Search PubMed⌕ Search

Biomedical subjects

A Fournier

Publications and source records attributed to A Fournier.

At least 361 records · Page 20Linked to original sources
PubMed1992

Electrophysiologic effects of sotalol on the immature mammalian heart.

Sotalol is a beta-blocker with class III antiarrhythmic properties that has recently been used in children for the treatment of supraventricular and ventricular arrhythmias. However, little is known about its electrophysiologic effects on the immature heart. Using intracardiac electrocardiographic recordings and stimulation techniques, 15 canine neonates (8-15 days) and 15 adult mongrel dogs were studied with cumulative doses of sotalol (0.5, 1, 2, and 4 mg/kg plus an additional dose of 8 mg/kg for neonates). Heart rate decreased significantly in the two groups, but more in adult dogs (-43% in adult dogs versus -25% in neonates, p less than 0.05). There was no significant change for QRS duration and His-Purkinje system conduction time interval. QT and atrioventricular nodal conduction time intervals increased in adult dogs and neonates. Sinus node recovery time increased significantly in the two groups, but more in adult dogs. Refractory periods of the atrioventricular (AV) node increased significantly in neonates. Atrial flutter was no longer inducible in 12 of 15 neonates after the 2 mg/kg dose. Atrial effective refractory period increased significantly more in neonates (96%, p less than 0.001) than in adult dogs (58%, p less than 0.001). Ventricular effective refractory periods increased significantly both in neonates (46%) and adult dogs (50%), in a similar way. In conclusion, sotalol has greater electrophysiologic effects on the immature heart at the atrial level when compared to the adult, and similar effects on the refractory period of AV node and ventricle.

Animals↗
PubMed1992

Control of predialytic hyperphosphatemia by oral calcium acetate and calcium carbonate. Comparable efficacy for half the dose of elemental calcium given as acetate without lower incidence of hypercalcemia.

Since Mai et al. found, with the intestinal lavage technique, that the same dose of elemental calcium given as acetate (Ca Ac) complexed in the gut of uremic patients twice as much phosphate as calcium carbonate (CaCO3) while inducing a rather low calcium absorption, we wanted to see if half the dose of elemental calcium given as Ca Ac could control, on medium term, the predialysis plasma phosphate as well as CaCO3 while inducing less frequent hypercalcemia. This was evaluated in a cross-over study of 3 periods of 10 weeks according to the sequence Ca Ac, CaCO3 and Ca Ac, in 12 compliant patients on chronic dialysis previously treated by CaCO3. Because of poor tolerance of Ca Ac during the first period, 4 patients were excluded and the results were assessed only on the 8 patients who completed the study. For half the doses of elemental calcium (620 +/- 250 mg versus 1,310 +/- 560 mg versus 710 +/- 200 mg/day), Ca Ac allowed the same control of predialytic hyperphosphatemia (1.67 +/- 0.34; 1.74 +/- 0.32; 1.75 +/- 0.38) with paradoxically comparable normal mean plasma calcium concentration (2.61 +/- 0.14; 2.56 +/- 0.13; 2.55 +/- 0.14 mmol/l). Plasma alkaline phosphatases and intact PTH concentrations remained also stable during the 3 periods. The frequency of hypercalcemia greater than 2.75 mmol/l (12; 9; 20%) and of hyperphosphatemia greater than 2 mmol/l (17; 22; 27%) were comparable with the 2 treatments. In conclusion, Ca Ac controls predialytic hyperphosphatemia as efficiently as CaCO3 for half the dose of elemental calcium without, however, decreasing the frequency of hypercalcemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1992

Involvement of the Y-1 receptor subtype in the regulation of luteinizing hormone secretion by neuropeptide Y in rats.

The present experiments were designed to investigate structure-function relationships, and identify the receptor subtype and postreceptor cellular mechanisms that mediate the ovarian hormone-dependent, excitatory, and inhibitory effects of neuropeptide Y (NPY) on LH release in female rats. Intracerebroventricular administration of NPY decreased plasma concentrations of LH in ovariectomized, hormonally untreated rats but stimulated LH release in ovariectomized rats pretreated with estradiol benzoate and progesterone. A similar dual response was also obtained after administration of NPY2-36. However, deletion of additional amino acids at the N terminus, as in NPY5-36, NPY11-36, NPY16-36, and NPY25-36, rendered the peptides inactive. An N-terminal fragment, NPY1-24-amide, and a discontinuous NPY analog, NPY1-4-epsilon-amino-caproic acid-25-36, similarly failed to influence LH release. The analog [Leu31,Pro34]NPY, a preferential agonist at the Y-1 NPY receptor subtype, also elicited the dual LH responses, but the preferential Y-2 receptor agonist, NPY13-36, was completely inactive. Further, only the peptides that stimulated LH release in vivo, i.e. NPY, NPY2-36, and [Leu31,Pro34]NPY, also stimulated the release of LHRH from median eminence fragments of steroid-primed rats in vitro, and the excitatory effect of [Leu31,Pro34] NPY was blocked by a noncompetitive NPY receptor antagonist, D-myo-inositol-1,2,6-trisphosphate. With the exception of NPY1-24-amide, all of the NPY fragments tested bound specifically to NPY binding sites in hypothalamic membrane preparations, but the highest binding affinities were found for the peptides that evoked biological responses in the in vivo and in vitro tests. Further analysis of the mode of action of NPY showed that the stimulation of LHRH release in vitro was unaffected by omission of Ca2+ from the incubation medium, but was prevented by two antagonists of intracellular Ca2+ mobilization, 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester and ryanodine. Inhibition of prostaglandin synthesis with indomethacin blocked the stimulatory effect of the alpha 1-adrenergic agonist methoxamine on LHRH release, but not the increase produced by NPY.(ABSTRACT TRUNCATED AT 400 WORDS)

Analysis of Variance↗
PubMed1992

Nonadrenergic and noncholinergic arterial dilatation and venoconstriction are mediated by calcitonin gene-related peptide1 and neurokinin-1 receptors, respectively, in the mesenteric vasculature of the rat after perivascular nerve stimulation.

In the present study, selective calcitonin gene-related peptide (CGRP) and neurokinin (NK) agonists and antagonists were used to characterize the receptors mediating the nerve-induced arterial vasodilation and venous vasoconstriction in the rat mesenteric vasculature. In guanethidine-pretreated preparations, perivascular nerve stimulation (PNS) induced a frequency-dependent vasodilation in the arterial vasculature (precontracted with methoxamine), yet only induced an atropine-resistant contraction in the venous mesenteric vasculature (precontracted with U46619) of the rat. hCGRP alpha induced a marked dose-dependent relaxation of the arterial side, whereas only a slight vasodilation was seen at a high dose on the precontracted venous side. The PNS or hCGRP alpha-induced arterial dilatation was markedly reduced by the antagonist hCGRP8-37, whereas the venoconstrictive response to PNS was not. Furthermore, [acetamidomethyl-Cys2,7]hCGRP was inactive on either side of the rat mesenteric vasculature. A selective NK-1 nonpeptidic antagonist (CP-96,345) reduced the response of the venous vasculature to PNS by 70% without affecting the response of the arterial side to the same stimulus. Furthermore, a selective NK-3 receptor antagonist ([Trp7,beta-Ala8]-NKA (4-10)) did not affect the venoconstriction induced by PNS, yet markedly reduced the pressor response induced by a selective NK-3 receptor agonist, [MePhe7]-NKB. Hence, PNS induces the release of CGRP which activates specifically CGRP1 receptors and induces relaxation on the arterial vasculature. On the venous side, the nerve stimulation activates transmural NK-1 receptors and evokes a venoconstriction.

Animals↗
PubMed1992

Use of alkaline calcium salts as phosphate binder in uremic patients.

In order to prevent aluminum toxicity induced by the association of aluminum phosphate binder with 1 alpha(OH) vitamin D3 derivatives and the use of deferoxamine with its own hazards to diagnose and treat this toxicity, we have shown in 1982 that it was possible to replace the iatrogenic association of aluminum phosphate binder with 1 alpha OH vitamin D derivatives by oral calcium carbonate taken with the meals in order to bind phosphate and correct the negative calcium balance. This led to the disappearance of the crippling aluminic osteomalacia and adynamic bone diseases in our center. The effectiveness of CaCO3 without 1 alpha(OH)D3 derivatives in the control of hyperparathyroidism in dialysis patients has been proven by the appearance in four patients of our dialysis population of an histological idiopathic adynamic bone disease associated with relative hypoparathyroidism, and by the finding that more than 50% of our dialysis population treated by this sole treatment have plasma concentration of intact PTH below twice the upper limit of normal (that is, the threshold above which only significant histological osteitis fibrosa is observed). Besides the compliance problem, the limit of CaCO3 is the occurrence of hypercalcemia which occurs in about 8% of the measurements. Since calcium acetate binds twice as much phosphate for the same dose of elemental calcium as CaCO3, its use has been recommended. However, clinical experience has shown that in spite of the fact that half the dose of calcium element given as acetate does actually control predialysis plasma phosphate as well as CaCO3, the incidence of hypercalcemia is not decreased, probably because calcium availability at the alkaline pH of the intestine is much greater with Ca acetate. When hypercalcemia is frequent (and not explained by autonomized hyperparathyroidism, adynamic bone disease, overtreatment with vitamin D, granulomatosis or neoplasia) it is necessary either to decrease the dose of calcium and complete the necessary binding of phosphate by adding small doses of Mg(OH)2 or Mg carbonate, provided the dialysate Mg is decreased to 0.2 to 0.35 mmol/liter to prevent hypermagnesemia or to decrease the dialysate calcium (DCa) concentration. The decrease of DCa can be made either just when hypercalcemia occurs or on a systemic basis according to the amount of CaCO3 used and to the necessity of associating 1 alpha(OH) vitamin D3 derivatives.(ABSTRACT TRUNCATED AT 400 WORDS)

Aluminum↗
PubMed1992

Use of transtelephonic electrocardiographic monitoring in children with suspected arrhythmias.

Arrhythmias in children can produce various symptoms and their assessment often is difficult with usual methods. Transtelephonic electrocardiographic monitoring was used in 136 symptomatic patients (palpitations [112], syncope [six], chest pain [18]) for a mean duration of 86 +/- 65 days; mean age was 11.1 +/- 4.8 years and 62% were female. Of 398 recordings sent (mean 2.9 per patient) 32 revealed significant arrhythmias (8%). Of the 67 patients reporting symptoms during the recording period, only 24 had documented arrhythmias - 23 supraventricular tachycardia and one junctional tachycardia. The negative predictive value is 100%, compared with a low positive predictive value of 36%; sensitivity and specificity are, respectively, 100 and 62%. Of the 24 patients with documented arrhythmias, 54% were treated versus 13% of those with normal recordings (P < 0.01). At the end of the follow-up (mean duration 1.6 +/- 1.2 years), 63% of the patients with negative recordings had not complained of further symptoms versus 22% of those with documented arrhythmias (P = 0.001). Transtelephonic electrocardiographic monitoring is an important tool for documenting infrequent arrhythmias in children and even more for reassuring the patient and his or her family in the absence of significant arrhythmias.

Adolescent↗
PubMed1992

Neuropeptide Y potentiates selectively the N-methyl-D-aspartate response in the rat CA3 dorsal hippocampus. I. Involvement of an atypical neuropeptide Y receptor.

Neuropeptide Y (NPY) has been reported to potentiate N-methyl-D-aspartate (NMDA)-induced neuronal activation in the rat CA3 region of the dorsal hippocampus in vivo. Three types of NPY receptors, denoted Y1, Y2 and Y3, have been identified thus far. The present studies were undertaken to characterize the type of NPY receptor involved in this effect of NPY on the neuronal response to NMDA. NPY, its analogs [Leu31, Pro34]NPY and desamido-NPY, the related peptides pancreatic polypeptide (PP) and peptide YY (PYY) and the C- and N-terminal NPY fragments, NPY2-36, NPY11-36, NPY13-36, NPY16-36, NPY18-36 and NPY1-24CONH2, were tested. The peptides NPY (which is active at Y1, Y2 and Y3 receptors), [Leu31, Pro34]NPY (a selective Y1 agonist) and NPY13-36 (which mimics the effects of NPY in Y2 models) dose dependently enhanced NMDA-induced activation of CA3 dorsal hippocampus pyramidal neurons, but did not alter the activation of the same neurons by quisqualate. In contrast, PYY (which mimics NPY on Y1 and Y2 receptors, but has no activity or elicits an effect opposite to that of NPY in Y3 models) and NPY18-36 (which has been reported to exert an antagonistic or a partial agonistic action at Y3 receptors) did not modify by themselves the NMDA response, but antagonized the potentiating effect of NPY on NMDA-induced activation. Additionally, the C-terminal desamido form of NPY, which has little or no activity at Y1 and Y2 receptor subtypes, reduced the neuronal response to NMDA and quisqualate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Neuropeptide Y potentiates the N-methyl-D-aspartate response in the CA3 dorsal hippocampus. II. Involvement of a subtype of sigma receptor.

In an in vivo electrophysiological paradigm, we have shown in the companion paper that neuropeptide Y (NPY) potentiates N-methyl-D-aspartate (NMDA)-induced neuronal activation via a non-Y1, non-Y2, non-Y3 receptor subtype, in the rat CA3 dorsal hippocampus. Because sigma ligands have also been shown to potentiate NMDA-induced activation and because NPY and peptide YY have been reported to have high affinity for sigma binding sites, the present study was carried out to assess the possibility that the modulation of the NMDA response by NPY might be mediated by a sigma receptor. In the same electrophysiological paradigm, low doses of haloperidol and alpha-(4-fluorophenyl)-4-(5-fluoro-2- pyrimidinyl)-1-piperazine butanol, two antagonists of sigma receptors, reversed the potentiation of the NMDA response induced by NPY, [Leu31, Pro34]NPY or NPY13-36 and blocked the suppressant effect of desamido-NPY on the NMDA response. In contrast, spiperone, which has low affinity for sigma sites, was ineffective in suppressing NPY, as well as desamido-NPY-induced modulation of the NMDA response. In our model, peptide YY, which acts as a NPY antagonist by suppressing the potentiation of the NMDA response induced by NPY, also antagonized the potentiation of the NMDA response induced by the administration of low doses of di(2-tolyl)guanidine and (+)N-cyclopropyl-methyl-N-,methyl-1,4- diphenyl-1-ethyl-but-3-en-1-ylamine hydrochloride, two high-affinity sigma agonists.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

[Acute renal failure complicating carbamazepine hypersensitivity].

A case of acute renal failure occurring during treatment with carbamazepine is reported. The clinical signs and biological abnormalities strongly supported the diagnosis of acute interstitial nephritis of immunoallergic origin. The outcome was favourable after drug withdrawal. We review the cases of carbamazepine-induced acute renal failure.

Acute Kidney Injury↗
PubMed1991

High-level secretion of correctly processed recombinant human interleukin-1 beta in Kluyveromyces lactis.

The lactose-assimilating yeast, Kluyveromyces lactis, has been developed as a microbial host for the synthesis and secretion of human proteins. Here, we report the use of multi-copy vectors based on the 2 mu-like plasmid pKD1 from Kluyveromyces drosophilarum [Chen et al., Nucleic Acids Res. 14 (1986) 4471-4481] for the secretion of recombinant human interleukin-1 beta (reIL-1 beta). High levels of reIL-1 beta were secreted into the growth medium when the structural gene was fused in-frame to a synthetic secretion signal derived from the 'pre'-region of the K. lactis killer toxin. N-terminal sequencing of the excreted protein showed highly efficient (greater than 95%) maturation of the signal sequence. Synthesis as prepro-IL-1 beta, the 'pro'-sequence being derived from the human serum albumin-encoding gene, resulted in equally efficient secretion of mature IL-1 beta. Cytoplasmic production of Met-IL-1 beta, without a secretion signal, was found to be toxic to K. lactis. As in Saccharomyces cerevisiae [Baldari et al., EMBO J. 6 (1987) 229-234], but unlike native human IL-1 beta, K. lactis reIL-1 beta is glycosylated. This glycosylation led to a 95% loss of its biological activity. Removal of the carbohydrate chains by endo-beta-N-acetyl-glucosamidase H treatment fully restored the biological activity. A modified form of IL-1 beta (Asn7----Gln7), in which the unique site for Asn-linked glycosylation was deleted, exhibited the same biological activity as native IL-1 beta. The level of secretion of mature recombinant IL-1 beta ws glycosylation-independent.

Amino Acid Sequence↗
PubMed1991

Age and castration modulate the inhibitory action of neuropeptide Y on neurotransmission in the rat vas deferens.

The potency of neuropeptide Y (NPY) to inhibit the electrically induced contractions of the epididymal half of the vas deferens diminishes markedly with age, being at least 20 times lower in the adult than in the 26-day-old rat. Castration sensitizes the epididymal segment to NPY in a testosterone-reversible manner. [Pro34]NPY was 3 times less potent than NPY in prepubertal rats and inactive in castrated adults, while NPY-(13-36) had no effect in either group. In the prostatic half, NPY and its analogs were active in rats from all ages studied; the order of potency being NPY greater than [Pro34]NPY greater than NPY-(13-36). The sensitivity of the prostatic segment from adult rats to NPY was unchanged by castration or testosterone replacement therapy. The NPY content of the ductus increases during development being higher in the prostatic than in the epididymal half at all ages studied. Castration decreases the peptide content in the two segments and the effect is prevented by testosterone administration. The present investigation demonstrated that the effect of NPY on vas deferens neurotransmission is subject to regulation by sex steroids, which affects differently the response of the two segments of the ductus.

Aging↗
PubMed1991

[Physiopathology, exploration and treatment of calcium lithiasis].

The main risk factors for calcium urolithiasis that are clinically detectable are low diuresis, hypercalciuria, hyperruricuria, alkaline urinary pH, hyperoxaluria, hypomagnesuria, hypocitraturia. They should be evaluated, all the more precisely that the disease is active, under both the urological and metabolic points of view, using 24 hour urine collection made at home on a free diet with a dietary record. In the majority of the cases the calcic urolithiasis is idiopathic, i.e. not related to a cause of secondary hypercalciuria like primary hyperparathyroidism, or to a hyperroxaluria either primary or of digestive or toxic origin. Its treatment if mainly dietary with high fluid intake (diuresis greater than 2 1/24 h), normoclacic diet (800-1000h mh/24 h) with meat but not dairy product restriction, oxalate salts, carbohydrate and alcohol restriction. These dietary recommendations should be controlled by measuring the above cited parameters in the 24 hour urine samples and by measuring urea excretion which should not exceed 0.33 g/kg of body weight. When diet fails, drugs may be added mainly allopurinol, thiazides and potassium citrate.

Calcium↗
PubMed1991

Characterization of melanotropin-release-inhibiting factor (melanostatin) from frog brain: homology with human neuropeptide Y.

A polypeptide was purified from frog brain extracts on the basis of its ability to inhibit alpha-melanotropin release from perifused frog neurointermediate lobes. Based on Edman degradation, amino acid analysis, and peptide mapping, the primary structure of this frog melanotropin-release-inhibiting factor (melanostatin) was determined to be H-Tyr-Pro-Ser-Lys-Pro-Asp-Asn-Pro-Gly-Glu-Asp-Ala-Pro-Ala-Glu-Asp-Met- Ala-Lys-Tyr-Tyr-Ser-Ala-Leu-Arg-His-Tyr-Ile-Asn-Leu-Ile-Thr-Arg-Gln-Arg- Tyr-NH2 . Frog melanostatin belongs to the pancreatic polypeptide/neuropeptide Y/peptide YY family, and the structure of this peptide differs from that of human neuropeptide Y by only one amino acid substitution in position 19. A synthetic replicate of frog melanostatin is coeluted with the native peptide on HPLC and is highly potent in inhibiting alpha-melanotropin secretion in vitro (IC50 = 60 nM).

Amino Acid Sequence↗
PubMed1991

A role for Na+/H+ exchange in contraction of guinea pig airways by endothelin-1 in vitro.

Endothelin-1-induced contractions of guinea pig tracheal and bronchial strips were dose-dependently attenuated by the amiloride analogues 5-(N-ethyl-N-isopropyl)amiloride (EIPA, 1-10 microM) and 5-(N,N-hexamethylene)amiloride (HMA, 1-10 microM). The calculated Ki values for EIPA and HMA were 0.11 +/- 0.02 microM and 0.06 +/- 0.02 microM in the trachea, and 0.28 +/- 0.11 microM and 0.70 +/- 0.25 microM in the bronchus, respectively. These values are in the same order of magnitude as those reported for inhibition of the Na+/H+ exchange in cells. Amiloride (1-10 microM) was ineffective. These data suggest that activation of the Na+/H+ exchange by ET-1 may be involved in mediating its myotropic action in guinea pig airway smooth muscle.

Amiloride↗
PubMed1991

Calcitonin gene-related peptide (hCGRP alpha) binding sites in the nucleus accumbens. Atypical structural requirements and marked phylogenic differences.

The distribution of [125I]hCGRP alpha binding sites was studied in tissue sections from rat brain and, at the level of the nucleus accumbens in the brains of 6 other species. In the rat, very high levels of binding were found in the nucleus accumbens, the amygdaloid complex and mammillary body while high amounts were localized to the superficial layers of the superior colliculus, temporal cortex, cerebellum (molecular layer), frontal cortex and inferior olive. Moderate densities of [125I]hCGRP alpha binding were observed in the medial geniculate nucleus, inferior colliculus and substantia nigra. Regional competition studies in rat brain showed that salmon calcitonin was almost as effective as hCGRP alpha in competing for [125I]hCGRP alpha binding sites in the nucleus accumbens but was mostly inactive in other regions such as the mesolimbic cortex and the striatum. On the basis of their atypical sensitivity to salmon calcitonin, [125I]hCGRP alpha binding sites in the rat nucleus accumbens, which appear between postnatal days 4 and 7, do not seem to correspond to either the CGRP1 or CGRP2 receptor subtypes. Marked species differences were observed in the distribution of [125I]hCGRP alpha binding sites, especially in the nucleus accumbens. In the mouse, low densities of hCGRP alpha sites were observed in striatum and fronto-parietal cortex while low to moderate levels were found in the medial and posterior aspects of the nucleus accumbens. A similar distribution was seen in the guinea pig brain albeit of generally higher density. In the rat, very high amounts of [125I]hCGRP alpha binding were seen in the nucleus accumbens while lower levels were found in the striatum and certain cortical areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗