[Electrophysiologic and hemodynamic effects of intravenous aminophylline in humans].
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Adult↗
Biomedical subjects
C Bianchi
Publications and source records attributed to C Bianchi.
[A case of retropharyngeal abscess of atypical presentation].
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Abscess↗
[Kaposi's sarcoma in the Monfalcone area].
The Monfalcone area (Italy) is a small industrial territory (60,000 inhabitants), characterized by a high incidence of asbestos-related diseases. In a review of the biopsy and necropsy records collected at the Monfalcone Hospital during the period October 1979-September 1985 two cases of Kaposi's sarcoma were found. Of the two patients one was resident out of the Monfalcone area; the second was already affected by the disease, when he came to this country. The present data suggest that Kaposi's sarcoma is a rare condition in Monfalcone territory.
Aged↗
[Hemoperitoneum in the 5th month of pregnancy].
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Adult↗
Asbestos exposure and Alzheimer disease.
10 cases in which an asbestos-related disease (malignant pleural mesothelioma or asbestosis) was associated with severe Alzheimer type lesions in the brain are reported. The patients, all males aged between 67 and 78 years, had been occupationally exposed to asbestos in the shipbuilding industry. The hypothesis that asbestos is a favoring factor in the genesis of Alzheimer disease is discussed.
Aged↗
The influence of 5-hydroxytryptamine on the release of acetylcholine from guinea-pig brain ex vivo and in vitro.
The effect of 5-hydroxytryptamine (5-HT) on the release of acetylcholine (ACh) from the brain of the guinea-pig was investigated in order to determine whether this amine plays a modulatory role on the cortical cholinergic projections. 5-Hydroxytryptamine (0.2-1 mumol), injected intracerebroventricularly (i.c.v.), caused mild excitation, stereotyped movements and ataxia. Simultaneously, it increased the output of ACh from the cortex in a dose-dependent manner. Methysergide (4.2 mumol Kg-1 i.p.) also increased the output of ACh by about 60-80%, but prevented the effect of 5-HT (1 mumol i.c.v.). Metitepine (1-4.2 mumol kg-1 i.p.) increased the output of ACh like methysergide but it changed the facilitation of the release of ACh by 5-HT into inhibition. At the same time the animals became hypothermic, sedated and their electroencephalogram (EEG) was synchronized. Pretreatment with 5,7-HT blocked the increase in release of ACh produced by 5-HT (1 mumol). D-Norfenfluramine (10.4 mumol kg-1) was ineffective alone but reduced the release of ACh in metitepine-pretreated animals. 5-Hydroxytryptamine (10-30 microM) did not affect the efflux of [3H]choline from electrically-stimulated slices of cerebral cortex. The increase in the release of ACh caused by 5-HT, abolished by pretreatment with methysergide and 5,7-HT, may be explained by activation of 5-HT autoreceptors, while the increase of transmitter outflow induced by methysergide may be due to a blockade of 5-HT receptors present on the cholinergic neurones. Metitepine appeared to unmask the tryptaminergic inhibition caused by injection of 5-HT intraventricularly or by the 5-HT-releasing drug, D-norfenfluramine, possibly by acting on the autoreceptors and preventing auto-inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)
5,7-Dihydroxytryptamine↗
Effects of chronic morphine treatment on opioid-induced inhibition and facilitation of acetylcholine release in guinea-pig thalamic slices.
The effect of chronic morphine treatment on acetylcholine (ACh) release from guinea-pig thalamic slices and on [3H]-dihydro-morphine binding to the brain of normal, tolerant and abstinent guinea-pigs was studied. Morphine (30 microM) inhibited the electrically-evoked ACh release to the same extent in normal and tolerant slices. This effect was antagonized by naloxone. Morphine (30 microM) in the presence of naloxone (10 microM) facilitated electrically-evoked release of ACh. This effect displayed tachyphylaxis in normal slices and was absent in the brain taken from tolerant animals. The reduction of [Ca++] in the medium increased the facilitatory response in normal slices and the inhibitory response in normal and tolerant tissue. The high and low affinity binding sites to [3H]-dihydro-morphine were the same in the thalami, caudate nuclei and cortices of normal, tolerant and abstinent animals. It is concluded that the cholinergic structures of the guinea-pig thalamus are unlikely to be involved in morphine tolerance. In fact, the facilitation appears to be an ancillary phenomenon which quickly displays tachyphylaxis in normal tissue while the inhibition of ACh release remains unchanged.
Acetylcholine↗
Cortical acetylcholine release is increased and gamma-aminobutyric acid outflow is reduced during morphine withdrawal.
The effects of naloxone on acetylcholine (ACh) and gamma-aminobutyric acid (GABA) outflow from the cerebral cortex of freely moving, morphine-dependent guinea-pigs was studied. The cortical efflux of ACh in chronically-treated guinea-pigs was about half of that of normal animals. GABA efflux was unaffected. During opioid withdrawal precipitated by naloxone (0.1-10 mg kg-1, i.p.) the guinea-pigs showed jumping, hyperactivity and wet dog shakes, the intensity of which was directly related to the dose of naloxone. The withdrawal syndrome was accompanied by a dose-dependent increase in ACh release and reduction in GABA outflow; ACh release was increased by naloxone at doses lower (0.1-3 mg kg-1) than those acting on GABA efflux (1-10 mg kg-1). Atropine (10 mg kg-1) and diazepam (5 mg kg-1) did not prevent GABA and ACh changes.
Acetylcholine↗
Distinct localization of atrial natriuretic factor and angiotensin II binding sites in the glomerulus.
A comparative study of the localization of 125I-labeled atrial natriuretic factor (ANF) and 125I-labeled angiotensin II (ANG II) binding sites in the glomerulus of the rat, after an intravascular injection, has been done by ultrastructural radioautography. 125I-ANF binding sites are localized predominantly on the podocytes of the visceral epithelium (63%) followed by the endothelium of capillaries (14%), the parietal epithelium (13%), and finally mesangial cells (10%). In a comparative study, it was confirmed that 125I-ANG II uptake is localized predominantly on mesangial cells (60%) followed by epithelial visceral cells (23%) and the endothelium of capillaries (16%). Using isolated rat glomeruli, it was confirmed that ANG II decreases glomerular size (maximum effect of 15%) with an apparent half maximum effective concentration (EC50) between 10(-9) and 10(-8) M. Although ANF alone has no apparent effect on glomerular size, it inhibits the contractile effect of ANG II with a half maximum inhibitory concentration (IC50) between 10(-11) and 10(-10) M. These results suggest that an intraglomerular mechanism other than glomerular arteriolar resistance may be involved in the modulation of glomerular filtration rate by ANF. The presence of 125I-ANF uptake mainly in foot processes of visceral epithelial cells of glomeruli in vivo and the inhibition of ANG II decrease in glomerular size by ANF in vitro raise the possibility that ANF may regulate the ultrafiltration coefficient by two mechanisms: modulation of glomerular permeability, and surface area.
Angiotensin II↗
Radioautographic localization of 125I-atrial natriuretic factor binding sites in the brain.
Rats were injected through the carotid artery (cephalad direction) with 18.9 mu Ci of either 125I-Arg 101-Tyr 126 atrial natriuretic factor alone or together with an excess of unlabeled hormone. At 2 min after injection, all rats were fixed in vivo by perfusion and serial sections of the whole brain were processed for light microscope radioautography. The radioautographic reaction produced by 125I-atrial natriuretic factor alone was localized in all circumventricular organs (except the subcommissural organ), the smooth muscle cells and endothelial cells of arteries, arterioles, veins, venules, the endothelial cells of intraparenchymal capillaries and the epithelial cells of the choroid plexus. In rats which received 125I-atrial natriuretic factor plus an excess of unlabeled hormone, the radioautographic reaction was reduced by 70-90%. Binding sites are thus localized in regions of the brain, some of them involved in the central monitoring of blood pressure and osmolarity. In addition, the presence of binding sites in the cerebral vasculature and in the epithelium of the choroid plexus suggests that circulating ANF may play a role in the control of cerebral blood flow and in the production of vertebrospinal fluid.
Animals↗
Fate of [125I]angiotensin II in adrenal zona glomerulosa cells.
Binding and internalization of [125I]angiotensin II (AII) were studied by morphological and biochemical methods in rats in vivo. Light microscope radioautography demonstrated that [125I]AII binds specifically to adrenal zona glomerulosa (ZG) cells. Ultrastructural radioautographic analysis revealed that [125I]AII binds to the cell surface, clusters in coated pits, is internalized in coated vesicles, and is transported by receptosomes to lysosomes in less than 20 min. Biochemical analysis revealed that as much as 40% of the adrenal radioactive uptake behaves as native [125I]AII as shown by electrophoresis, immunoprecipitation and radioligand binding studies. These results indicate that the effects of AII on the secretion of aldosterone by ZG cells are mediated by cell surface phenomena and not by binding to intracellular organelles involved in steroidogenesis. They also indicate that the half-life of AII bound to receptors and internalized seems to be much longer (min) than in the systemic circulation (sec).
Adrenal Cortex↗
Internalization and lysosomal association of [125I]angiotensin II in norepinephrine-containing cells of the rat adrenal medulla.
The morphological localization of [125I]angiotensin II (AII) in the rat adrenal medulla (AM) was studied by light- and electron-microscopic radioautography in vivo. With light microscopy the presence of binding sites for AII in both norepinephrine-containing (NE) and epinephrine-containing (E) cells was confirmed. With electron microscopy, it was found that AII binds to the cell surface of NE cells, is progressively internalized, and is associated with lysosomes and Golgi complex within 20 min, whereas in E cells AII seems to be internalized earlier and recycled back to the cell surface within 5 min without any appreciable association with intracellular organelles. These results suggest different intracellular pathways for AII in NE and E cells of the rat AM.
Adrenal Medulla↗
Localization and characterization of specific receptors for atrial natriuretic factor in the ciliary processes of the eye.
By light and electron microscope radioautography in vivo, competitive binding sites for 125I-Arg 101-Tyr 126 atrial natriuretic factor were localized mostly on the "pigmented" epithelium of the rat ciliary process. Further investigation using isolated ciliary processes from rabbits demonstrated the presence of specific receptors for 125I-atrial natriuretic factor. In addition, synthetic atrial natriuretic factor inhibited basal and stimulated adenylate cyclase activity. These results demonstrate for the first time the presence of specific receptors for atrial natriuretic factor in the ciliary processes which are negatively coupled to adenylate cyclase. The possible role of this peptide in the control of intraocular pressure is suggested.
Adenylyl Cyclases↗
Noradrenergic modulation of cortical acetylcholine release is both direct and gamma-aminobutyric acid-mediated.
The effect of norepinephrine (NE) on the outflow of gamma-aminobutyric acid (GABA) as well as the influence of endogenous GABA on NE-induced inhibition of acetylcholine (ACh) release have been investigated in guinea-pig cortical slices, in order to clarify the role of this amino acid in the noradrenergic control of the cholinergic signal. NE in the range of 9 to 30 microM increased GABA outflow from unstimulated slices, doubling it at 30 microM. This effect was antagonized by prazosin (0.1 microM) and by tetrodotoxin (0.5 microM), suggesting an involvement of alpha-1 receptors and of sodium-dependent mechanisms. 2,4-diaminobutyric acid (DABA), an inhibitor of neuronal GABA uptake, at 60 microM steadily doubled the amino acid outflow without affecting ACh release However, DABA increased the GABA-induced inhibition of electrically evoked ACh release by a factor of about 10 and the NE-induced inhibition by a factor of 2.8. Prazosin (1 microM) reduced the effects of NE (60 microM) on the spontaneous and evoked ACh release in normal slices and the effects of NE (30 microM) in DABA-treated slices. Thus, an alpha-1 GABA-mediated component of NE influence on ACh can be demonstrated even in vitro (beside the well-known alpha-2 direct inhibition), provided high NE concentrations are used or the GABA availability is enhanced. On the other hand, bicuculline and picrotoxin antagonized not only GABA but also NE, whereas yohimbine counteracted not only NE but also GABA inhibition of ACh release, suggesting a close assembly of alpha-2 and GABAA receptors on the cholinergic axons.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholine↗
The effect of nicotine and cytisine on 3H-acetylcholine release from cortical slices of guinea-pig brain.
Nicotine 1.8 X 10(-5)-1.8 X 10(-4) mol/l enhanced the spontaneous 3H-efflux from guinea-pig cortical slices preloaded with 3H-choline and perfused in the presence of hemicholinium (HC-3). The facilitation of tritium outflow was prevented by tetrodotoxin 5 X 10(-7) mol/l and by D-tubocurarine 4.5 X 10(-6) mol/l. Nicotine 1.8 X 10(-6)-1.8 X 10(-4) mol/l, and the agonist cytisine 5 X 10(-7)-5 X 10(-5) mol/l increased, in a concentration-dependent way, 3H-efflux from electrically-stimulated slices (0.2 Hz). The concentration-response curves of both drugs were parallelly shifted to the right by D-tubocurarine 4.5 X 10(-6) mol/l. The EC50 values (i.e. the concentrations required to cause a 50% increase in the S2/S1 ratio) changed for nicotine from 5.58 X 10(-5) to 4.34 X 10(-4) and for cytisine from 6.3 X 10(-6) to 2.75 X 10(-4) mol/l in the absence and in the presence of the antagonist, respectively. In the range of 0.2-2 Hz the magnitude of the effect of nicotine was inversely related to the rate of stimulation. The response to nicotine was subject to rapidly developing tachyphylaxis; it was resistant to atropine. It is concluded that nicotine and cytisine facilitate 3H-efflux from the cholinergic nerve endings of guinea-pig cerebral cortex. This effect involves sodium-dependent mechanisms and is due to an interaction of the drugs with receptors showing affinity for D-tubocurarine.
Acetylcholine↗
Radioautographic localization of 125I-atrial natriuretic factor (ANF) in rat tissues.
Rats were injected either with synthetic 125I-Arg 101-Tyr 126 atrial natriuretic factor (ANF) or with 125I-ANF together with an excess of cold Arg 101-Tyr 126 ANF. Binding sites in various tissues were accepted depending on two criteria: displacement of radioactivity by cold ANF and absence of localization of silver grains on putative target cells in the presence of cold ANF. Binding sites were localized on zona glomerulosa cells and on adrenergic and noradrenergic cells of adrenal medulla, on hepatocytes, on the base of mature epithelial cells of villi in the small intestine, on smooth muscle cells of the muscularis layer of the colon and on the base of epithelial cells of the ciliary bodies. In addition, binding sites were localized in the vasculature of kidney, adrenal cortex, lung and liver. Binding sites were particularly numerous on renal glomerular endothelial cells. These results indicate that ANF may have important hemodynamic effects in kidney, lung, liver and adrenal cortex, may regulate water and ion transport in small intestine and ciliary bodies and may have metabolic effects in the liver. The presence of binding sites on the zona glomerulosa is in agreement with the important inhibitory effect of the peptide on aldosterone secretion.
Adrenal Glands↗
The modulation of cortical acetylcholine release by GABA, GABA-like drugs and benzodiazepines in freely moving guinea-pigs.
In order to define the modulatory role played by gamma-aminobutyric acid (GABA) in corticopetal cholinergic projections, the effect of this amino acid and related drugs on gross behaviour, the EEG and the release of acetylcholine (ACh) from the cerebral cortex in freely moving guinea-pigs was studied. gamma Aminobutyric acid, injected intracerebroventricularly (20-50 mumol) induced a three-phase picture: first (5-15 min) behavioural activation and increased release of ACh, then (30-90 min) depression, EEG synchronization and reduced release of ACh, and finally "rebound" stimulation. Ethanolamine-O-sulphate (EOS) injected intraventricularly (28 mumol/kg) or intraperitoneally (14 mmol/kg) reproduced the first two phases of the effects of GABA (i.e. stimulation followed by inhibition), while diazepam (0.7 and 3.5 mumol/kg, i.p.) and flurazepam (32 mumol/kg, i.p.) caused, at first, only depression. Muscimol and 4,5,6,7-tetrahydroisoxazolo(4,5-c)pyridine-3-ol (THIP) injected intraventricularly (in the nmol range) or intraperitoneally (in the mumol range) produced behavioural activation and increased release of ACh; the depressant signs appeared only after very large, toxic doses. Picrotoxin and bicuculline, at sub-convulsive doses, reduced the symptomatology caused by GABA and antagonized the sedation produced by diazepam. Methysergide (8-16 mumol/kg, i.p.) prevented the behavioural activation and the increased release of ACh by GABA, unmasked the depression due to subthreshold doses of diazepam (i.c.v., 7-70 nmol) and reversed the stimulation induced by muscimol into sedation and reduced the outflow of ACh. Pretreatment with 5,7-HT also dampened and shortened the stimulation by muscimol.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholine↗
The effect of morphine on monoamine release and content in guinea-pig brain slices.
The effect of morphine on the efflux of (3H) monoamines as well as the endogenous monoamine contents in electrically stimulated brain slices was investigated. Only at a concentration at high as 30 microM did the drug reduce the tritium efflux and counteracted the monoamine depletion caused by prolonged electrical stimulation. This effect was antagonized by Naloxone 10 microM. Besides the good agreement between the two methods used to evaluate drug effects the discrepancy between morphine concentrations active on the neurosecretory process and those effective in the whole animal is stressed. The opioids may act in vivo either by modulating the firing rate of the monaminergic neurons or by affecting other related neuronal pools.
Animals↗