RICARDO COSTA PETRONI
Projetos de Pesquisa
Unidades Organizacionais
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina
4 resultados
Resultados de Busca
Agora exibindo 1 - 4 de 4
- Hypertonic saline solution reduces the inflammatory response in endotoxemic rats(2012) THEOBALDO, Mariana Cardillo; BARBEIRO, Hermes Vieira; BARBEIRO, Denise Frediani; PETRONI, Ricardo; SORIANO, Francisco GarciaOBJECTIVE: Volume replacement in septic patients improves hemodynamic stability. This effect can reduce the inflammatory response. The objective of this study was to evaluate the effect of 7.5% hypertonic saline solution versus 0.9% normal saline solution for volume replacement during an inflammatory response in endotoxemic rats. METHODS: We measured cytokines (serum and gut), nitrite, and lipid peroxidation (TBARS) as indicators of oxidative stress in the gut. Rats were divided into four groups: control group (C) that did not receive lipopolysaccharide; lipopolysaccharide injection without treatment (LPS); lipopolysaccharide injection with saline treatment (LPS + S); and lipopolysaccharide injection with hypertonic saline treatment (LPS + H). Serum and intestine were collected. Measurements were taken at 1.5, 8, and 24 h after lipopolysaccharide administration. RESULTS: Of the four groups, the LPS + H group had the highest survival rate. Hypertonic saline solution treatment led to lower levels of IL-6, IL-10, nitric oxide, and thiobarbituric acid reactive substances compared to 0.9% normal saline. In addition, hypertonic saline treatment resulted in a lower mortality compared to 0.9% normal saline treatment in endotoxemic rats. Volume replacement reduced levels of inflammatory mediators in the plasma and gut. CONCLUSION: Hypertonic saline treatment reduced mortality and lowered levels of inflammatory mediators in endotoxemic rats. Hypertonic saline also has the advantage of requiring less volume replacement.
conferenceObject Obesity alters sepsis induced pulmonary inflammation(2012) LIMA-SALGADO, T.; FUNGARO, T. P.; PETRONI, R. C.; OLIVEIRA, S. J. S.; BARBEIRO, D. F.; SORIANO, F. G.Purpose/Objective: Sepsis is a severe disease that represents a significant healthcare burden worldwide, while obesity has reached epidemic proportions over the last few decades. Although the mechanism is uncharted, it is known that obesity increases morbidity and mortality in sepsis through its multiple effects on many organ systems, including pulmonary function. Our aim was to investigate the effects of obesity in systemic and pulmonary inflammatory process in an experimental model of endotoxemic shock. Materials and methods: Animals were fed a high fat diet (30% of fat) for 6 weeks and then injected with 15 mg/kg LPS i.p. They were euthanatized after 6, 24 and 48 h. Inflammation was characterized by measurement of plasma and pulmonary cytokines. The mRN expression of cytokines and tissue remodeling proteins was determined by real time PCR. Results: Obesity decreased the survival rate of the animals 24 h after LPS injection. There was higher plasma concentration of IL1-beta, IL-6and TNF-alpha in these animals. Furthermore, there was higher concentration of IL-6 in the obese mice’s lungs after 6 h of endotoxemia. However, the mRNA expression of pro-inflammatory factors (IL-6, TNF-alpha, IL-1beta and MMP9) was lower, suggesting they may be converted to proteins. Obese mice presented higher mRNA expression of TGF-beta after 6 h, indicating a reparative process. Conclusions: Obesity may be an additional complication factor in sepsis induced pulmonary inflammation.- ROLE OF FOCAL ADHESION KINASE IN LUNG REMODELING OF ENDOTOXEMIC RATS(2012) PETRONI, Ricardo Costa; TEODORO, Walcy R.; GUIDO, Maria Carolina; BARBEIRO, Hermes Vieira; ABATEPAULO, Fatima; THEOBALDO, Mariana Cardillo; BISELLI, Paolo Cesare; SORIANO, Francisco GarciaDespite significant advances in the care of critically ill patients, acute lung injury continues to be a complex problem with high mortality. The present study was designed to characterize early lipopolysaccharide (LPS)-induced pulmonary injury and small interfering RNA targeting focal adhesion kinase (FAK) as a possible therapeutic tool in the septic lung remodeling process. Male Wistar rats were assigned into endotoxemic group and control group. Total collagen deposition was performed 8, 16, and 24 h after LPS injection. Focal adhesion kinase expression, interstitial and vascular collagen deposition, and pulmonary mechanics were analyzed at 24 h. Intravenous injection of small interfering RNA targeting FAK was used to silence expression of the kinase in pulmonary tissue. Focal adhesion kinase, total collagen deposition, and pulmonary mechanics showed increased in LPS group. Types I, III, and V collagen showed increase in pulmonary parenchyma, but only type V increased in vessels 24 h after LPS injection. Focal adhesion kinase silencing prevented lung remodeling in pulmonary parenchyma at 24 h. In conclusion, LPS induced a precocious and important lung remodeling. There was fibrotic response in the lung characterized by increased amount in total and specific-type collagen. These data may explain the frequent clinical presentation during sepsis of reduced lung compliance, oxygen diffusion, and pulmonary hypertension. The fact that FAK silencing was protective against lung collagen deposition underscores the therapeutic potential of FAK targeting by small interfering RNA.
conferenceObject ACTION OF HYPERTONIC SALINE SOLUTION (NaCl 7,5%) IN PULMONARY FIBROSIS IN A RODENT MODEL OF ENDOTOXEMIA(2012) PETRONI, Ricardo Costa; BISELLI, Paolo; MARTINS, Milton; CSABA, Szabo; SORIANO, FranciscoHypertonic saline solution (HSS, NaCl 7,5%) has shown to modulates immune function favorably and decrease pulmonary injury triggered by endotoxic shock. Therefore, our objective was to investigate the effects of HSS on the mechanism involved in pulmonary fibrosis, in an experimental model of endotoxemic shock. Wistar rats (220–260 g) received lipopolysaccharide - LPS (10mg/kg, intraperitoneal,ip) and volume after 15 minutes. The animals were assigned in four groups (n=7 per group): control group (not subjected to LPS); LPS group (injected with LPS 10mg/kg i.p); HSS group (injected with LPS and treated with hypertonic saline, 4 mL/Kg) and NS group (injected with LPS and treated with normal saline, 34 mL/kg). At 24h after treatment, pulmonary mechanics, type I collagen expression, metalloproteinase 9 expression and activity, and focal adhesion kinase (FAK) were measured. Normal saline increased pulmonary resistance and elastance, compared to other groups (p<0.05). HSS inhibited collagen expression compared to LPS and NS groups and prevented pulmonary injury by decreased MMP9 activity in tissue (p<0.05). Expression of FAK was decreased in HSS groups compared to LPS and NS groups (P<0.05). Therefore, we concluded that treatment of endotoxemic shock with HSS solution can decreased pulmonary fibrosis and injury through FAK pathway.