; all the patients were responders and blood pressure decreased by more than 20% in 13 out of them. Subjective tolerance was very good. Untoward effects of an immuno-allergic type have been noticed in 30% of these cases but disappeared in all instances when daily doses of the drug had been reduced, allowing maintenance of the treatment. Plasma renin activity increased during captopril administration but no relationship appeared between pretreatment plasma renin activity and the extent of blood pressure response to the drug. The use of captopril must be considered in severe and resistant hypertension but careful monitoring of this treatment is needed.

Adult↗
PubMed1981

[Borderline essential hypertension and the adrenergic nervous system. Identification assay].

The physiopathological participation of the sympathetic nervous system in borderline hypertension may be assessed on the following criteria: I) A quantitative rather than qualitative classification of hypertensive patients shows a group of patients with diastolic pressures between 75 and 95 mm Hg, in whom increases in cardiac output are closely related to increases in heart rate; 2) Clinical examination, which should include an assessment of personality, shows a higher incidence of signs in favour of an increase (absolute or relative) in sympathetic activity; 3) Plasma catecholamine levels are not helpful: the absence of raised concentrations could be related to increased excretion, especially by the kidney; 4) Urinary excretion of catecholamines is slightly raised: this is very evident when homovanillic acid levels are assessed.

Cardiac Output↗
PubMed1979

[Renovascular hypertension and beta blockers. Theoretical and practical implications].

Beta blockade was instituted in 10 patients with renovascular hypertension due to renal artery stenosis or thrombosis. The treatment was very effective in unilateral stenosis with a normal contralateral kidney (2 kidney Goldblatt) and in fibromuscular dystrophy of the renal artery. On the other hand many failures were observed in hypertension with a single kidney (1 kidney Goldblatt) and in renovascular hypertension with complex lesions or associated renal failure. Although a clear relationship was often observed between the increased plasma renin activity and the antihypertensive effect of beta blockade, this association was sometimes completely erroneous. Beta blockade, which is easy to perform, should be tried out systematically in renovascular hypertension, but, when no result is observed, this therapeutic test should not exclude surgical management thereafter.

Adrenergic beta-Antagonists↗
PubMed1977

Catecholamines, cyclic AMP and renin in two contrasting forms of essential hypertension.

Essential hypertension (EH) can be subdivided according to the sympathetic and renin activity into two contrasting forms: (1) borderline beta-hyperadrenergic renin hyperresponsive and (2) stable beta-hypoadrenergic renin hyporesponsive EH. These two forms probably represent two expreme poles in the spectrum of EH in which sympathetic and renin hyper- or hyporeactivity cannot be accounted for by catecholamine determinations solely. beta-Adrenergic responsiveness monitored by plasma cyclic AMP determinations revealed plasma cyclic AMP, renin and circulatory hyperresponsiveness to isoproterenol in borderline hyperadrenergic EH while the opposite, cyclic AMP and renin hyporesponsiveness to insulin-induced hypoglycemia have been described in low renin stable EH. The kidney is in the center of the adrenergic abnormality in the two forms of EH with the borderline one excreting into the urine catecholamines not accounted for by their glomerular filtration. Catecholamines solely, however, do not account for the differences in both forms of EH which can probably be attributed to their different beta-adrenergic responsiveness.

Adrenergic beta-Antagonists↗