857 resultados para sympathetic innervation
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The superior cervical ganglion (SCG) provides sympathetic input to the head and neck, its relation with mandible, submandibular glands, eyes (second and third order control) and pineal gland being demonstrated in laboratory animals. In addition, the SCG's role in some neuropathies can be clearly seen in Horner's syndrome. In spite of several studies published involving rats and mice, there is little morphological descriptive and comparative data of SCG from large mammals. Thus, we investigated the SCG's macro- and microstructural organization in medium (dogs and cats) and large animals (horses) during a very specific period of the post-natal development, namely maturation (from young to adults). The SCG of dogs, cats and horses were spindle shaped and located deeply into the bifurcation of the common carotid artery, close to the distal vagus ganglion and more related to the internal carotid artery in dogs and horses, and to the occipital artery in cats. As to macromorphometrical data, that is ganglion length, there was a 23.6% increase from young to adult dogs, a 1.8% increase from young to adult cats and finally a 34% increase from young to adult horses. Histologically, the SCG's microstructure was quite similar between young and adult animals and among the 3 species. The SCG was divided into distinct compartments (ganglion units) by capsular septa of connective tissue. Inside each ganglion unit the most prominent cellular elements were ganglion neurons, glial cells and small intensely fluorescent cells, comprising the ganglion's morphological triad. Given this morphological arrangement, that is a summation of all ganglion units, SCG from dogs, cats and horses are better characterized as a ganglion complex rather than following the classical ganglion concept. During maturation (from young to adults) there was a 32.7% increase in the SCG's connective capsule in dogs, a 25.8% increase in cats and a 33.2% increase in horses. There was an age-related increase in the neuronal profile size in the SCG from young to adult animals, that is a 1.6-fold, 1.9-fold and 1.6-fold increase in dogs, cats and horses, respectively. on the other hand, there was an age-related decrease in the nuclear profile size of SCG neurons from young to adult animals (0.9-fold, 0.7-fold and 0.8-fold in dogs, cats and horses, respectively). Ganglion connective capsule is composed of 2 or 3 layers of collagen fibres in juxtaposition and, as observed in light microscopy and independently of the animal's age, ganglion neurons were organised in ganglionic units containing the same morphological triad seen in light microscopy. Copyright (c) 2007 S. Karger AG, Basel.
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The mechanism by which adiposity can raise blood pressure is not fully understood. Leptin has been suggested as a possible cause of the arterial hypertension in obese subjects because leptin induces an increase in sympathetic activity. The aim of the present study is to evaluate serum leptin level, blood pressure, lipid profile, blood glucose, and insulin in obese women. Leptin, total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides were measured. Serum leptin was markedly higher in hypertensive obese women (92.3 +/- 22 ng/mL, n = 7) as compared with normotensive obese women (37.7 +/- 11 ng/mL, n = 7). Similarly, total cholesterol and LDL cholesterol were significantly elevated in the hypertensive group. No changes were observed in triglycerides and high-density lipoprotein cholesterol concentration between the 2 groups. There were no significant differences in plasma insulin concentration or blood glucose in both groups. In conclusion, our findings suggest a link among dyslipidemia, leptin level, and hypertension that might be relevant to the development of cardiovascular disease in obese subjects.
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Bilateral common carotid occlusion (BCO) over a period of 60 s in conscious rats produces a biphasic presser response, consisting of an early (peak) and late (plateau) phase. In this study we investigated 1) the effects of lesions of the commissural nucleus of the solitary tract (commNTS) on the cardiovascular responses produced by BCO in conscious rats and 2) the autonomic and humoral mechanisms activated to produce the presser response to BCO in sham- and commNTS-lesioned rats. Both the peak and plateau of the presser response produced by BCO increased in commNTS-lesioned rats despite the impairment of chemoreflex responses induced by intravenous potassium cyanide. In sham rats sympathetic blockade with intravenous prazosin and metoprolol, but not vasopressin receptor blockade with the Manning compound, reduced both components of BCO. In commNTS-lesioned rats the sympathetic blockade or vasopressin receptor blockade reduced both components of BCO. The results showed 1) the sympathetic nervous system, but not vasopressin, is important for the presser response to BCO during 60 s in conscious sham rats; 2) in commNTS-lesioned rats, despite chemoreflex impairment, BCO produces an increased presser response dependent on sympathetic activity associated with vasopressin release; and 3) the increment in the presser response to BCO in commNTS-lesioned rats seems to depend only on vasopressin secretion.
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The influence of testosterone on the development of the pressor response to common carotid occlusion was investigated in control and median eminence-lesioned male rats. In control rats (N = 9), gonadectomy performed 21 days before the experiments reduced by 22% (from 51 +/- 2 to 40 +/- 2 mmHg) and treatment with testosterone (300-mu-g for 4 days before the measurements) increased the initial peak pressor response (from 51 +/- 2 to 57 +/- 2 mmHg) which depends on carotid innervation. The maintained response which is of central origin (probably ischemic) was less affected. In nongonadectomized rats (N = 6), lesions of the median eminence (6 days) decreased the initial peak by 19% (from 52 +/- 2 to 42 +/- 3 mmHg) and the maintained response by 56% (from 32 +/- 2 to 14 +/- 1 mmHg). Sham-operated rats served as controls. In gonadectomized animals (N = 6) the lesion reduced only the maintained response (from 23 +/- 2 to 11 +/- 1 mmHg). Testosterone supplementation restored the maintained response but did not alter the initial peak. These results indicate that the pressor response to common carotid occlusion in male rats is modulated by testosterone and that the depression in the maintained response caused by median eminence lesion can be reversed by steroid supplementation.
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Progressive facial hemiatrophy (Romberg's syndrome) is of unknown cause and uncertain pathogenesis. The main pathogenetic hypotheses are: sympathetic system alterations, localized scleroderma, trigeminal changes, possibly of genetic origin. To test the hypothesis of sympathetic system alterations, we designed an experimental model with ablation of the superior cervical sympathetic ganglion in rabbits, cats and dogs. All the animals were operated upon when 30 days old and were examined monthly for 1 year. During this period localized alopecia, corneal ulceration, keratitis, strabismus, enophthalmos, ocular atrophy, hemifacial atrophy and slight bone atrophy on the side of the sympathectomy were observed. Thus, cervical sympathectomy reproduces in animals the principal clinical alterations of Romberg's syndrome. Our data suggest that the sympathetic system is involved in the pathogenesis of this syndrome.
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Rat isolated right atria obtained 1 wk after sinoaortic denervation were less sensitive to the chronotropic actions of beta-agonists than were tissues obtained from animals that underwent sham surgery or no surgery at all. The potencies, but not the maximal responses for two high efficacy agonists, norepinephrine and isoproterenol, were reduced about 3- to 4-fold. Sinoaortic denervation (SAD) caused about a 3-fold decrease in potency and about a 60% decrease in maximal response for a low efficacy agonist, prenalterol. The changes in the actions of these agonists occurred in the absence of any changes in the subtype of beta receptor mediating the chronotropic response. The results of analyses of the data for prenalterol showed that SAD caused a decrease in the operational efficacy of this agonist without any changes in its K-D value for beta-1 adrenoceptors. SAD had no effect on the responses of the tissue to blockade of uptake 1 and uptake 2, suggesting no compensatory changes in the removal processes caused the decreased potency. The results of radioligand binding assays showed that SAD caused a decrease in the maximal binding of I-125-cyanopindolol without altering its K-D. Also, the results of competition binding assays confirmed the lack of effect of SAD on the K-D for prenalterol. The SAD-induced changes in the actions of agonists acting at right atrial beta-1 receptors were caused by a down-regulation of beta-1 adrenoceptors, which probably occurred in response to SAD-induced increases in sympathetic tone.
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Selective chemical sympathectomy of the internal genital organs of prepubertal to mature male Wistar rats was performed by chronic treatment with low doses of guanethidine. Sympathetic denervation caused an increase in intratesticular progesterone levels in prepubertal and early pubertal rats in addition to a decrease in androstenedione and testosterone levels in prepubertal animals, thus indicating a decrease in the conversion of progesterone into androgen, probably by blocking the steroidogenic enzymatic pathway at the 17 alpha-hydroxylase/17,20 desmolase level. A lower degree of testicular maturation, probably related to reduced androgen activity, was observed in prepubertal and early pubertal sympathectomized rats. Concentration of spermatozoa, on the other hand, was increased in the enlarged cauda epididymidis of late pubertal and mature denervated animals. This result is discussed in terms of the impairment of epididymal mechanisms of seminal emission, fluid resorption and spermatozoal disposal.
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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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In order to test if the maximal velocity of shortening (V(max)TP) reflects the level of inotropism and is affected by preload and afterload, the behavior of this index was compared in two groups of anesthetized, atropinized dogs when preload and afterload were raised with an angiotensin II infusion. In seven dogs (group I), the arterial pressure elevation was allowed to inhibit reflectively the sympathetic tone and depress contractility. In eleven dogs (group II), the adrenergic activity was abolished by previous administration of reserpine. In group I, there was a significant decrease in V(max)TP during the angiotensin infusion. In group II, there was no significant change in the value of this index when the drug was infused. In six animals of this group, a further increase of arterial pressure was induced, but the values of V(max)TP remained similar to control. These results suggest that this index reflects the inotropic state of the myocardium and does not suffer significantly from the influence of preload and afterload elevations within our experimental limits.
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Cholinergic and adrenergic agonists and antagonists were injected directly into the subfornical organ (SFO), via implanted cannulae, and the volume of water ingested was recorded over a period of 1 hour after injection. Application of 2 nmol carbachol caused intense water intake in 100% of the animals (8.78±0.61 ml), with a very short intake latency. When the 2 nmol carbachol dose was preceded by increased doses of atropine, a progressive reduction in water intake was observed, with complete blockage of the thirst-inducing response to carbachol at the 20 nmol dose level with atropine. Followed by several doses of hexamethonium, the water intake caused by application of 2 nmol carbachol was reduced, although the response was not totally blocked. Injection of 80 nmol of nicotine had a significant thirst-inducing inducing effect in 50% of the animals studied (1.06±0.18 ml) and increase in water intake was further reduced by application of increased doses of hexamethonium. Raising the dose levels of noradrenaline into th SFO caused an increase in water intake although to a lesser degree than was observed after carbachol injection. When the 40 nmol dose of noradrenaline was preceded by increased doses of propranolol (5 to 40 nmol), there was a gradual reduction in water intake, with total blockage at the 40 nmol dose. Application of phentolamine in doses of 10 to 80 nmol caused no reduction in water intake after 40 nmol of noradrenaline. Application of isoproterenol at doses from 20 to 160 nmol into the SFO caused a dosedependent increase in water intake which was blocked by previous applications of propranolol. These results support the hypothesis that the water intake caused by chemical stimulation of the SFO is mainly due to muscarinic cholinergic receptors, although the influence of nicotinic receptors or participation of adrenergic mediation should not be ruled out. © 1984.
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1. 1. The aim of these experiments was to study the extent to which previous cold-acclimation improves the cold-tolerance of diabetic rats. 2. 2. Alloxan diabetic rats (fasting blood glucose higher than 200mg/dl) were used in the experiments. 3. 3. In Expt. 1, non-cold-acclimated control and diabetic rats were exposed to cold environment (7-9°C), and the percentage of survival calculated during a 12-day experimental period. In Expt. 2, the rats were previously cold-acelimated before alloxan or saline injection (diabetic and control cold-acclimated rats) and the survival rate was also assessed during a 12-day period in the cold. 4. 4. The percentage of survival of the non-cold-acclimated diabetic rats (Expt.l) was 19% compared with 79% of the diabetic cold-acclimated animals (Expt. 2). There were no deaths in the control groups. 5. 5. Cold-acclimated diabetic rats maintained a near-normal thermogenic response after noradrenaline injection. This response was impaired in non-cold-acclimated diabetic rats. 6. 6. The results of these experiments suggest that the enhanced cold-tolerance of diabetic cold-acclimated rats could be related to the increased sympathetic activity and enhanced insulin sensitivity in thermogenic tissues, such as brown fat. © 1987.
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Termino-lateral neurorrhaphies have been used up to the beginning of this century. After this period, they have no longer been reported. We tested the efficacy of a new type of latero-terminal neurorrhaphy and evaluated the role of the epineural sheath. A group of 10 rats had the fibular nerve sectioned and the distal ending was sutured to the lateral face of the tibial nerve without removing the epineurium. All experiments were made on the right side, the left one remaining untouched in half of the animals of each group. The other half were denervated by sectioning and inverting the endings of the fibular nerves. In this way, tibial cranial muscles were either normal or denervated in the left side and reinnervated through latero-terminal neurorrhaphy in the right side. After 7.7 months, the animals were subjected to electrophysiological tests, sacrificed, and the nerves and muscles were taken for histological exams. A response of the tibial cranial muscle was obtained in 75% of the animals. The distal ending of the fibular nerve showed an average of 498 nerve fibers. The average areas of the reinnervated tibial cranial muscles were (mu 2):841.30 for M2n and 1798.33 for M2d. We concluded that the termino-lateral neurorrhaphy was functional, conducting electrical stimuli and allowing the passage of axons from the lateral surface of a healthy nerve, to reconstitute the distal segment of a sectioned nerve. The presence of the epineurium was no impediment to axonal regeneration or to the passage of electrical stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)