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Biomedical subjects

C Bianchi

Publications and source records attributed to C Bianchi.

At least 253 records · Page 14Linked to original sources
PubMed1989

Lack of excitatory amino acid-induced effects on calcium fluxes measured with 45Ca2+ in rat cerebral cortex synaptosomes.

Ca2+ uptake was measured in purified rat cerebral cortex synaptosomes (P3 pellets) using 45Ca2+ as a tracer. Ca2+ influx increased in time, and with an increase in external K+ concentration and temperature. The net (external K+-induced, depolarization-dependent) uptake follows a two-component course. The exponential term, due to the opening of voltage-operated calcium channels (VOC), has a rate constant which increases with an increase in the depolarization level (1.04 versus 0.54 nmol/s/mg protein for 50 mM - versus 15 mM [K+]-dependent net influx). The linear term, due to the Na+/Ca2+ exchange system, has a similar rate constant at all depolarization levels (0.16 +/- 0.05 and 0.11 +/- 0.02 nmol/s/mg protein). Excitatory amino acids (glutamate, kainate and n-methyl-d-aspartate-NMDA-) were tested on this preparation at doses ranging between 5 x 10(-5) M and 5 x 10(-3) M and at multiple incubation times, under resting conditions and under two depolarizing conditions (partial depolarization: 15 mM external K+ and maximal depolarization: 50 mM external K+). NMDA was also tested in the absence of Mg2+. No effect was detectable under any of these experimental conditions. Hypotheses to interpret these data are discussed. Further studies on other preparations are needed in order to directly investigate the presynaptic effects of excitatory amino acids.

Amino Acids↗
PubMed1989

Alpha 1-adrenoreceptor-mediated increase in acetylcholine release in brain slices during morphine tolerance.

Norepinephrine, clonidine, and phenylephrine increased the electrically evoked release of endogenous acetylcholine in cortical slices taken from morphine-tolerant guinea pigs. This effect was alpha 1-adrenoreceptor mediated and was opposite to the alpha 2-adrenoreceptor-mediated inhibition of acetylcholine release, normally elicited by norepinephrine and clonidine. In the presence of prazosin, clonidine recovered its normal inhibitory properties, suggesting that morphine tolerance induced the appearance of an alpha 1-adrenoreceptor-mediated response that overshadowed, but did not cancel, the still present alpha 2-adrenoreceptor inhibitory control. The attempt to prove the presence of alpha-adrenoreceptors on the nerve endings by testing the effect of norepinephrine in synaptosomal preparations (preloaded with [3H]choline and depolarized with KCl and veratridine) was unsuccessful. Therefore the problem of the exact location of this excitatory input remains to be solved. These results confirm previous findings reporting the increase in cortical acetylcholine release induced by the alpha-adrenoreceptor agonists in morphine-tolerant, freely moving guinea pigs and demonstrate that opiate tolerance inverts the direction of the noradrenergic modulation even in the isolated intracortical cholinergic structures.

Acetylcholine↗
PubMed1989

Effect of 5-hydroxytryptamine on [3H]-acetylcholine release from guinea-pig striatal slices.

1. The effect of 5-hydroxytryptamine (5-HT) on spontaneous and electrically-evoked tritium efflux was studied in guinea-pig caudate nucleus slices preloaded with [3H]-choline. 2. 5-HT, 10-300 mumol l-1, temporarily increased the spontaneous tritium efflux (as well as the endogenous acetylcholine (ACh) release) and, after 15 min perfusion, inhibited it. The facilitatory effect of 5-HT on spontaneous efflux was increased while the inhibitory effect did not occur in slices taken from dopamine-depleted guinea-pigs. 3. The increase in spontaneous tritium efflux by 5-HT was blocked by methiothepin, methysergide (pA2 8.7) and by the selective 5-HT2 antagonist, ritanserin (pA2 6.7). 4. The inhibition of spontaneous tritium efflux by 5-HT was prevented by methysergide and methiothepin but not by ritanserin and (-)-propranolol. 5. 5-HT, 100 mumol l-1, inhibited the electrically-evoked tritium efflux and this effect was unchanged in dopamine-depleted slices. 6. The inhibition of electrically-evoked tritium efflux by 5-HT was blocked by methiothepin and methysergide but not by (-)-propranolol or ritanserin. 7. These results suggest that 5-HT may exert a rapid and transient (excitatory) and a more prolonged (inhibitory) control over striatal cholinergic neurones.

Acetylcholine↗
PubMed1989

Effect of acute and subchronic nicotine treatment on cortical acetylcholine release and on nicotinic receptors in rats and guinea-pigs.

1. The effect of acute and chronic (16 days) administration of nicotine on cortical acetylcholine (ACh) release, gross behaviour and brain nicotinic binding sites was investigated in rats and guinea-pigs. 2. The drug, injected either subcutaneously (0.45-0.90 mg kg-1) or intracerebroventricularly (1, 3 and 5 micrograms) increased the cortical ACh release, in a dose-dependent manner, through mecamylamine-sensitive receptors for 1-2 h in both species. 3. Chronic treatment significantly increased basal ACh release in the rat and slightly lowered it in the guinea-pig, but the response to a challenging dose of nicotine was proportionally maintained in both species. 4. The number of nicotinic receptors was four times higher in the rat than in the guinea-pig and was not dependent on the radioligand used ([3H]-nicotine or [3H]-ACh, in the presence of atropine) to determine this. The nicotinic binding sites showed an apparent increase in chronically treated rats but no change in guinea-pigs. 5. Tolerance to the inhibitory effect of the drug, assessed with the T maze test, was found in the rat. No apparent change in gross behaviour was detected in the guinea-pig. 6. It is concluded that chronic nicotine treatment causes evident tolerance to its inhibitory effect on behaviour in the rat, but no adaptation to its excitatory properties on the cholinergic brain structures in rats and guinea-pigs.

Acetylcholine↗
PubMed1989

Bowel frequency in healthy children.

Bowel frequency was recorded, on a diary sheet basis, in 662 children from six Italian cities. There is a wide interindividual variability, showing a sharp decrease with age; we report the distribution of the percentiles in the different age groups. Among infants, the breast-fed ones pass significantly more stools than the formula-fed.

Child↗
PubMed1989

Atrial natriuretic factor binding sites in the jejunum.

We have studied the localization and the characterization of atrial natriuretic factor (ANF) binding sites by radioautographic techniques. Quantitative in vitro radioautography with a computerized microdensitometer demonstrated the presence of high-affinity, low-capacity 125I-ANF-(99-126) binding sites (Kd, 48 pM; Bmax, 63 fmol/mg protein) mainly in the villi of 20-microns slide-mounted transverse sections of the rat jejunum. Competition curves showed 50% inhibitory concentrations of 55 and 1,560 pM for ANF-(99-126) and ANF-(103-123), respectively. In vivo electron microscope radioautography showed that 80% of the silver grains were localized on the lamina propria fibroblast-like cells, 18% on mature enterocytes, and 2% on capillaries. Bradykinin and adrenocorticotropin did not compete with ANF binding. These results demonstrate that ANF binding sites in the rat jejunum possess the pharmacological characteristics of functional ANF receptors encountered in other rat tissues, and ultrastructural radioautographs show their cellular distribution. Taken together, these results demonstrate the presence and the localization of specific binding sites for ANF in the jejunal villi of the rat small intestine.

Animals↗
PubMed1989

Atrial natriuretic factor binding sites in experimental congestive heart failure.

A quantitative in vitro autoradiographic study was performed on the aorta, renal glomeruli, and adrenal cortex of cardiomyopathic hamsters in various stages of heart failure and correlated, in some instances, with in vivo autoradiography. The results indicate virtually no correlation between the degree of congestive heart failure and the density of 125I-labeled atrial natriuretic factor [(Ser99, Tyr126)ANF] binding sites (Bmax) in the tissues examined. Whereas the Bmax was increased in the thoracic aorta in moderate and severe heart failure, there were no significant changes in the zona glomerulosa. The renal glomeruli Bmax was lower in mild and moderate heart failure compared with control and severe heart failure. The proportion of ANF B- and C-receptors was also evaluated in sections of the aorta, adrenal, and kidney of control and cardiomyopathic hamsters with severe heart failure. (Arg102, Cys121)ANF [des-(Gln113, Ser114, Gly115, Leu116, Gly117) NH2] (C-ANF) at 10(-6) M displaced approximately 505 of (Ser99, Tyr126)125I-ANF bound in the aorta and renal glomeruli and approximately 20% in the adrenal zona glomerulosa in both series of animals. These results suggest that ANF may exert a buffering effect on the vasoconstriction of heart failure and to a certain extent may inhibit aldosterone secretion. The impairment of renal sodium excretion does not appear to be related to glomerular ANF binding sites at any stage of the disease.

Adrenal Glands↗
PubMed1989

[Efficacy of propylthiouracil in the treatment of amiodarone-induced hyperthyroidism].

Amiodarone is a benzofuranic derivative widely used in cardiologic practice because of its excellent antiarrhythmic properties. Due to its high iodine content, it interferes with thyroid physiology and can cause either hyper or hypothyroidism. Amiodarone-induced hyperthyroidism should be considered as a serious complication since it develops in cardiac patients, the clinical diagnosis can be difficult and because conventional methods of therapy are said to be often ineffective. We analyze the outcome of 10 pts, chronically treated with Amiodarone (16-60 mo, mean 37.6 mo) who develop hyperthyroidism during the antiarrhythmic therapy. All patients had multinodular goiter. Overt clinical picture for thyrotoxicosis was seen in 7 of them and lab tests showed: rT3 = 101.1 +/- 14.9 ng/dl; T3 = 220.2 +/- 25 ng/dl; T4 = 15.6 +/- 1.9 micrograms/dl, TSH = 0.8 +/- 0.2 microU/ml and TRH response 0.0 microU/ml. Thyroid microsomal antibodies were negative in 3 pts studied. After Amiodarone was discontinued, patients were followed-up monthly. In 2, normalization of clinical and laboratory indexes were obtained at 40-60 d and no other medication was given. In the remaining, due to the intensity of clinical manifestations, PTU treatment was started (300 mg/d) After 4 mo, euthyroidism was achieved in 6 and it persisted after discontinuation of PTU has patient failed to respond to PTU, 131I was administered with excellent results. Patients have been followed-up up to 3 years after therapy without observing thyrotoxic relapses nor deterioration of their cardiological condition.2+ conventional therapies (PTU or 131I) have been, very effective.

Adult↗
PubMed1989

Changes in cortical acetylcholine and gamma-aminobutyric acid outflow during morphine withdrawal involve alpha-1 and alpha-2 receptors.

Naloxone (0.3-9 mumol kg-1), electrical stimulation of locus ceruleus or clonidine at low doses (7.5-112 nmol kg-1) increased the release of acetylcholine from the exposed parietal cortex of freely moving, morphine-tolerant guinea pigs. This increase was not additive and was prevented by prazosin (35.8 nmol kg-1), suggesting the involvement of alpha-1 receptors. At high doses (374 nmol kg-1 or more) clonidine inhibited acetylcholine release through alpha-2 receptors, as it did in naive animals at 7.5 nmol kg-1. Clonidine (374 nmol kg-1) and prazosin (35.8 nmol kg-1) reduced the objective signs of naloxone-precipitated withdrawal. Electrical stimulation of the locus ceruleus or naloxone treatment reduced the release of gamma-aminobutyric acid (GABA) from the exposed parietal cortex of morphine-tolerant guinea pigs. This reduction was not additive and was prevented by idazoxan (84 nmol kg-1), suggesting the involvement of alpha-2 receptors. Clonidine (7.5 nmol kg-1), too, reduced the release of GABA in morphine-tolerant animals. However, when tested jointly with naloxone, clonidine (7.5-112 nmol kg-1) induced alpha-1-mediated facilitation of GABA release (like that elicited in naive animals at 112-374 nmol kg-1) leaving the signs of withdrawal unchanged. This points to the stimulation of alpha-1 receptors highly responsive to this agonist (but not to locus ceruleus stimulation) during naloxone-precipitated withdrawal. In conclusion, chronic morphine treatment modifies the alpha-1- and alpha-2-mediated control of GABA and acetylcholine neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1989

[A case of diffuse hemangioma of the placenta].

The paper reports a case of diffuse placental hemangioma leading to intrauterine fetal death. Contrary to other cases reported in the literature, polyhydramnios, oligohydramnios and fetal malformations were not observed. The sole finding was a dilatation of the cardiac auricle, in particular on the right-hand side. It is hypothesised that fetal death was due to two concomitant factors: the severe hypoxemic state and the difficulty of venous drainage from the fetus to the mother owing to increased materno-fetal placental shunts.

Adult↗
PubMed1989

Juvenile nephronophthisis associated with new skeletal abnormalities, tapetoretinal degeneration and liver fibrosis.

This report concerns a boy presenting renal disease with tubulointerstitial nephropathy which suggests familial juvenile nephronophthisis, hepatosplenomegaly due to congenital hepatic fibrosis, tapetoretinal degeneration, probable endocrine involvement and congenital skeletal abnormalities. The associations presented in this paper have not previously been reported.

Abnormalities, Multiple↗
PubMed1989

[Vascular leiomyoblastoma of the liver. A personal case].

A case of vascular leiomyoblastoma of the liver is reported. This rare type of liver tumour is noteworthy for the associated paroxysmal pain attacks which are the first symptom of the disease. It should be considered in the wide range of liver tumours because, although benign, it is potentially malignant.

Hemangioma↗
PubMed1988

Modulation of adriamycin uptake by lonidamine in Ehrlich ascites tumor cells.

The effect of Lonidamine, 1-(2,4 dichlorobenzyl)-1-H-indazol-3-carboxylic acid, on the uptake of Adriamycin by Ehrlich ascites tumor cells has been investigated. The uptake of Adriamycin is greatly stimulated by Lonidamine and the increase depends on the energy sources of the cell. In the presence of glucose the intracellular drug content is remarkably lower than that in its absence. This difference lies in the mechanism by which Lonidamine enhances the uptake of Adriamycin. The Adriamycin efflux is via an active transport process and, in the presence of glucose, both aerobic glycolysis and oxidative phosphorylation contribute to ATP synthesis. Although Lonidamine inhibits both these pathways, there is still sufficient ATP to extrude a certain amount of Adriamycin. The elevated intracellular concentration of Adriamycin depends not only on the Lonidamine-inhibited outward transport but also on higher membrane permeability which allows a low concentration of Adriamycin (18 microM) to interfere also with the oxidative metabolism of Ehrlich ascites tumor cells.

Animals↗
PubMed1988

Effect of ethylketocyclazocine on acetylcholine release in guinea-pig brain slices.

The effect of ethylketocyclazocine (EKC) on 3H-Choline (Ch) efflux and on endogenous acetylcholine (ACh) release from guinea-pig brain slices was studied. The drug inhibited the 3H-Ch efflux at a low concentration (0.1 mumol/l) in thalamus slices, while only at high concentrations (30-100 mumol/l) did EKC induce deep inhibition in the caudate nucleus and slight reduction in the cerebral cortex. Dynorphin (1-13) and morphine (Mo) inhibited the ACh release from thalamus slices as well. Naloxone (Nx) was more effective in antagonizing Mo than EKC. The experiments carried out with the endogenous ACh bioassay technique confirmed the above results. Mr 2266 and Mr 1452, both proposed as preferential k antagonists, per se enhanced 3H-Ch efflux from thalamus slices, while the dextrorotatory isomer Mr 1453, devoid of opioid properties, did not share such action. The role of k-opioid receptors in cholinergic system modulation in the guinea-pig brain is discussed.

Acetylcholine↗