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Acute but not chronic metabolic acidosis potentiates the acetylcholine-induced reduction in blood pressure: an endothelium-dependent effect BJMBR
Celotto,A.C.; Ferreira,L.G.; Capellini,V.K.; Albuquerque,A.A.S.; Rodrigues,A.J.; Evora,P.R.B..
Metabolic acidosis has profound effects on vascular tone. This study investigated the in vivo effects of acute metabolic acidosis (AMA) and chronic metabolic acidosis (CMA) on hemodynamic parameters and endothelial function. CMA was induced by ad libitum intake of 1% NH4Cl for 7 days, and AMA was induced by a 3-h infusion of 6 M NH4Cl (1 mL/kg, diluted 1:10). Phenylephrine (Phe) and acetylcholine (Ach) dose-response curves were performed by venous infusion with simultaneous venous and arterial blood pressure monitoring. Plasma nitrite/nitrate (NOx) was measured by chemiluminescence. The CMA group had a blood pH of 7.15±0.03, which was associated with reduced bicarbonate (13.8±0.98 mmol/L) and no change in the partial pressure of arterial carbon dioxide...
Tipo: Info:eu-repo/semantics/article Palavras-chave: Acid-base balance; Metabolic acidosis; Hemodynamic failure; Endothelium; Nitric oxide.
Ano: 2016 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2016000200604
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Effects of NO/cGMP inhibitors in a rat model of anaphylactoid shock BJMBR
Albuquerque,A.A.S.; Ferreira,L.G.; Carvalho,M.T.M.; Capellini,V.K.; Evora,P.R.B.; Celotto,A.C..
Anaphylactic shock can be defined as an acute syndrome, and it is the most severe clinical manifestation of allergic diseases. Anaphylactoid reactions are similar to anaphylactic events but differ in the pathophysiological mechanism. Nitric oxide (NO) inhibitors during anaphylaxis suggest that NO might decrease the signs and symptoms of anaphylaxis but exacerbate associated vasodilation. Therefore, blocking the effects of NO on vascular smooth muscle by inhibiting the guanylate cyclase (GC) would be a reasonable strategy. This study aimed to investigate the effects of NO/cGMP pathway inhibitors methylene blue (MB), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME), and indigo carmine (IC) in shock induced by compound 48/80 (C48/80) in rats. The...
Tipo: Info:eu-repo/semantics/article Palavras-chave: Endothelial cells; Allergy; Rodent; Nitric oxide; Anaphylaxis.
Ano: 2020 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2020000300606
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Erythropoietin reduces the expression of myostatin in mdx dystrophic mice BJMBR
Feder,D.; Rugollini,M.; Santomauro Jr,A.; Oliveira,L.P.; Lioi,V.P.; dos Santos,R.; Ferreira,L.G.; Nunes,M.T.; Carvalho,M.H.; Delgado,P.O.; Carvalho,A.A.S.; Fonseca,F.L.A..
Erythropoietin (EPO) has been well characterized as a renal glycoprotein hormone regulating red blood cell production by inhibiting apoptosis of erythrocyte progenitors in hematopoietic tissues. EPO exerts regulatory effects in cardiac and skeletal muscles. Duchenne muscular dystrophy is a lethal degenerative disorder of skeletal and cardiac muscle. In this study, we tested the possible therapeutic beneficial effect of recombinant EPO (rhEPO) in dystrophic muscles in mdx mice. Total strength was measured using a force transducer coupled to a computer. Gene expression for myostatin, transforming growth factor-β1 (TGF-β1), and tumor necrosis factor-α (TNF-α) was determined by quantitative real time polymerase chain reaction. Myostatin expression was...
Tipo: Info:eu-repo/semantics/article Palavras-chave: Muscular dystrophy; Erythropoietin; Myostatin; Skeletal muscle; Quadriceps.
Ano: 2014 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2014001100966
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