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Ana Cristina Simões e Silva

Publications and source records attributed to Ana Cristina Simões e Silva.

8 recordsLinked to original sources
PubMed2006

The renin-angiotensin system in a rat model of hepatic fibrosis: evidence for a protective role of Angiotensin-(1-7).

BACKGROUND/AIMS: The circulating renin-angiotensin system (RAS) [plasma renin activity (PRA), Angiotensin (Ang) I, Ang II and Ang-(1-7)] was evaluated in a model of hepatic fibrosis in rats. To investigate the pathophysiological involvement of Ang-(1-7), animals were treated with the Ang-(1-7) Mas receptor antagonist, A-779. METHODS: RAS components, liver function and histology were examined in male Wistar rats (220-300 g). Animals were submitted to sham-surgery or ligature of the bile duct and evaluated 1, 2, 4 and 6 weeks later. Blood samples were obtained to determine biochemical parameters and RAS components. A second group was treated with A-779 or vehicle to measure liver hydroxyproline and total transforming growth factor beta-1 (TGFbeta1). RESULTS: PRA and Ang I were significantly elevated in rats at 4 and 6 weeks compared to sham-operated animals. Ang II and Ang-(1-7) progressively increased over the 6 weeks. Changes in RAS profile correlated with histological signs of fibrosis and deterioration in liver function. Pharmacological blockade of the Ang-(1-7) receptor aggravated liver fibrosis with a significant elevation in hydroxyproline and total TGFbeta(1). CONCLUSIONS: Hepatic fibrosis was associated with RAS activation in our model. Our data also suggested that Ang-(1-7) played a protective role in hepatic fibrosis.

Angiotensin I↗
PubMed2006

Morphine versus remifentanil for intubating preterm neonates.

A double-blind, randomised controlled study was conducted to evaluate the intubation conditions in 20 preterm neonates following the use of either morphine or remifentanil as premedication. The findings suggest that the overall intubation conditions were significantly better (p=0.0034) in the remifentanil group than in the morphine group. No severe complications were observed in either group.

Analgesics, Opioid↗
PubMed2006

The therapeutic potential of Angiotensin-(1-7) as a novel Renin-Angiotensin System mediator.

In this review, we show Angiotensin-(1-7) as a novel Renin Angiotensin System mediator that antagonizes cardiovascular and proliferative effects of Angiotensin II and exerts complex renal actions. We also speculate the possibility of new drugs for the treatment of cardiovascular, genitourinary and hepatic diseases by interfering with ACE2-Angiotensin-(1-7)-Mas axis.

Angiotensin I↗
PubMed2005

Successful management of concomitant omphalocele, accessory hepatic lobe, and biliary atresia in a 44-day-old boy.

We report the second case in literature of a boy with the association of large omphalocele, accessory hepatic lobe, and biliary atresia, and the first successful treatment. The patient was submitted to a surgical treatment at 44 days of life, including Kasai procedure, correction of the remnant abdominal wall defect, and removal of a hepatic accessory lobe. The boy evolved with normalization of hepatic function tests. After 15 years of follow-up, the patient is completely healthy, weights 45 kg, and is 1.64 m tall.

Biliary Atresia↗
PubMed2005

Remifentanil for sedation and analgesia in a preterm neonate with respiratory distress syndrome.

We present the efficacy and safety of the use of remifentanil for intubation, sedation and analgesia in a preterm infant during mechanical ventilation for respiratory distress syndrome. A 34-week-old baby, born by cesarean delivery that developed respiratory distress, required intubation and ventilatory support. For intubation, the baby was given midazolam (0.2 mg.kg(-1)) and remifentanil (1 microg.kg(-1)). The intubation conditions were assessed and classified as excellent. The remifentanil infusion was started at dose 0.75 microg.kg(-1).min(-1) and the dose adjustments were made depending on the neonatal infant pain scale (NIPS), hemodynamic and respiratory changes or the presence of spontaneous movements. Pulse oximetry, respiratory rate, ECG and invasive blood pressure were continuously monitored. He was given surfactant within 2.5 h of life after which ventilator parameters could be progressively decreased. Three hours later, the remifentanil infusion was decreased to 0.5 microg.kg(-1).min(-1), and he remained sedated (NIPS < 2). Six hour after surfactant administration, blood gases and chest X ray were normal. The remifentanil infusion was then discontinued and 30 min later the baby was awake and extubated with success. There were no side effects after intubation or during the continuous infusion. The profile of remifentanil allowing a rapid recovery, the absence of side effects and a good level of sedation and analgesia support the choice of this opioid for sedation in the NICU.

Analgesics↗
PubMed2004

Nonpeptide AVE 0991 is an angiotensin-(1-7) receptor Mas agonist in the mouse kidney.

It has been described recently that the nonpeptide AVE 0991 (AVE) mimics the effects of angiotensin-(1-7) [Ang-(1-7)] in bovine endothelial cells. In this study, we tested the possibility that AVE is an agonist of the Ang-(1-7) receptor Mas, in vitro and in vivo. In water-loaded C57BL/6 mice, AVE (0.58 nmol/g body weight) produced a significant reduction in urinary volume (0.06+/-0.03 mL/60 min [n=9] versus 0.27+/-0.05 [n=9]; P<0.01), associated with an increase in urinary osmolality. The Ang-(1-7) antagonist A-779 completely blocked the antidiuretic effect of AVE. As observed previously for Ang-(1-7), the antidiuretic effect of AVE after water load was blunted in Mas-knockout mice (0.37+/-0.10 mL/60 min [n=9] versus 0.27+/-0.03 mL/60 min [n=11] AVE-treated mice). In vitro receptor autoradiography in C57BL/6 mice showed that the specific binding of 125I-Ang-(1-7) to mouse kidney slices was displaced by AVE, whereas no effects were observed in the binding of 125I-angiotensin II or 125I-angiotensin IV. Furthermore, AVE displaced the binding of 125I-Ang-(1-7) in Mas-transfected monkey kidney cells (COS) cells (IC50=4.75x10(-8) mol/L) and of rhodamine-Ang-(1-7) in Mas-transfected Chinese hamster ovary (CHO) cells. It also produced NO release in Mas-transfected CHO cells blocked by A-779 but not by angiotensin II type-1 (AT1) and AT2 antagonists. Contrasting with these data, the antidiuretic effect of AVE was totally blocked by AT2 antagonists and partially blocked (approximately 60%) by AT1 antagonists. The binding data, the results obtained in Mas-knockout mice and in Mas-transfected cells, show that AVE is a Mas receptor agonist. Our data also suggest the involvement of AT2/AT1-related mechanisms, including functional antagonism, oligomerization or cross-talk, in the renal responses to AVE.

Angiotensin I↗
PubMedDate not supplied

[Liddle's syndrome: late diagnosis of a rare cause of arterial hypertension].

OBJECTIVE: The aim of this article is to highlight the importance of a rare disease that causes severe arterial hypertension in children. It is important to advise pediatricians to measure arterial pressure in children in order to avoid late diagnosis and renal insufficiency. DESCRIPTION: We report a case of a 13-year-old patient that presented typical clinical and laboratorial features of Liddle's syndrome. The diagnosis was established based on the clinical picture associated with the presence of chronic hypokalemia, increase of urinary potassium excretion with sodium retention and reduction of renin plasma activity, and circulating levels of angiotensin II and aldosterone. In a spite of the initial therapeutic response to triamterene, the patient developed progressive renal failure due to the delay in the diagnosis and the poorly controlled hypertension. COMMENTS: Liddle's syndrome consists of a form of pseudoaldosteronism characterized by arterial hypertension, hypokalemia, metabolic alkalosis and failure to thrive. Some aspects regarding physiopathology, diagnosis and treatment are discussed.

English Abstract↗