86 resultados para Intraventricular


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OBJETIVO: Avaliar os efeitos na função ventricular esquerda do uso precoce e tardio de dopamina, em modelo experimental de coração isolado. MÉTODO: Foram utilizados 60 coelhos em modelo de coração isolado mantido por animal suporte. Um balão intraventricular foi locado no ventrículo esquerdo. Três grupos foram constituídos: grupo controle (GC); grupo que recebeu dopamina precoce (Dopa P) e grupo que recebeu dopamina tardia (após 20 minutos) (Dopa T). Foram realizadas leituras hemodinâmicas diretas e indiretas. RESULTADOS: Fluxo sangüíneo coronariano: GC(7,196 ± 1,275ml/min); Dopa P (9,477 ± 1,160ml/min); Dopa T (14,316 ± 2,308ml/min), com GC=Dopa P, GC ¹Dopa T e Dopa P¹Dopa T. Primeira derivada temporal da pressão intraventricular (dp/dt+): GC (719,61 ± 127,53ml/min); Dopa P (719,61 ± 127,53ml/min); Dopa T (1431,60 ± 230,87ml/min), p<0,05, Dopa P¹Dopa T, GC=Dopa P e GC ¹ Dopa T. Primeira derivada temporal da pressão intraventricular negativa (dp/dt-): GC (469,85 ± 107,16mmHg/s); Dopa P (716,07 ± 215,66mmHg/s); Dopa T (931,24 ± 181,46mmHg/s), p<0,05, Dopa P¹Dopa T¹GC. Delta V: GC (1,355 ± 0,2432ml); Dopa P (0,97 ± 0,3199ml); Dopa T (1,27 ± 0,2983ml), p>0,05, Dopa P=Dopa T=GC. Estresse sistólico desenvolvido: GC (27,273 ± 10,276g/cm²); Dopa P (55,219 ± 24,625g/cm²); Dopa T (79,152 ± 12,166g/cm²), Dopa P=Dopa T, Dopa P=GC e GC ¹ Dopa T.Dialdeído Malônico (MDA): GC (4,5 ± 0,527mmol/L); Dopa P (4,7 ± 1,16mmol/L); Dopa T (4,1 ± 0,7379mmol/L), p>0,05, Dopa P=Dopa T=GC. CONCLUSÕES: Concluiu-se que, no modelo experimental delineado, o uso precoce da dopamina foi deletério, segundo algumas variáveis hemodinâmicas.

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O objetivo foi a padronização de modelo experimental de coração isolado parabiótico em coelhos, testando sua estabilidade e durabilidade, para fins de pesquisa cardiovascular. Foram utilizados 66 coelhos raça Norfolk-2000 divididos em grupo doador do coração isolado e animais suporte, totalizando 33 preparações. Mediante auxilio de bombas peristálticas estabeleceu-se suporte circulatório para o coração isolado mantendo-se fluxo constante(16ml/min.). Um balão intraventricular foi inserido no ventrículo esquerdo, sendo ajustado para gerar pressão diastólica de ± 10mmHg. A freqüência foi fixada em 120 batimentos por minuto mediante o uso de marcapasso. Foram avaliadas variáveis hemodinâmicas, laboratoriais e anatomopatológicas. Das 33 preparações, 13 foram excluídas mediante critérios pré-estabelecidos. Das 20 restantes, 10 cumpriram o tempo máximo do protocolo(180 minutos). Com relação ao animal suporte houve deterioração hemodinâmica progressiva c/ queda da pressão arterial média(89,30±6,09mmHg->47,50±6,35mmHg). Com relação ao corações isolado, das 10 preparações que cumpriram os 180 minutos de protocolo, houve estabilidade hemodinâmica. As variáveis laboratoriais mostraram queda progressiva do sódio, potássio e hemoglobina, sendo compatível com hemodiluição. O exame anatomopatológico mostrou espaçamento maior entre fibras, compatível com edema. O presente modelo mostrou estabilidade e atividade de 100% das preparações em 60 minutos, havendo perdas progressivas chegando a 50% das preparações em atividade em 180 minutos. O presente modelo, dentro das limitações estabelecidas é viável para pesquisas cardiovasculares.

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Objetivos: avaliar a evolução ultra-sonográfica de cistos subependimários (CSE) do ângulo externo dos ventrículos laterais, e a evolução clínica dos pacientes. Comparar os pacientes com CSE isolados e os com CSE associados a outras lesões. Métodos: foram diagnosticados um a vários cistos no ângulo externo de um ou de ambos os ventrículos laterais, por meio de ultra-som transfontanelar (US) de rotina, realizado nos primeiros dias de vida, caracterizando os CSE. Durante o período de 1981-2000, 66 recém-nascidos tiveram CSE evidenciados na UTI neonatal do Hospital de Port-Royal. Foram constituídos dois grupos: G-I, com CSE isolados (n=21), e G-II, com CSE associados a outras lesões (n=45). Resultados: os recém-nascidos do GI apresentaram maior maturidade, melhores condições de nascimento e menor morbidade respiratória em relação a GII. A incidência de malformações congênitas foi elevada em ambos os grupos. Houve baixa taxa de infecção bacteriana e ausência de infecção congênita. Os CSE foram uni ou bilaterais, únicos ou múltiplos (colar de pérolas), sem diferença entre os grupos estudados, e predominaram à esquerda. US seriados foram realizados em 49/66 pacientes (74%), mostrando aumento no tamanho do cisto em 21/49 (45%), no primeiro mês de vida, enquanto 12 CSE (24%) desapareceram. O óbito ocorreu em dez recém-nascidos com lesões neurológica graves (quatro leucomalácias periventriculares, cinco hemorragias peri e intraventriculares), e somente um com hérnia diafragmática não apresentava outras lesões ao US transfontanelar. Conclusões: as características dos CSE não diferiram quando esses estavam associados a outras lesões. O nítido predomínio no lado esquerdo sugere uma etiologia vascular. Foi encontrada uma alta taxa de malformações associadas, alertando para a possibilidade de uma etiologia malformativa. Ambas hipóteses sugerem um desvio de desenvolvimento, e não de uma fetopatia viral.

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BACKGROUND:Guidelines for red blood cell (RBC) transfusions exist; however, transfusion practices vary among centers. This study aimed to analyze transfusion practices and the impact of patients and institutional characteristics on the indications of RBC transfusions in preterm infants.STUDY DESIGN and METHODS:RBC transfusion practices were investigated in a multicenter prospective cohort of preterm infants with a birth weight of less than 1500 g born at eight public university neonatal intensive care units of the Brazilian Network on Neonatal Research. Variables associated with any RBC transfusions were analyzed by logistic regression analysis.RESULTS:Of 952 very-low-birth-weight infants, 532 (55.9%) received at least one RBC transfusion. The percentages of transfused neonates were 48.9, 54.5, 56.0, 61.2, 56.3, 47.8, 75.4, and 44.7%, respectively, for Centers 1 through 8. The number of transfusions during the first 28 days of life was higher in Center 4 and 7 than in other centers. After 28 days, the number of transfusions decreased, except for Center 7. Multivariate logistic regression analysis showed higher likelihood of transfusion in infants with late onset sepsis (odds ratio [OR], 2.8; 95% confidence interval [CI], 1.8-4.4), intraventricular hemorrhage (OR, 9.4; 95% CI, 3.3-26.8), intubation at birth (OR, 1.7; 95% CI, 1.0-2.8), need for umbilical catheter (OR, 2.4; 95% CI, 1.3-4.4), days on mechanical ventilation (OR, 1.1; 95% CI, 1.0-1.2), oxygen therapy (OR, 1.1; 95% CI, 1.0-1.1), parenteral nutrition (OR, 1.1; 95% CI, 1.0-1.1), and birth center (p < 0.001).CONCLUSIONS:The need of RBC transfusions in very-low-birth-weight preterm infants was associated with clinical conditions and birth center. The distribution of the number of transfusions during hospital stay may be used as a measure of neonatal care quality.

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A case of intraventricular meningioma in a 17 year old white man located in the right lateral ventricle is presented. The tumor was successfully removed at operation, and weighed 470 grams. The patient made a good recovery; however, hemiparesis and amaurosis amaurosis, remained.

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The development of a fever in response to intravenous (IV, 1.5 μg/kg body mass) and intracerebroventricular (ICV, 1.5 μg/animal) injections of Escherichia coli lipopolysaccharide (LPS) was studied in control, thyroidectomised and protein-calorie malnourished rabbits (New Zealand Whites, n = 55). ICV injection of LPS is control rabbits produced a fever response, the characteristics of which differed from those obtained after IV pyrogen injection. Thyroid deficiency caused an attenuated fever response, irrespective of whether LPS had been administered by IV or ICV injection. Protein-calorie malnourished rabbits showed a smaller fever response after IV or ICV pyrogen injections. Malnourished rabbits, refed over a period of 15 days, showed a typical biphasic fever response, but with lower magnitude than controls. The results of these experiments suggest that ICV injection of LPS is not an appropriate model for the study of fever mechanisms in disease states, and that the attenuated fever response observed in protein-calorie malnourished rabbits may be related, at least in part, to a decreased ability to produce the endogenous pyrogen interleukin-1.

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Cardiovascular responses to central losartan (LOS), a non-peptide angiotensin II (ANG II) receptor antagonist, were investigated by comparing the effects of LOS injection into the 3rd and 4th cerebral ventricles (3rdV, 4thV) on mean arterial pressure (MAP) and heart rate (HR). Adult male Holtzman rats were used (N=6 animals per group). Average basal MAP and HR were 114±3 mmHg and 343±9 bpm (N=23), respectively. LOS (50, 100 or 200 nmol/2 μl) injected into the 3rdV induced pressor (peak of 25±3 mmHg) and tachycardic (peak of 60±25 bpm) responses. LOS injected into the 4thV had no effect on MAP, but it induced bradycardia (peak of -35±15 bpm). KCl (200 nmol/2 μl) injected into the 3rdV or into the 4thV had no effect on either MAP or HR compared to 0.9% saline injection. The results indicate that LOS injected into the third ventricle acts on forebrain structures to induce its pressor and tachycardic effects and that bradycardia, likely dependent on hindbrain structures, is obtained when LOS is injected into the fourth ventricle.

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Angiotensin II (Ang II) non-peptide antagonists were injected i.c.v. (6.25-200 nmol, n = 5-8 rats/group): In sodium replete rats, losartan (AT1 receptor antagonist) induced an increase in mean arterial pressure (MAP) and in heart rate (HR) by 3rd ventricular (3rdV) injection, and a weaker pressor response and bradycardia by 4th ventricular (4thV) injection. PD123319 (AT2 receptor antagonist) induced an increase in MAP and in HR by 3rdV injection, and an increase in MAP and no alteration in HR by 4thV injection. In sodium deplete (furosemide plus removal of ambient sodium for 24 h) rats, losartan induced an increase in MAP and no alteration in HR by 3rdV injection, and no alteration in MAP and bradycardia by 4thV injection. PD123319 induced an increase in MAP and in HR by 3rdV injection, and an increase in MAP and bradycardia by 4thV injection. Thus, there was no fall in MAP by central injections of Ang II antagonists. Intravenous injection of losartan, but not of PD123319, induced a fall in MAP in both sodium replete and sodium deplete animals. Therefore, losartan and PD123319 can have similar effects on MAP and HR when injected intracerebroventricularly, although some differences are also present. The bradycardia is consistent with an withdrawal of Ang II inhibitory action on baroreflex.

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We determined the effects of losartan and CGP42112A (selective ligands of the AT1 and AT2 angiotensin receptors, respectively) and salarasin (a relatively nonselective angiotensin receptor antagonist) on urinary volume and urinary sodium and potassium excretion induced by administration of angiotensin II (ANG II) into the paraventricular nucleus (PVN) of conscious rats. Both the AT1 and AT2 ligands and salarasin administered in the presence of ANG II elicited a concentration-dependent inhibition of urine excretion, but losartan inhibited only 75% of this response. The IC50 for salarasin, CGP42112A, and losartan was 0.01, 0.05, and 6 nM, respectively. Previous treatment with saralasin, CGP42112A and losartan competitively antagonized the natriuretic responses to PVN administration of ANG II, and the IC50 values were 0.09, 0.48, and 10 nM, respectively. The maximum response to losartan was 65% of that obtained with saralasin. Pretreatment with saralasin, losartan, and CGP42112A injected into the PVN caused shifts to the right of the concentration-response curves, but the losartan concentrations were disproportionately greater compared with salarasin or CGP42112A. The IC50 values were 0.06, 0.5, and 7.0 for salarasin, CGP42112A, and losartan, respectively. These results suggest that both AT1 and AT2 receptor subtypes in the PVN are involved in ANG II-related urine, sodium, and potassium excretion, and that the inhibitory responses to AT2 blockade are predominant. Copyright (C) 1999 Elsevier Science B.V.

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Bilateral injections of the GABAA agonist muscimol into the lateral parabrachial nucleus (LPBN) disrupt satiety and induce strong ingestion of water and 0.3M NaCl in fluid-replete rats by mechanisms not completely clear. In the present study, we investigated the effects of the blockade of central muscarinic cholinergic receptors with atropine injected intracerebroventricularly (i.c.v.) on 0.3M NaCl and water intake induced by muscimol injections into the LPBN in fluid-replete rats. Male Holtzman rats with stainless steel cannulas implanted bilaterally into the LPBN and unilaterally into the lateral ventricle (LV) were used. Bilateral injections of muscimol (0.5nmol/0.2μL) into the LPBN induced 0.3M NaCl (32.2±9.9mL/4h, vs. saline: 0.4±0.2mL/4h) and water intake (11.4±4.4mL/4h, vs. saline: 0.8±0.4mL/4h) in fluid-replete rats previously treated with i.c.v. injection of saline. The previous i.c.v. injection of atropine (20nmol/1μL) reduced the effects of LPBN-muscimol on 0.3M NaCl (13.5±5.0mL/4h) and water intake (2.9±1.6mL/4h). The i.c.v. injection of atropine did not affect 0.3M NaCl (26.8±6.2mL/2h, vs. saline i.c.v.: 36.5±9.8mL/2h) or water intake (14.4±2.5mL/2h, vs. saline i.c.v.: 15.6±4.8mL/2h) in rats treated with furosemide+captopril subcutaneously combined with bilateral injections of moxonidine (α2-adrenoceptor/imidazoline agonist, 0.5nmol/0.2μL) into the LPBN, suggesting that the effect of atropine was not due to non-specific inhibition of ingestive behaviors. The results show that active central cholinergic mechanisms are necessary for the hypertonic NaCl and water intake induced by the blockade of the inhibitory mechanisms with injections of muscimol into the LPBN in fluid-replete rats. The suggestion is that in fluid-replete rats the action of LPBN mechanisms inhibits facilitatory signals produced by the activity of central cholinergic mechanisms to maintain satiety. © 2012 Elsevier B.V.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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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)