102 resultados para blood response


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Maternal separation is known to exert long-term effects on both behavior and the neuroendocrine system. We investigated cocaine-induced locomotor activation as well as the locomotor and corticosterone response to forced novelty in maternally separated adolescent and adult rats. Maternal separation consisted of separating litters from their darns daily during 5 h from postnatal days 2 to 6. Control animals were subjected only to regular cage changes. Cocaine- (10 mg/kg, i.p.) and novelty-induced locomotion were recorded in an activity cage. After the animals were tested for behavioral response to novelty, trunk blood samples were collected and plasma corticosterone levels were determined by radioimmunoassay. Adolescent rats exposed to maternal separation exhibited an increased locomotor response to novelty and cocaine; corticosterone levels were lower in these adolescent animals, after exposure to the novel environment. These effects of materrial separation were not observed in rats that were tested as adults. Thus the maternal separation protocol produced enduring but transient changes in the behavioral response to cocaine and in the stress response to novelty. (C) 2004 Elsevier B.V. All rights reserved.

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Os autores investigaram a relação entre dermatofitose e grupo sanguíneo ABO através da tipagem sanguínea, identificação do dermatófito isolado e resposta imune celular específica de 40 indivíduos portadores desta micose. Verificaram que o fungo Trichophyton rubrum foi isolado em 54,5% dos pacientes, sendo mais frequente em indivíduos pertencentes ao grupo sanguíneo A. A resposta imune celular, avaliada através do antígeno tricofitina, foi positiva em 25% dos pacientes estudados; a presença de reações imediatas (30 min) foi verificada em 35%. A distribuição dos grupos sanguíneos entre pacientes com dermatofitose e grupo controle foi a seguinte: 47,5% x 36% grupo A, 40% x 50% grupo O, 12,5% x 11% grupo B. Embora os autores tenham encontrado um número maior de pacientes pertencentes ao grupo sanguíneo A e infectados pelo T. rubrum, não obtiveram evidência estatística de que esses indivíduos sejam mais suscetíveis as dermatofitoses.

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

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Background Mucocutaneous lesions in paracoccidioidomycosis are granulomatous and result from tissue responses to Paracoccidioides brasiliensis, the aetiological agent.Objectives and methods In this study we investigate the expression of tumour necrosis factor (TNF)-alpha, interleukin (IL)-10 and transforming growth factor (TGF)-beta 1 by immunohistochemistry in skin and mucosa lesions from patients with the chronic form of paracoccidioidomycosis, evaluated before and at day 20 of trimethoprim-sulfamethoxazole treatment. Cytokine production by peripheral blood monocytes was also studied by enzyme immunoassay.Results Intense immunostaining for TNF-alpha was detected in mononuclear cells that infiltrated granulomas in all skin and mucosa lesions before treatment simultaneously with low IL-10 granular deposits in these cells. At day 20 of treatment, there was reduced TNF-alpha and IL-10 deposition. Immunoreactive TGF-beta 1 was observed diffusely in the dermis and generally in the cytoplasm of macrophages and giant cells, before treatment, and as increased TGF-beta 1 deposits in the fibrosis area at day 20 of treatment. Peripheral blood monocytes from patients with paracoccidioidomycosis, evaluated before treatment, produced high endogenous levels of TNF-alpha, TGF-beta 1 and IL-10 in relation to healthy controls. Lipopolysaccharide-stimulated monocytes from patients secreted lower levels of TNF-alpha in both periods of evaluation while no impairment in capacity of IL-10 and TGF-beta production was observed.Conclusions Trimethoprim-sulfamethoxazole therapy was effective in decreasing fungal load in the lesions, allowing patient immune response to control the infection leading to the healing of the lesions.

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Em agosto de 1983, os Autores, estudaram 36 doentes com infecção causada pelo Plasmodium falciparum e 14 indivíduos normais, nascidos na região de Humaitá, que nunca tiveram malária, sem esplenomegalia, com exame parasitológico de sangue e hemaglutinação passiva negativas. Todos eles foram submetidos à observação clínica completa, exame hematológico, exame parasitológico de sangue e tipagem de linfócitos. Os linfócitos foram isolados e congelados em nitrogênio líquido, para posterior tipagem pela formação de rosetas. Os doentes foram classificados em dois grupos de acordo com a presença (13 doentes), ou ausência (23 doentes) de gametócitos antes do tratamento. Houve predomínio de formas graves no grupo de doentes sem gametócitos. Os resultados mostraram diminuição do número de linfócitos T em ambos os grupos de doentes, com ou sem gametócitos antes do tratamento, enquanto que o número de linfócitos B foi normal apenas no grupo de doentes com gametócitos. Essas observações, assim como as que foram relatadas pelos Autores anteriormente, permitem associar a presença de gametócitos circulantes com o número normal de células B em doentes com formas leves de malária causada pelo Plasmodium falciparum.

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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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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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

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We investigated the effects of injection into the supraoptic nucleus (SON) of losartanand PD 123319 (nonpeptide AT(1) and AT(2)- angiotensin II [ANG II] receptor antagonists, respectively); d(CH2)(5)-Tyr(Me)-AVP (AVPA; an arginine-vasopressin [AVP] V-1 receptor antagonist), FK 409 (a nitric oxide [NO] donor), and N-W-mtro-(L)-arginine methyl ester ((L)-NAME; an NO synthase inhibitor) oil water intake, sodium chloride 3% (NaCl) intake and arterial blood pressure induced by injection of ANG 11 into the lateral septal area (LSA). Mate Holtzman rats (250-300 g) were implanted with cannulae into SON and LSA unilaterally. The drugs were injected in 0.5 mul over 30-60 s. Controls were injected with a similar volume of 0.15 M NaCl. ANG II was injected at a dose of 10 pmol. ANG II antagonists and AVPA were injected at doses of 80 nmol. FK 409 and (L)-NAME were injected at doses of 20 and 40 mug, respectively. Water and NaCl intake was measured over a 2-h period. Prior administration of losartan into the SON decreased water and NaCl intake induced by injection of ANG II. While there was a decrease in water intake, ANG II-induced NaCl intake was significantly increased following injection of AVPA. FK 409 injection decreased water intake and sodium intake induced by ANG II. L-NAME alone increased water and sodium intake and induced a pressor effect. (L)-NAME-potentiated water and sodium intake induced by ANG II. PD 123319 produced no changes in water or sodium intake induced by ANG II. The prior administration of losartan or AVPA decreased mean arterial pressure (MAP) induced by ANG II. PD 123319 decreased the pressor effect of ANG II to a lesser degree than losartan. FK 409 decreased the pressor effect of ANG II while (L)-NAME potentiated it. These results suggest that both ANG II AT, and AVP V, receptors and NO within the SON may be involved in water intake, NaCl intake and the pressor response were induced by activation of ANG II receptors within the LSA. These results do not support the involvement of LSA AT(2) receptors in the mediation of water and NaCl intake responses induced by ANG II, but influence the pressor response. (C) 2004 Elsevier B.V. All rights reserved.

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In the present experiments we investigated a possible involvement of imidazoline receptors of the paraventricular nucleus (PVN) of the hypothalamus on the presser effects of the angiotensin LI (ANG II) injected into the subfornical organ (SFO), in male Holtzman rats (250-300 g) with a cannula implanted into the third ventricle (3rdV), PVN and SFO. At first we tested the participation of alpha(2) and imidazoline agonist and antagonist compounds on the presser effect of ANG II injected into the 3rdV. Based on the results we may conclude that clonidine associated with rilmenidine was able to block the hypertensive response to ANG IT. The ANG II (20 pmol) injected into SFO induced a robust increase in blood pressure (37 +/- 2 mmHg). Isotonic saline (0.15 M) NaCl did not produce any change in blood pressure (5 +/- 2 mmHg). The injection of rilmenidine (30 mu g/kg/l mu L), an imidazoline agonist agent injected into PVN before ANG II injection into SFO, blocked the presser effect of ANG II (5 +/- 2 mmHg). Also, the injection of idazoxan (60 mu g/kg/mu L) before rilmenidine blocked the inhibitory effect of rilmenidine on blood pressure (39 +/- 4 mmHg). The injection of clonidine (20 nmol/mu L) prior to ANG II into the 3rdV produced a decreased in arterial blood pressure (37 +/- 2 mmHg) to (15 +/- 4 mmHg). The injection of yohimbine (80 nmol/mu L) prior to clonidine blocked the effect of clonidine on the effect of ANG II (27 +/- 2 mmHg). The injection of rilmenidine prior to ANG TI also induced a decrease in arterial blood pressure (10 +/- 3 mmHg). The injection of idazoxan prior to rilmenidine also blocked the inhibitory effect of rilmenidine (24 +/- 3 mmHg). In summary, the present study demonstrated that rilmenidine decreases the hypertensive effect of ANG II, with more potency than clonidine, even when injected into 3rdV or PVN. This study established that the PVN interacts with SFO by imidazoline receptors in order to control the arterial blood pressure. (C) Elsevier, Paris.

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Purpose: To evaluate clinically and microscopically the human pulp response when directly capped with an adhesive system or calcium hydroxide over short (9-12 days) and long (53-204 days) experimental periods. Materials and Methods: Fifty-one sound human premolars scheduled for orthodontic extraction, had their pulp horns gently exposed with a diamond point. Debris in the pulp wound was washed out with a sterile saline solution. The pulps were then capped with either an adhesive system (Scotchbond Multi-Purpose Plus) or calcium hydroxide. All teeth were subsequently restored with resin-based composite (Z-100) according to the manufacturer's instructions. After the experimental periods, the teeth were extracted and processed for light microscopic examination. Results: Short-term: the pulp tissue capped with SBMP-P exhibited dilated and congested blood vessels associated with a mo;derate inflammatory response and blanching of pulp cell nuclei. Long-term: no evidence of healing and bridge formation was observed. A persistent mild inflammatory pulp response was present. Micro-abscesses were detected in three cases associated with bacterial infiltration. Calcium hydroxide stimulated early pulp repair and dentin bridging which extended into the longest period.

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Injections of the excitatory amino acid L-glutamate (L-glu) into the rostral ventrolateral medulla (RVLM) directly activate the sympathetic nervous system and increase mean arterial pressure (MAP). A previous study showed that lesions of the anteroventral third ventricle region in the forebrain reduced the pressor response to L-glu into the RVLM. In the present study we investigated the effects produced by injections of atropine (cholinergic antagonist) into the lateral ventricle (LV) on the pressor responses produced by L-ghl into the RVLM. Male Holtzman rats (280-320 g, n=5 to 12/group) with stainless steel cannulas implanted into the RVLM, LV or 4th ventricle (4th V) were used. MAP and heart rate (HR) were recorded in unanesthetized rats. After saline into the LV, injections of L-glu (5 nmol/100 nl) into the RVLM increased MAP (51 +/- 4 mm Hg) without changes in HR. Atropine (4 nmol/1 PI) injected into the LV reduced the pressor responses to L-glu into the RVLM (36 +/- 5 mm Hg), However, atropine at the same dose into the 4th V or directly into the RVLM did not modify the pressor responses to L-glu into the RVLM (45 +/- 2 and 49 +/- 4 mm Hg, respectively, vs. control: 50 +/- 4mmHg). Central cholinergic blockade did not affect baro and chemoreflex nor the basal MAP and HR. The results suggest that cholinergic mechanisms probably from forebrain facilitate or modulate the pressor responses to L-glu into the RVLM. The mechanism is activated by acetylcholine in the forebrain, however, the neurotransmitter released in the RVLM to facilitate the effects of glutamate is not acetylcholine. (C) 2007 Elsevier B.V. All rights reserved.

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Peripheral treatment with the cholinergic agonist pilocarpine induces intense salivation that is inhibited by central injections of the alpha(2)-adrenergic/imidazoline receptor agonist moxonidine. Salivary gland blood flow controlled by sympathetic and parasympathetic systems may affect salivation. We investigated the changes in mean arterial pressure (MAP) and in the vascular resistance in the submandibular/sublingual gland (SSG) artery, superior mesenteric (SM) artery and low abdominal aorta (hindlimb) in rats treated with intraperitoneal (i.p.) pilocarpine alone or combined with intracerebroventricular (i.c.v.) moxonidine. Male Holtzman rats with stainless steel cannula. implanted into lateral ventricle (LV) and anesthetized with urethane were used. Pilocarpine (4 mumol/kg of body weight) i.p. reduced SSG vascular resistance (-50 +/- 13% vs. vehicle: 5 +/- 3%). Pilocarpine i.p. also increased mesenteric vascular resistance (15 +/- 5% vs. vehicle: 2 +/- 3%) and MAP (16 +/- 3 mmHg, vs. vehicle: 2 +/- 3 mmHg). Moxonidine (20 nmol) i.c.v. increased SSG vascular resistance (88 +/- 12% vs. vehicle: 7 +/- 4%). When injected 15 min following i.c.v. moxonidine, pilocarpine i.p. produced no change on SSG vascular resistance. Pilocarpine-induced pressor responses and increase in mesenteric vascular resistance were not modified by i.c.v. moxonidine. The treatments produced no change in heart rate (HR) and hindlimb vascular resistance. The results show that (1) i.p. pilocarpine increases mesenteric vascular resistance and MAP and reduces salivary gland vascular resistance and (2) central moxonidine increases salivary gland vascular resistance and impairs pilocarpine-induced salivary gland vasodilatation. Therefore, the increase in salivary gland vascular resistance may play a role in the anti-salivatory response to central moxonidine. (C) 2003 Elsevier B.V. All rights reserved.