Programa de Pós-graduação em Ciências Biológicas
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Navegando Programa de Pós-graduação em Ciências Biológicas por Autor "Amaral, Nathalia Oda"
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Item Envolvimento do núcleo pré-óptico mediano (MnPO) na recuperação cardiovascular induzida pela infusão de salina hipertônica em animais submetidos ao choque hemorrágico(Universidade Federal de Goiás, 2014-04-16) Amaral, Nathalia Oda; Custodio, Carlos Henrique Xavier; Pedrino, Gustavo Rodrigues; http://lattes.cnpq.br/1155446449250341; Oliveira, André Henrique Freiria de; Ferreira Neto, Marcos Luiz; Ferreira, Patrícia Maria; Castro, Carlos Henrique deIn recent decades, several studies have demonstrated that hyperosmolarity induced by hypertonic saline infusion (HS) it’s a benefit for hypovolemic hemorrhage treatment. The median preoptic nucleus (MnPO) is known to receive information from central osmoreceptors and peripheral afferents about plasma osmolarity changes, reflexively modulating autonomic and neuroendocrine adjustments, primarily through its projections to the paraventricular nucleus (PVN). The present study aim to determine MnPO involvement in cardiovascular recovery induced by HSI in rats subjected to hemorrhagic shock (HC). Wistar rats (250 - 300 g) were prepared to record mean arterial pressure (MAP), heart rate (HR), renal blood flow (RBF) and aortic (ABF). The renal vascular conductance (RVC) and aortic (AVC) were calculated through the ratio between RBF and ABF with MAP, respectively. Hemorrhagic shock was induced by blood withdrawal over 10 min until the MAP reached approximate values of 60 mmHg. The sodium overload by infusion HS (3 M NaCl, 1.8 ml ∙ kg-1 body mass index) was made 2 min after the nanoinjection (100 nL) of GABA agonist muscimol (4 mM experimental group 1 - EXP 1 ), α-adrenergic antagonist phentolamine (13 mM ; experimental group 2 - EXP 2) or isotonic saline (NaCl, 0.15 M, control group - CON) in MnPO. This resulted in HC CON (n=6) MAP reduction (98.4 ± 5.3 to 62.2 ± 1.1 mmHg after 20 min HC, p<0.05), a decrease in RVC (- 59.4 ± 9.2%, 20 min after HC, p<0.05) and did not alter the AVC (-11.5 ± 10.5%, 20 min after HC) and HR (387.2 ± 12 to 351.7 ± 13 bpm after 20 min HC). HC promoted in EXP 1 (n=6) MAP reduction (98 ± 5.4 to 61 ± 0.7 mmHg after 20 min HC, p<0.05), a decrease in RVC (-64.8 ± 10.9%, 20 min after CH, p<0.05) and CVA (-32.3 ± 4.4%, 20 min after HC, p<0.05) and did not alter HR (389 ± 23.9 ± 17.1 to 360 bpm after 20 min HC). In EXP 2 (n=6) HC resulted in a MAP reduction (102.0 ± 4.2 to 62.0 ± 1.1 mmHg, 20 min after HC, p<0.05), a decrease in CVR (-27.6 ± 5.8% after 20 min HC, p <0.05), CVA (-4.5 ± 4.1% after 20 min HC, p<0.05) and HR (387 ± 14 to 347 ± 7.4 bpm after 20 min HC). HS infusion enabled MAP restoration (105.2 ± 3 mmHg, 60 min after infusion of HS, p<0.05), did not alter HR (400 ± 18.4 bpm, 60 min after infusion of HS) raised the RVC to baseline xi levels (-14.6 ± 14.2%, 60 min after infusion of HS, p<0.05) and reduced AVC (- 27.4 ± 4.3%, 60 min after infusion HS, p<0.05) in CON. HS infusion in EXP 1 was not able to restore MAP (54 ± 3.8 mmHg, 60 min after infusion of HS, p<0.05) and RVC (- 48.1 ± 9.7%, 60 min after infusion of HS, p<0.05), did not alter HR (361 ± 15.3 bpm, 60 min after infusion of HS) and was able to promote an increase in AVC similar to baseline (-23.2 ± 10.6%, 60 min after infusion HS, p<0.05) levels. In EXP 2, HS infusion enabled MAP restoration (89 ± 3.3 mmHg, 60 min after infusion of HS, p<0.05) but this return to baseline was delayed and occurred only 50 min after HS infusion (88 ± 3.3 mmHg), HR return (379 ± 6.5 bpm, 60 min after infusion of HS) and RVC to basal levels (-16.1 ± 8.9%, 60 min after infusion HS, p<0.05) and an increase in AVC 10 min after HS infusion (20.3 ± 6.4%, p<0.05), which was restored to levels similar to baseline at registration end (-15.7 ± 6.2%, 60 min after infusion of HS, p<0.05). Together, the results obtained in this study showed that MnPO plays an important role in cardiovascular recovery induced by HS infusion in HC cases. Furthermore, the cardiovascular adjustments involved in this resuscitation seem to depend partly on adrenergic neurotransmission in this nucleus.Item Dieta hiperlipídica e hipernatremia: alterações autonômicas e cardiovasculares(Universidade Federal de Goiás, 2018-02-02) Amaral, Nathalia Oda; Colombari, Débora Simões de Almeida; http://lattes.cnpq.br/1684467594359403; Pedrino, Gustavo Rodrigues; http://lattes.cnpq.br/1155446449250341; Pedrino, Gustavo Rodrigues; Oliveira, André Henrique Freiria; Gomes, Rodrigo Mello; Amaral, Vanessa Cristiane de Santana; Rebelo, Ana Cristina SilvaHypertension is the most common pathologies which affect population. Of the factors that can promote hypertension, food behavior is highlighted in relation to unhealthy eating habits present in western diet. Thus, present study sought to evaluate some aspects of this pathology in several situations, and themes were discussed separately in two chapters. In the first moment, effect of maternal hyperlipidic diet on metabolic and autonomic parameters in offspring was evaluated. It is known which obesity induced by maternal diet can modify central regulatory pathways of the fetus, mainly long-term regulation of appetite, but no work sought to evaluate the influence of the maternal hyperlipidic diet (HD) on cardiovascular and autonomic parameters in the offspring . Female Holtzman rats (280-300 g) were divided into two groups. One group received standard diet (SD) and other HD. The animals had free access to SD or HD for 6 weeks prior and during gestation and lactation period. All pups were weaned after 21 days of life and had free access to SD. After one week some offspring and mothers were submitted to glycemic test and later euthanized for removal of adipose tissue and blood. Other offspring were submitted to in situ preparation. DH increased adipose tissue in all females, but was able to change only metabolic triacylglycerols concentration. Offspring of HFD dams (OffHFD) showed an increase in adipose tissue and total cholesterol and HDL levels. Offspring of SD dams (OffSD) showed decrease in sympathetic activity after pre-colicular transection. This effect was not observed in males offspring of mothers with HFD (OffHFD). KCN infusion caused similar increases in abdominal activity (ABD), in phrenic nerve frequency (PNA f) and sympathetic activity (SNA), but in OffHFD this increase in SNA was smaller. KCN caused increase in phrenic nerve amplitude (PNA) and was higher in OffHFD. Hypercapnia resulted in increase in SNA, ABD and PNA and decrease in PNA f in both groups. The decrease in PNA f was more pronounced in OffHFD and increased PNA was higher in OffHFD. Phenylephrine caused in both groups decrease in SNA, ABD and PNA, and generated an increase in PNA f. The reduction of SNA was higher in OffHFD. These results suggest that maternal HFD during fetal development alters central connections in offspring. In second moment oxytocin effects on vascular reactivity and its role in hypernatremia-induced responses were evaluated. Changes in volume and/or extracellular compartments composition are known to evoke various autonomic, cardiovascular and hormonal responses that to modulate renal excretion of water and sodium. The main vegetative adjustments are: renal vasodilation and oxytocin secretion. Regulation of osmolarity and volume is critical for survival. Despite knowledge, no study evaluated interaction between renal sympathetic activity and oxytocin secretion on renal and cardiovascular responses induced by sodium overload. Male Wistar rats (280–350 g) were anesthetized with sodium thiopental (40 mg/kg, i.v.). Animals were also instrumented for measurement of mean arterial pressure (MAP) and renal blood flow (RBF). Renal vascular conductance (RVC) was calculated as the ratio of RBF by MAP. In anesthetized rats (n = 6), OT infusion (0.03 μg/kg, i.v.) induced renal vasodilation. Ex vivo experiments demonstrated that OT caused renal artery relaxation. Blockade of OT receptors (OTR) reduced these responses to OT, indicating a direct effect of this peptide on OTR on this artery. Hypertonic saline (3 M NaCl, 1.8 ml/kg b.wt., i.v.) was infused over 60 s. In sham rats (n=6), hypertonic saline induced renal vasodilation. The OXTR antagonist (AT; n=7) and renal denervation (RX) reduced the renal vasodilation induced by hypernatremia. Atosiban with renal denervation (RX+AT; n=7) completely abolished renal vasodilation induced by sodium overload. Intact rats excreted 51% of the injected sodium within 90 min. Natriuresis was slightly blunted by atosiban and renal denervation (42% and 42% of load, respectively), whereas atosiban with renal denervation reduced sodium excretion to 16% of the load. These results suggest that OT and renal nerves are involved in renal vasodilation and natriuresis induced by acute plasma hypernatremia. The understanding of regulatory mechanisms activated both during obesity and during hyperosmolarity allows greater possibility development new therapeutic tools for hypertension prevention and treatment.