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Biomedical subjects

F Moroni

Publications and source records attributed to F Moroni.

At least 199 records · Page 11Linked to original sources

Inhibition of acetylcholine turnover in rat hippocampus by intraseptal injections of beta-endorphin and morphine.

Intraseptal administration of morphine (70 nmol) or beta-endorphin (0.7 nmol) reduced the rate of acetylcholine (ACh) turnover (TRACh) in rat hippocampus but not in striatum or cortex. These intraseptal injections failed to modify the ACh content and did not elicit analgesia. Naltrexone (15 mumol/kg, i.p.) completely antagonized the decrease of hippocampal TRACh elicited by the two opiate receptor agonists. Furthermore, intraseptal injections of naltrexone partially blocked the decrease in hippocampal TRACh induced by intraperitoneal administration of morphine (70 mumol/kg, i.p.). These data suggest that opiate agonists decrease hippocampal TRACh by regulating septal cholinergic neurons, and that this effect is not associated with analgesia.

Acetylcholine↗

The modulation of histamine release by alpha-adrenoceptors: evidences in murine neoplastic mast cells.

Murine neoplastic mast cells which have been loaded with exogenous labelled histamine, released 14C-histamine when exposed to increasing concentrations of phenylephrine and noradrenaline. Adrenaline was only slightly effective, while isoprenaline and dibutyryl-cyclic-AMP were fully inactive. The release of histamine evoked by alpha-adrenergic agonists was antagonized by phentolamine, and left unchanged by practolol and cocaine. It is concluded that alpha-adrenoceptors may be valuable in evoking histamine release by murine neoplastic mast cells.

Animals↗

A trend in the therapy of Amanita phalloides poisoning.

Recent experimental evidences have been produced on the protection afforded by penicillin G in rats poisoned by Amanita phalloides extracts. A therapeutic trend which combines penicillin G infusions to the classical supportive measures was applied to 33 cases of severe A. phalloides poisoning, with 100% survival rates. The possible mechanism of the protective effect of penicillin G in A. phalloides poisoning is discussed.

Adult↗

Studies on the 14C-histamine release induced by noradrenaline in mouse neoplastic mast cells.

Murine neoplastic mast cells incubated with labelled histamine released 14C-histamine when exposed to increasing concentrations of noradrenaline. This process was blocked by low temperature, by inhibiting oxidative metabolism and glycolysis, by calcium deprivation and by cytochalasin B. Electron microscope observations of cells exposed to noradrenaline revealed an increase of the Juxtanuclear Golgi Apparatus, and the appearance of a pronounced peripheral vacuolization. Cells exposed simultaneously to noradrenaline and cytochalasin B were characterized by a further increase of the Golgi apparatus, and by the appearance of many electron dense cytoplasmic granules. The possible mechanisms of the noradrenaline induced histamine release were discussed.

Animals↗

Interaction of histamine H1-and H2-receptor antagonists with histamine uptake and metabolism by guinea-pig isolated atrium and mouse neoplastic mast cells cells in vitro.

1. Burimamide, metiamide, chlorpheniramine, triprolidine and cocaine, were tested as inhibitors of histamine uptake and metabolism in the guinea-pig atrium and in mouse neoplastic mast cells. 2. Cocaine did not affect the uptake and metabolism of histamine, either in the atrium or in the mast cells. All the antihistamines tested blocked the uptake and metabolism of histamine in both preparations. The order of potency was burimamide greater than chlorpheniramine greater than triprolidine greater than metiamide in the atrium; and burimamide greater than metiamide greater than triprolidine greater than chlorpheniramine, in the mase cells. 3. Comparison of the present results with the antihistamine activity of these blocking agents suggests that no correlation exists between the receptor blocking activity and the ability of these substances to act as inhibitors of histamine uptake and metabolism.

Animals↗

The inhibition of histamine uptake and metabolism by burimamide in the guinea-pig atrium and in mouse neoplastic mast cells, in vitro.

Burimamide, an H(2)-receptor blocking agent, has been shown capable of blocking the uptake and metabolism of [(14)C]-histamine, both in the guinea-pig isolated atrium and in murine neoplastic mast cells. This occurs even at concentrations far below the dose range capable of blocking the positive chronotropic effect of histamine in the isolated atrium. In the atrium, very low concentrations of burimamide were found capable of blocking histamine metabolism.

Animals↗

Uptake, disposition and metabolism of histamine in isolated heart preparations.

1. The uptake and metabolism of histamine by the guinea-pig heart and by the isolated electrically driven guinea-pig left atria was studied with both labelled and unlabelled histamine.2. Histamine uptake took place against a concentration gradient and, at low concentrations, this was blocked by hypoxia plus glucose deprivation or by a toxic dose of ouabain.3. The histamine taken up was retained by cardiac tissues and mainly metabolized into methyl-histamine and other metabolites. The uptake and metabolism of histamine was higher in atria than in ventricles thus reflecting the regional distribution of endogenous histamine and mast cell numbers.4. The uptake and metabolism of histamine were greatly reduced in hearts which had been depleted of mast cells, by combining cardiac anaphylaxis and (+)-tubocurarine (1 mg/ml), but pretreatment of guinea-pigs with 6-hydroxy-dopamine failed to affect uptake of total radioactivity in the isolated left atria.5. In the guinea-pig heart histamine appears to be taken up, stored and metabolized in at least two pools, one of which is linked to the mast cells.

Anaphylaxis↗

Hepatic encephalopathy: lack of changes of gamma-aminobutyric acid content in plasma and cerebrospinal fluid.

The aim of the study was to verify the role of gamma-aminobutyric acid in the pathogenesis of hepatic encephalopathy occurring in cirrhotic patients by attempting to correlate plasma and cerebrospinal fluid content of authentic gamma-aminobutyric acid with the neurological manifestations of hepatic encephalopathy. For this purpose, plasma and cerebrospinal fluid gamma-aminobutyric acid levels were measured by means of mass fragmentography in 17 cirrhotic patients with hepatic encephalopathy and in 6 cirrhotics without neurological symptoms. Moreover, in all patients, a second sample was obtained during the clinical course of hepatic encephalopathy. The mean plasma and cerebrospinal fluid gamma-aminobutyric acid levels were not different in patients with or without hepatic encephalopathy and did not change during the evolution of the neurological symptoms. The lack of changes in the gamma-aminobutyric acid content in plasma and cerebrospinal fluid during hepatic encephalopathy is in contrast with the hypothesized importance of increased entry into the brain of gamma-aminobutyric acid in the pathogenesis of hepatic encephalopathy.

Adult↗

Food restriction in female Wistar rats. I. Survival characteristics, membrane microviscosity and proliferative response in lymphocytes.

The effect of food restriction on the survival characteristics, membrane microviscosity and proliferative response in lymphocytes of female Wistar undernourished rats has been evaluated. Diet restriction was applied starting from the age of 3.5 months by feeding the animals on an every-other-day schedule (EOD). Diet restricted animals showed an increase of both mean, median and maximal life span as compared to the rats fed ad libitum (AL). Analyzing the survival curves by a parametric model, it emerged that undernutrition increased the individual resistance to environmental insults. In particular, it could be speculated that the positive influence was more pronounced in individuals with the lowest physiological capacities. The membrane microviscosity of lymphocytes was lower in EOD animals as compared to the AL ones even if one assumes a decrease in body temperature of 1-2 degrees C in EOD groups. The improvement of membrane microviscosity due to diet restriction may in part explain the improvement of proliferative response of lymphocytes from EOD groups.

Journal Article↗

Food restriction in female Wistar rats. II. Beta-adrenoceptor density in the cerebellum and in the splenic lymphocytes.

The effect of diet restriction, applied on an every-other-day schedule from 3.5 months of age on, has been investigated on the beta-adrenoceptor density in the cerebellum and in the splenic lymphocytes of old female Wistar rats. Comparing animals 6 months and 24 months old fed ad libitum, a 75% age-dependent reduction in specific binding of the agonist dihydroalprenolol was observed in cerebellar membrane preparations, while the beta-adrenoceptor density of lymphocytes remained unaltered. Diet restriction induced a partial recovery of the age-related decrease of this parameter in the cerebellum without affecting the receptor density of lymphocytes. Present results suggest that undernutrition delays the appearance of those alterations related to aging.

Journal Article↗

Food restriction in female Wistar rats. III. Thermotropic transition of membrane lipid and 5'-nucleotidase activity in hepatocytes.

The effect of diet restriction was measured on the anisotropy parameter of 1,6-diphenyl-1,3,5-hexatriene (DPH) and 5'-nucleotidase enzyme activity in liver plasma membrane preparates. Diet restriction was applied to rats 3.5 months old on an every-other-day schedule (EOD) and the rats were killed at the age of 28-29 months. Six months and 24 months rats, fed ad libitum (AL), were used as controls. The Arrhenius plots of anisotropy parameter of liver membranes from young, old AL and old EOD animals exhibited well defined breakpoints at 16.3 degrees C, 19.5 degrees C and 16.7 degrees C, respectively. The breakpoint temperature of 5'-nucleotidase activity was lower in samples from young rats as compared to those from old AL rats, whereas no difference was observed comparing young and EOD fed rats. Present results support the hypothesis that diet restriction modifies lipid composition of liver plasma membranes in such a way that the appearance of age-dependent alterations is delayed.

Journal Article↗

Diet restriction, body temperature and physicochemical properties of cell membranes.

This paper summarizes some recent results of the effect of diet restriction upon body temperature and membrane microviscosity of lymphocytes, hepatocytes and cerebellar cells of diet-restricted female Wistar rats. The treated animals were fed on an every-other-day schedule starting from the age of 3.5 months. It is suggested that a decrease in average body temperature (-1 degree C) of diet-restricted animals as compared to the ad libitum fed ones may stimulate the cells to synthesize more fluid membranes. Together with these the maintenance of the activity of protective enzymes is another key event which helps to prevent the age-dependent deterioration of cell membrane functions.

Journal Article↗