Evaluation of nitric oxide in murine renal tissue subjected to acute hemorrhage under anesthesia with sevoflurane use of glyburide

• Grant number: 11/09161-1
• Support Opportunities: Regular Research Grants
• Start date: August 01, 2011
• End date: January 31, 2014
• Field of knowledge: Health Sciences - Medicine - Surgery
• Principal Investigator: Yara Marcondes Machado Castiglia
• Grantee: Yara Marcondes Machado Castiglia
• Host Institution: Faculdade de Medicina (FMB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil

Abstract

In this experimental study, will evaluate nitric oxide (NO) produced in murine renal tissue subjected to acute hemorrhage under anesthesia with sevoflurane in use of glibenclamide. In the intervention group in prior research, there was attenuation of renal injury at the histopathological level, significant compared to the control group. Based on previous studies that suggest NO as an important modulator of renal function, because they show an increase in blood pressure resulting from the inhibition of NO production, whereas NO acts as antagonist substances reactive oxygen species (ROS) in renal tissue, suggests that the acute kidney injury would result from the loss of this mechanism. Thus, the imbalance between the loss of renal protection and NO-dependent deleterious effects of ROS would represent the path way of injury in acute renal failure. The glibenclamide attenuates acute kidney injury by interfering with this balance by decreasing the production of ROS or by protecting the enzyme producing NO? The nitrite measurement, a product of NO, using biochemical test, the modified method of Granger, we intend to clarify this mechanism, reproducing the same methodological conditions, developted in experiment conducted by Diego et al., 2007. We will add the intervention group SHAM (glibenclamide) and controls without bleeding. (AU)