246 resultados para sympathetic hyperactivity


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The expansion of psychiatric labeling does not reach only the adult population, but also the problematic related to childhood have been captured by the speeches and practices of the medical-psychiatric knowledge and turned into psychopathologies which tend to be treated with the main resource made available by psychiatrics in the present times: the psychotropic drugs. This work presents a critical thinking on the expansion of the diagnoses of “attention deficit disorder and hyperactivity” (ADHD) both in children and teenagers and on the conduction of drug therapies. It follows that the processes of childhood psycho-pathologization and the trivializing of psychotropic drug prescription are related to the overvaluation of the biological conception of psychic suffering and to the economic interests of the great pharmaceutical laboratories which by means of several strategies influence the medical practices, factors that lead to exposure of these patients to possible side effects and the risks of stigmatization that must be considered.

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The present paper is a reflection on the diagnosis of Attention Deficit Hyperactivity Disorder (ADHD) and its relations to the process of medicalization as well as the meanings and perspectives apprehended through three case studies of children diagnosed with such disorder in a doctoral research in which the main purpose was to understand the meanings and peculiarities of ADHD symptomatology .We’ve utilized the model of qualitative research, grounded in psychoanalytic perspective, and conducted the psychodiagnosis for three children who were referred for psychological treatment. The survey found that those children had few experiences of both continence and frustration tolerance. It was evidenced how the school uses the logic of medicalization to try solving the problems with their children when it came to the school dimension. The variety of symptomatic manifestations and psychic dynamics presented by the cases that were studied revealed the weaknesses and inconsistencies of the referred diagnosis.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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The acute effects after exposure to different styles of music on cardiac autonomic modulation assessed through heart rate variability (HRV) analysis have not yet been well elucidated. We aimed to investigate the recovery response of cardiac autonomic modulation in women after exposure to musical auditory stimulation of different styles. The study was conducted on 30 healthy women aged between 18 years and 30 years. We did not include subjects having previous experience with musical instruments and those who had an affinity for music styles. The volunteers remained at rest for 10 min and were exposed to classical baroque (64-84 dB) and heavy metal (75-84 dB) music for 10 min, and their HRV was evaluated for 30 min after music cessation. We analyzed the following HRV indices: Standard deviation of normal-to-normal (SDNN) intervals, root mean square of successive differences (RMSSD), percentage of normal-to-normal 50 (pNN50), low frequency (LF), high frequency (HF), and LF/HF ratio. SDNN, LF in absolute units (ms (2) ) and normalized (nu), and LF/HF ratio increased while HF index (nu) decreased after exposure to classical baroque music. Regarding the heavy metal music style, it was observed that there were increases in SDNN, RMSSD, pNN50, and LF (ms (2) ) after the musical stimulation. In conclusion, the recovery response of cardiac autonomic modulation after exposure to auditory stimulation with music featured an increased global activity of both systems for the two musical styles, with a cardiac sympathetic modulation for classical baroque music and a cardiac vagal tone for the heavy metal style.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Nitric oxide (NO) is a free radical gas, inorganic, which has seven electrons of nitrogen and oxygen eight, possessing an unpaired electron. This radical is produced from L-arginine by a reaction mediated by the enzyme NO synthase. NO it is about a radical of who acts abundant on a variety of biological processes, particularly when produced by endothelial cells plays a significant role in cardiovascular control, as a modulator of peripheral vascular resistance and platelet aggregation. This free radical has also a neurotransmitter and mediator of the immune system. NO kidney function has been considered in many physiological functions such as: (a) regulation of hemodynamics and glomerular function tubuloglomerular, (b) participation in pressure natriuresis (c) maintaining medullar perfusion (d) inhibiting sodium reabsorption tubular, and (e) acting as a modulator of the activity of the sympathetic nervous system. Given these functions, the occurrence of its deficiency is associated with chronic kidney disease (CKD) in vasoconstriction and consequently glomerular hypertension, high blood pressure (HBP), proteinuria and progression of renal dysfunction. This work has the scope to describe the role of NO in renal physiology and pathophysiology of CKD.

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Selective chemical sympathectomy of the internal sex organs of adult male rats was undertaken by long term administration of low doses of guanethidine. The spermatogenic activity of the testis was unaffected by treatment. Examination of the vas deferens using morphometric methods revealed a marked increase in luminal area in contrast to a decrease in muscle layer area and in epithelial height. This is morphological evidence of sperm accumulation caused by a disorder in ductal contractile activity. No structural changes were observed in the epididymis. However, the concentration of spermatozoa in the sperm suspension stored in the cauda epididymidis was significantly increased in denervated rats. This result is discussed in terms of a sympathetic control of resorption mechanisms in the epididymis.

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The present study was performed to investigate the effect of treatment with furosemide on the pressor response induced by intracerebroventricular (i.c.v.) injections of cholinergic (carbachol) and adrenergic (norepinephrine) agonists, angiotensin II (ANGII) and hypertonic saline (HS, 2 M NaCl). The changes induced by furosemide treatment on the pressor response to intravenous (i.v.) norepinephrine, ANGII and arginine vasopressin (AVP) were also studied. Rats with a stainless-steel cannula implanted into the lateral ventricle (LV) were used. Two injections of furosemide (30 mg/kg b.wt. each) were performed 12 and 1 h before the experiments. Treatment with furosemide reduced the pressor response induced by carbachol, norepinephrine and ANGII i.c.v., but no change was observed in the pressor response to i.c.v. 2 M NaCl. The pressor response to i.v. ANGII and norepinephrine, but not AVP, was also reduced after treatment with furosemide. These results show that the treatment with furosemide impairs the pressor responses induced by central or peripheral administration of adrenergic agonist or ANGII, as well as those induced by central cholinergic activation. The results suggest that the treatment with furosemide impairs central and peripheral pressor responses mediated by sympathetic activation and ANGII, but not those produced by AVP. © 1992.

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In this study, we investigated an interaction between noradrenergic and cholinergic pathways of the medial septal area (MSA) on the control of water intake and urinary electrolyte excretion by means of injection of their respective agonists. Noradrenaline (a nonspecific α-adrenergic agonist) and clonidine (an α2-adrenergic agonist), but not phenylephrine (an α1-adrenergic agonist), induced natriuresis and kaliuresis. α-Adrenergic activation had no effect on the natriuresis and kaliuresis induced by carbachol (a cholinergic agonist) and it inhibited the antinatriuresis and antikaliuresis induced by isoproterenol (a ß-adrenergic agonist). Interactions related to volume excretion are complex. α-Adrenergic activation induced a mild diuresis and inhibited the antidiuresis induced by isoproterenol, but phenylephrine combined with carbachol induced antidiuresis. The water intake induced by carbachol was inhibited by clonidine and noradrenaline, but not phenylephrine. These results show an asymmetry in the interaction between α-adrenergic and cholinergic receptors concerning water intake and electrolyte excretion. © 1992.