RESUMEN
In this work we present a simple, inexpensive, and easily scalable industrial paper process to prepare sheets of conductive cellulose fibers coated with polyanilines. First, bare fibers were coated by in situ oxidative polymerization of polyaniline then, the resulting composite fibers were used to fabricate electroactive sheets. The resistivity of the sheets is 14 ± 1 Ω sq-1, a value around 1000 times lower than those reported in literature. The superior electronic proprieties of the sheets were demonstrated by assembling a capacitive touch sensor device with optimized geometry. The touch sensor shows an increase of 3-4 % of the starting electric capacity after compression and a fast response time of 52 ms. To our knowledge this is the first time that a device is prepared in this way and therefore, the herein presented results can bring an significant improvement in the development of low-cost, green and high-tech electronic devices.
RESUMEN
We report on the effectiveness and safety of gamma-hydroxybutyric acid in the therapy of overt alcohol withdrawal syndromes, their prevention, and the prevention of relapses in formerly detoxified alcoholics. We studied 321 patients (236 men, 85 women), divided into two open-study groups for the treatment and prevention of alcohol withdrawal syndromes and one double-blind study group to evaluate the effects of gamma-hydroxybutyric acid versus placebo on alcoholic craving and relapses in detoxified patients. Gamma-hydroxybutyric acid treatment promptly reduced withdrawal symptoms in all patients and prevented alcohol withdrawal syndromes in 55% of cases. The attenuation of craving in detoxified patients was significantly greater in the gamma-hydroxybutyric acid-treated group in comparison with the placebo-treated group. The therapeutic use of gamma-hydroxybutyric acid was not accompanied by serious side effects. Gamma-hydroxybutyric acid diversion was poorly represented: gamma-hydroxybutyric acid-induced abuse was reported in 4 (1.1%) of 345 treated patients, and only 9 cases of gamma-hydroxybutyric acid acute poisoning were reported in the years 1992-1995. Our results suggest that gamma-hydroxybutyric acid, with a favorable risk/benefit ratio, is a clinically useful drug in the treatment of alcohol dependence.
Asunto(s)
Trastornos Relacionados con Alcohol/tratamiento farmacológico , Alcoholismo/tratamiento farmacológico , Hidroxibutiratos/uso terapéutico , Adolescente , Adulto , Anciano , Delirio por Abstinencia Alcohólica/tratamiento farmacológico , Delirio por Abstinencia Alcohólica/prevención & control , Trastornos Relacionados con Alcohol/prevención & control , Método Doble Ciego , Femenino , Humanos , Hidroxibutiratos/administración & dosificación , Masculino , Persona de Mediana Edad , Placebos , RecurrenciaRESUMEN
Anaphylaxis in the isolated guinea-pig heart was associated with a sudden release of histamine with a long-lasting release of nitrite (NO2-), an oxidation product of NO. NG-monomethyl-L-arginine (MeArg, 300 microM) increased the severity of cardiac anaphylaxis, as shown by the decrease in the coronary flow and by a prolonged duration of antigen-induced arrhythmias. Concomitantly, MeArg increased the release of histamine while decreasing the release of nitrite. Sodium nitroprusside (NaNP, 10(-5)-10(-4) M) reduced the severity of cardiac anaphylaxis by increasing coronary flow and shortening the duration of antigen-induced arrhythmias. Concomitantly, NaNP decreased the release of histamine while increasing the release of nitrite. In mast cells isolated from actively sensitized guinea-pigs, the release of histamine elicited by specific antigen was increased by MeArg and decreased by NaNP. In conclusion, endogenous and exogenous NO antagonizes the effect of vasoconstrictor mediators released after antigen challenge and plays a protective role in anaphylactic reactions "in vitro".
Asunto(s)
Anafilaxia/fisiopatología , Corazón/fisiopatología , Mastocitos/fisiología , Óxido Nítrico/fisiología , Aminoácido Oxidorreductasas/antagonistas & inhibidores , Animales , Arginina/análogos & derivados , Arginina/farmacología , Circulación Coronaria/efectos de los fármacos , Cobayas , Corazón/efectos de los fármacos , Liberación de Histamina/efectos de los fármacos , Técnicas In Vitro , Masculino , Mastocitos/efectos de los fármacos , NG-Nitroarginina Metil Éster , Óxido Nítrico/antagonistas & inhibidores , Óxido Nítrico/metabolismo , Óxido Nítrico Sintasa , Nitroprusiato/farmacología , Ovalbúmina/inmunologíaRESUMEN
The effect of organic and inorganic nitrovasodilators (sodium nitroprusside; 3-morpholinosydnonimine; glyceryl trinitrate; isosorbide dinitrate; sodium nitrite, was studied on the release of histamine evoked by compound 48/80 and calcium ionophore A 23187 in isolated purified rat serosal mast cells. All the compounds tested were capable of significantly reducing the release of histamine in a concentration-dependent fashion, at different levels of potency. This effect was reverted by oxyhaemoglobin. The inhibitory effect of glyceryl trinitrate on the release of histamine was potentiated in cells taken from animals pretreated with Escherichia coli lipopolysaccharide, and decreased by NG-nitro-L-arginine methyl ester. Glyceryl trinitrate and isosorbide dinitrate concentration-dependently increase the generation of nitric oxide by rat serosal mast cells. The inhibitory effect of glyceryl trinitrate and isosorbide dinitrate on the release of histamine from mast cells was potentiated by N-acetylcysteine, which significantly increases the generation of nitric oxide by mast cells. It is concluded that nitrovasodilators inhibit the release of mast cell histamine through the generation of nitric oxide. The effect may be relevant in considering the perivascular location of mast cells and the role played by these cells in cardiovascular pathophysiology.
Asunto(s)
Liberación de Histamina/efectos de los fármacos , Mastocitos/metabolismo , Óxido Nítrico/biosíntesis , Vasodilatadores/farmacología , Acetilcisteína/farmacología , Animales , Calcimicina/antagonistas & inhibidores , Calcimicina/farmacología , Supervivencia Celular/efectos de los fármacos , Masculino , Mastocitos/efectos de los fármacos , Nitratos/metabolismo , Nitratos/farmacología , Oxihemoglobinas/farmacología , Ratas , Ratas Wistar , p-Metoxi-N-metilfenetilamina/farmacologíaRESUMEN
The effects of reduced glutathione (GSH) administration (1.2 g/day and 2.4 g/day intravenously) on erythrocyte glutathione levels, serum gamma-glutamyl transpeptidase activity (GGTP) and urinary glucaric acid elimination were studied in a population of 24 chronic alcoholics voluntarily admitted to a 30 day detoxification protocol in comparison to a 12 patient control group treated only with chlordiazepoxide (initial dose 75-100 mg/day). Glutathione treatment increases dose-dependently and in a significant way erythrocyte glutathione levels and hastens the recovery of serum GGTP and urinary glucaric acid elimination. The relationship between glutathione, GGTP and glucaric acid is discussed, suggesting the possible role of GSH against the oxidative damage of alcohol.
Asunto(s)
Alcoholismo/tratamiento farmacológico , Glutatión/uso terapéutico , Adulto , Alcoholismo/sangre , Alcoholismo/orina , Clordiazepóxido/uso terapéutico , Eritrocitos/química , Femenino , Ácido Glucárico/orina , Glutatión/administración & dosificación , Glutatión/sangre , Humanos , Masculino , Persona de Mediana Edad , Factores de Tiempo , gamma-Glutamiltransferasa/sangreAsunto(s)
Liberación de Histamina , Miocardio/metabolismo , Óxido Nítrico/metabolismo , Daño por Reperfusión/metabolismo , Animales , Arginina/análogos & derivados , Arginina/farmacología , Relación Dosis-Respuesta a Droga , Cobayas , L-Lactato Deshidrogenasa/metabolismo , Superóxido Dismutasa/farmacología , Vasodilatadores/farmacología , omega-N-MetilargininaRESUMEN
A group of 122 drug addict patients were studied to evaluate the incidence of HIV, HBV, HCV infections and of laboratory findings of hepatic damage. Our data show that hepatic damage is more frequent in patients affected by HBV-HCV coinfection than those with HBV or HCV infection alone and that HIV positivity supports HBV-HCV coinfection.
Asunto(s)
Infecciones por VIH/epidemiología , Hepatitis B/epidemiología , Hepatitis C/epidemiología , Hepatopatías/etiología , Abuso de Sustancias por Vía Intravenosa/complicaciones , Adolescente , Adulto , Femenino , Infecciones por VIH/complicaciones , Hepatitis B/complicaciones , Hepatitis C/complicaciones , Humanos , Hígado/patología , Hepatopatías/epidemiología , Masculino , Persona de Mediana EdadRESUMEN
Minute amounts of histamine and a discrete histamine-forming capacity was present in quiescent human platelets. Aggregation of human platelets induced by thrombin was concomitant with the release of histamine. In platelets obtained from actively sensitized guinea pig, the exposure to the specific antigen results in aggregation and histamine release which was not reproduced by the exposure to an unspecific protein or in platelets taken from unsensitized animals. The present results lend further support to positioning platelets among the inflammatory cells.
RESUMEN
Experiments were carried out to provide evidence of the effect of L-arginine (L-Arg), its analogue NG-monomethyl-L-arginine (MeArg) and of some nitrovasodilators (sodium nitroprusside, NaNP; 3-morpholino-sydnonimine, SIN-1) which spontaneously release nitric oxide (NO) on ischemia-reperfusion injury, histamine release and mast cell degranulation, occurring after multiple ligature and release of the left anterior descending (LAD) coronary artery in isolated perfused guinea-pig hearts. The reopening of the LAD coronary artery leads to a release of histamine related to a decrease in microdensitometry of cardiac mast cells and to calcium overload. The perfusion of the heart with NO-donors significantly reduces either the release of histamine, the loss of mast cell metachromasia and the overload of calcium. These effects were potentiated by SOD. The results suggest that the endogenous formation of NO and molecules able to generate NO have a role in the prevention of post-ischemic tissue injury.
Asunto(s)
Liberación de Histamina/efectos de los fármacos , Daño por Reperfusión Miocárdica/fisiopatología , Óxido Nítrico/metabolismo , Animales , Arginina/análogos & derivados , Arginina/farmacología , Calcio/metabolismo , Vasos Coronarios/fisiopatología , Gránulos Citoplasmáticos/ultraestructura , Cobayas , Masculino , Mastocitos/ultraestructura , Molsidomina/análogos & derivados , Molsidomina/farmacología , Daño por Reperfusión Miocárdica/patología , Nitroprusiato/farmacología , omega-N-MetilargininaRESUMEN
The release of histamine from rat serosal mast cells induced by coincubation with resting and activated human platelets, or by exposure of mast cells to supernatants obtained from activated platelets, is significantly reduced by anti-free radical interventions, and is coupled with the generation of membrane lipid peroxidation products. These results suggest free radical participation in the activity of PDHRF. Human platelets possess specific binding sites for an H1-receptor antagonist, suggesting that H1-receptors could modulate the intracellular calcium levels in a pro-aggregatory fashion.
Asunto(s)
Plaquetas/fisiología , Liberación de Histamina , Peroxidación de Lípido , Mastocitos/fisiología , Agregación Plaquetaria/fisiología , Receptores Histamínicos H1/fisiología , Animales , Membrana Celular/metabolismo , Depuradores de Radicales Libres , Radicales Libres , Histamina/farmacología , Liberación de Histamina/efectos de los fármacos , Humanos , Masculino , Malondialdehído/metabolismo , Pirilamina/sangre , Ratas , Ratas EndogámicasAsunto(s)
Factores Biológicos/fisiología , Liberación de Histamina/fisiología , Agregación Plaquetaria/fisiología , Receptores Histamínicos/fisiología , Animales , Ácido Araquidónico , Ácidos Araquidónicos/farmacología , Plaquetas/fisiología , Radicales Libres , Humanos , Técnicas In Vitro , Mastocitos/metabolismo , Ratas , Trombina/farmacologíaRESUMEN
In an ischemia-reperfusion model obtained in isolated perfused guinea pig heart by means of a double ligature of the left anterior descending coronary artery, the reperfusion of the ischemic myocardium leads to a release of lactate dehydrogenase and histamine, related to a decrease in the microdensitometry of cardiac mast cells and to a tissue calcium overload. The perfusion of the heart with L-arginine and with nitric oxide donors significantly reduces the release of histamine, the loss of mast cell metachromasia and calcium overload. These effects were potentiated by superoxide dismutase.
Asunto(s)
Liberación de Histamina , Daño por Reperfusión Miocárdica/metabolismo , Miocardio/metabolismo , Óxido Nítrico/metabolismo , Animales , Arginina/análogos & derivados , Arginina/farmacología , Cobayas , Técnicas In Vitro , Perfusión , omega-N-MetilargininaRESUMEN
Endogenous and exogenous free radical scavengers significantly decrease mast cell histamine release induced by coincubation with resting, activated platelets or with platelet-derived supernatant. Histamine and pyridylethylamine dose-dependently enhance platelet aggregation; the effect is potentiated by ranitidine and blocked by mepyramine. Histamine increases also cytosolic calcium concentration in platelets stimulated with thrombin, and binding sites for [3H]-mepyramine are present on platelet membranes.
Asunto(s)
Plaquetas/fisiología , Liberación de Histamina/efectos de los fármacos , Agregación Plaquetaria , Receptores Histamínicos/fisiología , Plaquetas/química , Calcio/metabolismo , Radicales Libres , Humanos , Técnicas In VitroRESUMEN
Experiments were carried out to provide further information on the biochemical and morphological changes occurring in the guinea-pig heart after multiple ligature and reopening of the left anterior descending (LAD) coronary artery. In isolated perfused guinea-pig heart the reopening of LAD coronary artery leads to a release of histamine related to a loss of metachromasia by cardiac mast cells. The process is associated with malonyldialdehyde (MDA) production, cellular overload of calcium and ventricular arrhythmias which can be modulated by pharmacological interventions.
Asunto(s)
Corazón/fisiopatología , Liberación de Histamina/efectos de los fármacos , Daño por Reperfusión Miocárdica/fisiopatología , Miocardio/metabolismo , Animales , Vasos Coronarios/fisiología , Cobayas , Corazón/efectos de los fármacos , Técnicas In Vitro , L-Lactato Deshidrogenasa/metabolismo , Masculino , Mastocitos/efectos de los fármacos , Mastocitos/metabolismo , Daño por Reperfusión Miocárdica/metabolismo , Miocardio/citología , Miocardio/enzimologíaRESUMEN
Coincubation of rat serosal mast cells with human platelets leads to a significant release of histamine. which dose-dependently increases when platelet aggregation is induced by various concentrations of arachidonic acid. In turn, histamine enhances platelet aggregation induced by different agonists, this effect being mimicked by pyridyl-ethyl-amine (PEA), blocked by mepyramine and amplified by ranitidine. The data suggest the existence of a platelet-derived histamine releasing factor (PDHRF) and indicate the presence of platelet H1 and H2 receptors, capable of modulating platelet aggregation.
Asunto(s)
Plaquetas/metabolismo , Liberación de Histamina/efectos de los fármacos , Mastocitos/metabolismo , Agregación Plaquetaria/efectos de los fármacos , Animales , Ácidos Araquidónicos/farmacología , Plaquetas/enzimología , Técnicas In Vitro , L-Lactato Deshidrogenasa/metabolismo , Masculino , Mastocitos/enzimología , Piridinas/farmacología , Pirilamina/farmacología , Ranitidina/farmacología , Ratas , Ratas EndogámicasRESUMEN
Polyunsaturated fatty acids (PUFA: arachidonic and linoleic acid) release histamine from isolated purified rat serosal mast cells only in the presence of oxidizing systems such as phenobarbital-induced rat liver microsomes, prostaglandin-H-synthetase (PHS) or soybean lipoxygenase. The release of mast cell histamine by activated PUFA has a long time-course and the electron microscopical features are consistent with an exocytotic secretion in the case of arachidonic acid and cell lysis in the case of linoleic acid. The phenomenon is associated with a significant increase in malonyldialdehyde (MDA) and conjugated diene generation, suggesting a relationship between histamine release and membrane lipid peroxidation. The secretion of histamine was inhibited by anti-free radical interventions such as D-mannitol, reduced glutathione and alpha-tocopherol. Some cyclooxygenase and lipoxygenase inhibitors, cimetidine and carnitine derivatives, are differentially active in the inhibition of mast cell histamine release by activated arachidonic acid. These results suggest that free radical derivatives of PUFA, generated by metabolic activation, trigger mast cell histamine release.
Asunto(s)
Ácidos Araquidónicos/farmacología , Liberación de Histamina/efectos de los fármacos , Ácidos Linoleicos/farmacología , Mastocitos/efectos de los fármacos , Animales , Ácido Araquidónico , Ácidos Araquidónicos/farmacocinética , Biotransformación/efectos de los fármacos , Radicales Libres , L-Lactato Deshidrogenasa/metabolismo , Ácido Linoleico , Ácidos Linoleicos/farmacocinética , Peroxidación de Lípido , Masculino , Mastocitos/metabolismo , Mastocitos/patología , Fenobarbital/farmacología , Ratas , Ratas EndogámicasRESUMEN
Free radicals produced by the occlusion and opening of the left anterior descending coronary artery and/or by perfusion of isolated guinea-pig heart with FeCl3/ADP (10 microM/100 microM) induce a differential release of histamine and lactate dehydrogenase (LDH) in the perfusates with a preferential liberation of histamine in the reperfusion phase, associated with an increase of ventricular arrhythmias. The release of histamine has been correlated with malonyldialdehyde (MDA) production and tissue calcium content in left ventricular tissue. MDA increased during ischemia, while the calcium content increased when the tissue was reperfused. Under these conditions, N-t-butyl-alpha-phenylnitrone (BPN), a molecule capable of forming spin adducts with free radicals, and D-mannitol are active in preventing reperfusion-induced arrhythmias.