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Biomedical subjects

A Fournier

Publications and source records attributed to A Fournier.

At least 307 records · Page 17Linked to original sources
PubMed1993

High levels of 2',5'-oligoadenylate synthetase and 2',5'-oligoadenylate-dependent endonuclease in human trophoblast.

Human placenta contains a high level of 2',5'-oligoadenylate (2-5A) synthetase activity of the 100-kD form of the enzyme. About 20% of the placental 2-5A synthetase activity was found to be cytosolic, whereas the remaining 80% was released by 0.5 M KCl in the presence of detergent. Most of the enzyme activity was localized in trophoblast cells, which also contain a high level of 2-5A-dependent RNase L activity. The purified trophoblast 100-kD 2-5A synthetase was shown to be activated by human immunodeficiency virus type 1 (HIV-1) 5' RNA 1-311 and 1-707, which both contain the TAR and primer binding site (PBS) structured regions. These two HIV-1 RNAs activated human trophoblast 2-5A synthetase at the same level as poly(I).poly (C), a standard highly efficient activator of the enzyme, and at the same optimal concentration. On the contrary, HIV-1 RNA 311-618, a poorly structured region missing TAR and PBS, was shown to be a poor activator of the enzyme. The specific cellular location of the 2-5A synthetase and its efficient activation by HIV 5' RNA favors the idea that the trophoblast 2-5A system negatively controls HIV replication in trophoblasts.

2',5'-Oligoadenylate Synthetase↗
PubMed1993

Calcium metabolism, plasma parathyroid hormone, and calcitriol in transient hypertension of pregnancy.

In order to know if abnormalities of calcium metabolism may be involved in the pathophysiology of pregnancy-induced hypertension (PIH), as it has been incriminated in essential hypertension, we measured plasma and urinary calcium and phosphate as well as plasma PTH and free calcitriol index (ratio of total calcitriol on the D binding protein) in normotensive pregnant women (n = 25), in women with PIH after the same duration of amenorrhea (> 28 wk, n = 21:preeclampsia and 20 transient hypertensions), and in age-matched nonpregnant women (n = 15). The severity of PIH was mild since blood uric acid was not increased and plasma volume, measured with the Evans blue technique, was found only moderately decreased (-10.5 +/- 3.1% of normal value). The results show that normotensive pregnant women showed the expected increase of the vitamin D parameters in comparison to nonpregnant controls. Hypertensive pregnant women were not different from the normotensive ones regarding plasma corrected calcium and phosphate and urinary excretion of calcium and phosphate, but had higher plasma PTH (13 +/- 1 v 8.8 +/- 1.6 pg/mL) and lower total and free calcitriol index (86 +/- 7 v 110 +/- 6 pg/mL and 1.72 +/- 0.10 v 2.25 +/- 0.13 x 10(-5)). Correlative studies showed PIH having a negative correlation between blood pressure and plasma corrected calcium (r = -0.43, P < .05), which is in agreement with epidemiological studies of essential hypertension. In conclusion, disturbances of calcium regulating hormones do exist in transient forms of pregnancy-induced hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Structure-activity relationships of ET-1 and selected analogues in the isolated guinea pig trachea: evidence for the existence of different ETB receptor subtypes.

We tested endothelin-1 (ET-1) derivatives on the guinea pig trachea (GPT) and compared their biologic activities to ET-1 in this tissue and to published reports using similar analogues in different assay systems, such as vascular smooth-muscle preparations. Six ET-1 analogues with no intramolecular disulfide bridges and/or with the substitution of one or more amino acids at position 7 and/or 21 were synthesized. Oxidation of the Met7 or formylation of the indole moeity of the Trp21 did not affect the biologic activity of ET-1 on the trachea. Acetamidomethylation of the Cys1-15 decreased the potency and intrinsic activity, but not as much as had been reported on vascular preparations. However, modifications involving one or both disulfide bridges, combined with formylation of the Trp21, yielded analogues with very weak contractile activity. These findings, when compared with the biologic activity of ET-1 analogues in other assay systems, suggest that a different population of receptors, probably non-ETA (i.e., an ETB subtype different from the one reported to be involved in ET-1-induced binding or activities in rabbit pulmonary artery or in rat cerebellum or vasculature) is present and responsible for ET-1-induced bronchoconstriction on the GPT.

Amino Acid Sequence↗
PubMed1993

Management of hyperphosphatemia in patients with renal failure.

Phosphate retention plays a major role in the pathogenesis of hyperparathyroidism at all stages of renal insufficiency. Dietary phosphate restriction is mandatory only for adults and is not advised for children because of the recommended diet allowance. Dietary restriction is usually not sufficient, and phosphate binders are almost always necessary when the glomerular filtration rate falls below 40 mL/min. Because long-term administration of aluminum phosphate binders is associated with risk of aluminum intoxication despite the use of so-called "safe doses", alternative phosphate binders should be used. Magnesium hydroxide and carbonate can be used only for dialysis patients because a low dialysate magnesium concentration is necessary to prevent the hazards of hypermagnesemia. Therefore, the major alternative is the use of alkaline salts of calcium. The most recently proposed salt, acetate, has a higher phosphate-binding capacity than carbonate but exposes patients to the same incidence of hypercalcemia despite the use of half the dose of elemental calcium. These salts should be taken with meals in order to complex more dietary phosphate and decrease calcium absorption and therefore the risk of hypercalcemia. Oral calcium alone, without 1 alpha OH-vitamin D3 derivatives, can prevent hyperphosphatemia and hyperparathyroidism in most uremic patients before dialysis and in about half of the patients dialyzed with a dialysate calcium of 1.5 to 1.65 mmol/L. 1 alpha OH-vitamin D3 derivatives, which increase intestinal absorption of phosphate, should be used only when hyperphosphatemia has been prevented by oral calcium and diet and when plasma parathyroid hormone levels increase above three times the upper limit of normal. To decrease hypercalcemic risk, patients should be given 1 alpha OH-vitamin D3 derivatives, preferably at night, as an intermittent bolus (intravenous or oral). In dialysis patients, the dialysate concentration of calcium may have to be further decreased in order to prevent hypercalcemia when high doses of oral calcium are necessary to control hyperphosphatemia.

Adult↗
PubMed1993

Neuroanatomical and physiological evidence for the involvement of pituitary adenylate cyclase-activating polypeptide in the regulation of the distal lobe of the frog pituitary.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a 38 amino-acid peptide which belongs to the glucagon/secretin/vasoactive intestinal peptide superfamily. The sequence of PACAP is identical in all mammalian species studied so far but frog PACAP differs by one amino-acid from mammalian PACAP. The aim of the present study was to investigate the presence of PACAP in the hypothalamo-pituitary complex of the frog Rana ribibunda and to determine the biological activity of frog PACAP on homologous pituitary cells. The distribution of PACAP-containing neurons and fibers was examined by the indirect immunofluorescence method using an antiserum raised against the N-terminal region of the peptide. In the hypothalamus, PACAP-immunoreactive perikarya were localized in the preoptic nucleus and the dorsal and ventral infundibular nuclei. Beaded nerve fibers were observed coursing from the ventral infundibular nucleus to the external vascular layer of the median eminence. A dense network of immunoreactive axons terminated in the vicinity of the capillaries of the hypophysial portal system. The neurointermediate lobe and the distal lobe of the pituitary were devoid of immunoreactive elements. The amount of PACAP-like immunoreactive material in hypothalamus extracts was measured by radioimmunoassay; the apparent concentration of PACAP was 4.5 ng/mg protein. Synthetic frog PACAP38 and PACAP27 induced a similar dose-dependent stimulation of cAMP production in isolated frog distal lobe pituitary fragments (ED50 = 2 x 10(-8) M). At the maximum dose tested (5 x 10(-6) M), both frog PACAP38 and PACAP27 produced a 4-fold increase in cAMP production.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Enhancement by endothelin-1 of microvascular permeability via the activation of ETA receptors.

1. The objective of the present experiments was to assess the involvement of endothelin-A (ETA) receptors in mediating the effects of endothelin-1 on microvascular permeability in conscious rats. 2. Bolus injection of endothelin-1 (0.1 and 1 nmol kg-1, i.v.) resulted in a dose-dependent prolonged pressor effect preceded by a transient depressor response. These changes were accompanied by a dose-dependent loss of plasma volume. Endothelin-1 (1 nmol kg-1) enhanced the vascular permeability of the upper and lower bronchi, kidney, stomach, duodenum and spleen (up to 270%) as measured by the extravasation of Evans blue dye. 3. Pretreatment of the animals with the selective ETA receptor antagonist, BQ-123 (1 mg kg-1, i.v.) significantly blunted the pressor response to endothelin-1 without affecting the depressor response. BQ-123 inhibited by 87% the endothelin-1 (1 nmol kg-1)-induced plasma volume loss. BQ-123 markedly attenuated protein extravasation elicited by endothelin-1 in the upper and lower bronchi and kidney, whereas it completely inhibited the permeability effect of endothelin-1 in the stomach and duodenum. BQ-123 by itself had no significant effect on the parameters studied. 4. The endothelin-1 analogue, [Trp(For)21]-endothelin-1, in which Trp21 is formylated, was as potent a pressor agent as endothelin-1, but had no depressor action. Bolus injection of [Trp(For)21]-endothelin-1 (0.1 and 1 nmol kg-1, i.v.) evoked similar plasma volume losses to those observed following administration of equimolar doses of endothelin-1. Furthermore, 1 nmol kg-1 [Trp(For)21]-endothelin-l evoked increases in protein extravasation similar to endothelin-l, 1 nmol kg-1.5. The present findings suggest that endothelin- 1 enhances microvascular permeability, in part, via the activation of ETA receptors.

Amino Acid Sequence↗
PubMed1993

Antagonism of the inhibitory action of neuropeptide Y (NPY) in guinea-pig trachea by the C-terminal fragment NPY (2-36).

The C-terminal fragment of neuropeptide Y (NPY), NPY(2-36) was used as a means of discriminating between two differently located NPY receptor sites in guinea-pig trachea. Both NPY and NPY(2-36) reduced the maximal relaxation elicited by vasoactive intestinal peptide (VIP). In contrast, the C-terminal fragment did not mimic the inhibitory action of NPY on the noradrenaline-(NA) evoked response. However, pretreatment of the trachea with 30 nM NPY(2-36), 5 min before generating NA and VIP concentration-response curves in the presence of NPY, abolished the inhibitory effect of NPY on NA-elicited response but did not affect the modulatory action of NPY on VIP-induced relaxation. These results suggest that the two differently located NPY receptor sites in guinea-pig trachea are of two distinct subpopulations.

Animals↗
PubMed1993

Vascular responses to endothelin-1 following inhibition of nitric oxide synthesis in the conscious rat.

1. The objectives of the present experiments were to assess the role of endogenous nitric oxide (NO) in mediating and/or modulating the effects of endothelin-1 (ET-1) on blood pressure and microvascular permeability in conscious rats. 2. Intravenous administration of the NO synthesis inhibitors, NG-monomethyl-L-arginine (L-NMMA) or NG-nitro-L-arginine methyl ester (L-NAME) at a dose (25 mg kg-1 or 2 mg kg-1, respectively) which evoked maximum increase in mean arterial blood pressure (MABP) significantly attenuated (by about 40%) the vasodepressor response and potentiated (by 100-180%) the pressor response to ET-1 (1 nmol kg-1, i.v.) compared to the effects of ET-1 in animals where the peripheral vasoconstrictor effects of L-arginine analogues were mimicked by an infusion of noradrenaline (620-820 ng kg-1 min-1). Similar inhibition of the depressor and potentiation of the pressor actions of ET-1 were observed when the MABP which had been elevated by L-NMMA or L-NAME was titrated to normotensive levels with hydralazine or diazoxide before injection of ET-1. 3. L-NAME (2 mg kg-1) increased the vascular permeability of the large airways, stomach, duodenum, pancreas, liver, kidney and spleen (up to 280%) as measured by the extravasation of Evans blue dye. The permeability of pulmonary parenchyma, skeletal muscle and skin was not affected significantly by L-NAME treatment. Elevation of MABP by noradrenaline infusion did not evoke protein extravasation in the vascular beds studied with the exception of the lung. In the large airways, tissue Evans blue content was similar following noradrenaline infusion and L-NAME.4. Both the pressor and permeability effects of L-NAME (2 mg kg-1) were effectively reversed by L-arginine (300 mg kg- 1) but not by D-arginine (300 mg kg-1 ). The D-enantiomer of L-NAME, D-NAME(2 mg kg-1) had no effect on the parameters studied.5. Protein extravasation was significantly enhanced by ET-1 (1 nmol kg-1) in the upper and lower bronchi, stomach, duodenum, kidney and spleen (up to 285%). This was potentiated by L-NAME(2 mg kg-1), resulting in marked increases in tissue Evans blue accumulation (up to 550%) in these tissues. The effects of L-NAME and ET-1 were additive in the trachea, duodenum, pancreas and liver.Combined administration of L-NAME plus ET-1 significantly increased protein extravasation in the pulmonary parenchyma, where neither L-NAME nor ET-1 alone caused significant increases.6. Noradrenaline infusion (620-820 ng kg-1 min-1) potentiated the permeability action of ET-1(1 nmol kg-1) in the pulmonary circulation, whereas it did not modify ET-1-induced protein extravasation in the other vascular beds.7. These results indicate that endogenous NO mediates, in part, the vasodepressor effect and attenuates the vasopressor action of ET-1 and modulates the effects of ET-1 on vascular permeability. These findings confirm the role of NO in the maintenance of blood pressure and suggest an important role for NO in the regulation of microvascular permeability.

Animals↗
PubMed1993

Long-term (6 months) cross-over comparison of calcium acetate with calcium carbonate as phosphate binder.

A previous short-term study of 10 weeks in 8 patients had shown us that with half the dose of elemental calcium, calcium acetate (CaAc) could control predialysis plasma phosphate (PPO4) as well as calcium carbonate (CaCO3) but that the incidence of hypercalcemia was not decreased. To better appreciate the value of CaAc in comparison to CaCO3, CaAc was given to 28 patients on chronic hemodialysis (6 men, 22 women, age 61 +/- 14 years; dialyzate Ca:1.5 mmol/l) for 6 months to replace CaCO3 at half the dose of elemental calcium (1,235 +/- 521 versus 2,375 +/- 1,470 mg/day). Because of gastrointestinal intolerance, CaAc had to be discontinued in 5 patients after 1-5 months. Magnesium hydroxide [Mg(OH)2] given in 18 of them in association with CaCO3 was discontinued and reintroduced in 6 patients in order to keep PPO4 < 2 mmol/l. Mean dosage of Mg(OH)2 was 2.09 +/- 1.4 g/day with CaCO3 and 0.9 +/- 0.5 with CaAc. Predialysis plasma concentrations of calcium and phosphate were monitored weekly during the 3 months of the control period under CaCO3 and during the 6-month administration of CaAc. Plasma calcium (PCa) was comparable with the 2 treatments (2.47 +/- 0.11 vs. 2.5 +/- 0.10 mmol/l), but PPO4 was significantly lower with CaAc (1.82 +/- 0.26 vs. 1.73 +/- 0.23 mmol/l). Plasma alkaline phosphatase remained constant (122 +/- 66 vs. 122 +/- 70; normal < 170 UI/l) as well as plasma intact PTH (121 +/- 153 vs. 121 +/- 146; normal < 54 pg/ml) and plasma aluminum (0.34 +/- 0.23 vs. 0.32 +/- 0.20 mumol/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1993

Natriuretic and vasoactive hormones and glomerular hyperfiltration in hyperglycaemic type 2 diabetic patients: effect of insulin treatment.

Evidence that an increase in plasma atrial natriuretic peptide (ANP) concentrations mediates, at least in part, glomerular hyperfiltration in diabetic rats prompted us to study the relationship between ANP and renal haemodynamics in hyperfiltering type 2 diabetic patients in association with other hormones implicated in the control of glomerular filtration rate (GFR) (catecholamines, vasopressin, renin) and in sodium tubular transport (aldosterone, ouabain-displacing factor, ODF). Since hyperglycaemia is also associated to hyperfiltration, diabetic patients who presented with secondary drug failure were studied both in hyperglycaemic and in normoglycaemic condition. For this purpose, 11 normotensive non-macroproteinuric hyperfiltering patients with type 2 diabetes were treated with an 8-day continuous insulin infusion (days 0-7). Dehydration was prevented or corrected and natriuresis was on day 0 above 100 mmol/day. The following parameters were determined on days 0 and 7: GFR and renal plasma flow (RPF) by 99mTc-DTPA and 131I-hippuran clearances; the extracellular volume, assimilated to the DTPA diffusion volume; urinary ODF by receptor-binding assay and urinary as well as plasma catecholamines by HPLC after extraction on alumin. Plasma ANP and antidiuretic hormone (ADH) were measured by radioimmunoassay after extraction on phenyl-silylsilica (ANP) and with ether (ADH). Unextracted plasma was used for radioimmunological measurement of plasma renin activity and aldosterone. When correcting hyperglycaemia to normoglycaemia GFR decreased from high to normal mean value (138 +/- 27 and 115 +/- 6 ml/min, p < 0.001), RPF followed the same trend, and the DTPA diffusion volume did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

The long QT syndrome in children. An international study of 287 patients.

BACKGROUND: The Pediatric Electrophysiology Society studied children with the long QT syndrome (LQTS) to describe the features of LQTS in patients less than 21 years old, define potential "low-risk" and "high-risk" subpopulations, and determine optimal treatment. METHODS AND RESULTS: Patients less than 21 years old were included if either QTc was more than 0.44; they had unexplained syncope, seizures, or cardiac arrest preceded by emotion or exercise; or family history of LQTS. We found 287 patients from 26 centers in seven countries. Mean +/- SD age at presentation was 6.8 +/- 5.6; 9% presented with cardiac arrest, 26% with syncope, and 10% with seizures. Of those with symptoms, 67% had symptoms related to exercise. Family history was positive for long QT interval in 39% and for sudden death in 31%. Hearing loss was present in 4.5%. A normal QTc was present in 6%, and QTc of more than 0.60 was in 13%. Atrioventricular block occurred in 5%, but 13 of 15 patients had second-degree atrioventricular block (2:1), and only two of 287 had complete atrioventricular block. Ventricular arrhythmias were found on 16% of initial routine ECGs: 4% uniform premature ventricular contractions, 5% multiform premature ventricular contractions, 1% monomorphic ventricular tachycardia, and 6% torsade de pointes. Overall, treatment was effective for symptoms in 76% and for ventricular arrhythmias in 60%. There was no difference between propranolol and other beta-blockers in effective treatment. Left stellectomy was performed in nine patients, and defibrillators were implanted in four; no sudden death occurred in these 13 patients. In follow-up (duration, 5.0 +/- 4 years; age, 10.9 +/- 6.3 years), 5% had cardiac arrest, 4% had syncope, and 1% had seizures. The two multivariate predictors of symptoms at follow-up were symptoms at presentation and propranolol failure. Sudden death occurred in 8%; multivariate predictors of sudden death were length of QTc at presentation of more than 0.60 and medication noncompliance. CONCLUSIONS: The appearance of 2:1 atrioventricular block, multiform premature ventricular contractions, and torsade de pointes are relatively more common in children with LQTS than other children and should raise the index of suspicion for LQTS. Because 9% of patients presented with cardiac arrest and no preceding symptoms, perhaps prophylactic treatment in asymptomatic children is indicated. Asymptomatic patients with normal QTc and positive family history may be a low-risk group. Patients with QTc of more than 0.60 are at particularly high risk for sudden death, and if treatment is not effective, consideration should be given to cardiac sympathetic denervation, pacemaker implantation, and perhaps implantation of a defibrillator.

Adrenergic beta-Antagonists↗
PubMed1993

Localization, characterization and activity of pituitary adenylate cyclase-activating polypeptide in the frog adrenal gland.

Pituitary adenylate cyclase-activating polypeptide (PACAP) has recently been isolated from the frog brain and the sequence of the peptide appears to be strikingly similar to that of mammalian PACAP. In the present study, we have investigated the localization of PACAP in the frog interrenal (adrenal) gland by immunocytochemistry using antisera directed against PACAP 38 or PACAP 27. Two types of PACAP-immunoreactive fibres were observed: thick varicose fibres coursing between adrenal cells and thin processes located in the walls of blood vessels irrigating the gland. Bilateral transection of the splanchnic nerves did not affect the intensity and distribution of PACAP immunoreactivity. The mean +/- S.E.M. concentration of PACAP, measured by radioimmunoassay in crude adrenal extracts, was 0.65 +/- 0.16 nmol/g wet tissue. Two molecular forms of PACAP in the adrenal gland were characterized by reversed phase high-performance liquid chromatography combined with radioimmunoassay quantification. The elution profiles revealed the existence of two peaks exhibiting the same retention times as synthetic frog PACAP 38 (fPACAP 38) and PACAP 27, the predominant form being PACAP 38. The possible involvement of PACAP in the regulation of adrenal steroidogenesis was investigated in vitro using a perifusion system for frog adrenal slices. Graded doses of fPACAP 38 (0.1-10 mumol/l) increased the secretion of both corticosterone and aldosterone in a dose-dependent manner. Administration of repeated pulses of fPACAP 38 (1 mumol/l), at 120-min intervals, led to a reproducible stimulation of corticosteroid secretion without any tachyphylaxis. Prolonged infusion (2 h) of the peptide induced a rapid increase in corticosterone and aldosterone output, followed by a gradual decline in the secretion rate, suggesting the occurrence of a desensitization phenomenon. Synthetic porcine vasoactive intestinal peptide, which is structurally related to PACAP, was about ten times less potent than fPACAP 38 in stimulating steroidogenesis while the [Des-His1]-fPACAP 38 analogue was 100 times less effective. These results demonstrate that a peptide closely related to fPACAP 38 is present in fibres innervating the frog adrenal gland and could participate in the regulation of corticosteroid secretion, particularly during neurogenic stress.

Adrenal Glands↗
PubMed1993

[Clinical value of studying hematuria using phase-contrast microscopy].

To evaluate the examination of urine erythrocytes with a contrast phase microscope for the etiological diagnosis of haematuria (erythrocytes > 10/mm3 of non centrifuged urine) the charts of 84 patients with haematuria were reviewed. A nephrological origin had been established with certainty in 56 cases with a renal biopsy and an urological origin was also established with certainty in 28 cases thanks to appropriate radiological, endoscopical and pathological examinations. The morphological criteria of the erythrocytes deformation were those of Birch and Fairley but the quantitative criteria of these authors (either 80 or 100%) were found to be of no value. By successive approaches the threshold of 20% of deformed erythrocytes was selected and found to be the best criterion for diagnosing glomerular hematuria: the sensitivity of the test is then 73% and its specificity 60%. As these results were relatively modest, conditions which decrease the percentage of deformed erythrocytes were excluded to improve the sensitivity, such as macroscopic haematuria and also examinations made during the 6 hours following furosemide administration whereas conditions which increase the percentage of deformed erythrocytes and which are easily diagnosed such as urinary infections, lithiasis and renal insufficiency associated with an uropathy were excluded in order to improve the specificity. Then the examination has a sensitivity and a specificity of 90% which makes it clinically relevant, authorizing a wait and see attitude in case there is an isolated microscopic haematuria of glomerular type.

Diagnosis, Differential↗
PubMed1993

[Percutaneous aortic valvuloplasty in children, non invasive evaluation and criteria of success].

The results of percutaneous aortic valvuloplasty in 15 children (average 8.4 years) were evaluated by echocardiography and non-invasive criteria of the indication of this procedure were defined. The aortic valve was unthickened in 7 patients (Group I) and dystrophic in the other 8 (Group II). Valvuloplasty decreased the transvalvular pressure gradient by 47 +/- 33%. Aortic regurgitation was aggravated in 4 patients. The reduction in pressure gradient was significantly greater in Group I than in Group II (64 +/- 19% vs 31 +/- 35%, p < 0.05). In Group I, in contrast to Group II, the results remained stable after an average follow-up of 14.5 months. When the maximal instantaneous pressure gradient on Doppler examination was < 80 mmHg, the peak-to-peak gradient at catheterisation was on average 21% less, whereas when the Doppler gradient was 80 mmHg or more, the percentage difference was only 8%. The myocardial mass index was over the 95th percentile in 7/8 patients with gradients > 80 mmHg whilst it was only increased in 1 patient with a gradient < 80 mmHg. Electrocardiographic LVH was observed in 6 of the 8 patients with a gradient > 80 mmHg but in none of the others. Although valvuloplasty reduced the transvalvular pressure gradient, the results were much less satisfactory in the dystrophic valves. The following indications were proposed for this techniques: a Doppler maximal pressure gradient > or = 80 mmHg, associated with at least one criterion of left ventricular hypertrophy.

Adolescent↗
PubMed1993

Evidence for in vivo interactions between neuropeptide Y-related peptides and sigma receptors in the mouse hippocampal formation.

Recently, it was proposed that neuropeptide Y (NPY) and peptide YY (PYY) could act as endogenous ligands for sigma binding sites, as both NPY and PYY competed with high affinity (nanomolar) for 3H-(+)SKF 10,047 binding sites in rat brain membrane homogenates (Roman et al., 1989). However, various laboratories failed to replicate these in vitro findings. In order to clarify this apparent discrepancy and investigate further possible interactions between NPY and sigma related sites, we evaluated the effects of NPY, PYY and homologs, as well as nonrelated peptides, on in vivo 3H-(+)SKF 10,047 binding parameters in the mouse hippocampal formation. As expected, haloperidol (2 mg/kg), a prototypical sigma receptor ligand, competed for 90% of in vivo hippocampal labeling observed following a peripheral intravenous injection of 3H-(+)SKF 10,047. Intracerebroventricular injections of 300-3000 pmol of either NPY, PYY, NPY2-36, or the Y1 agonist Leu31,Pro34-NPY inhibited significant proportions (17-35%) of haloperidol-sensitive in vivo 3H-(+)SKF 10,047 hippocampal labeling. However, a Y2 receptor agonist, NPY13-36, and nonrelated peptides such as neurotensin and vasoactive intestinal polypeptide, as well as adrenalin, failed to alter in vivo 3H-(+)SKF 10,047 hippocampal binding. It thus appears that NPY, PYY, and a selective Y1 agonist can interact in a concentration-dependent manner, with in vivo 3H-(+)SKF 10,047 labeling in the mouse hippocampal formation. This effect demonstrates selectivity as a Y2 agonist, unrelated peptides, and adrenalin failed to alter in vivo sigma labeling. This in vivo interaction may be relevant to some of the respective biological actions of NPY and sigma-related molecules.

Animals↗