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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Treatment of hemorrhagic shock with hypertonic saline solution modulates the inflammatory response to live bacteria in lungs

Full text
Author(s):
Fernandes, C. I. [1] ; Llimona, F. [1] ; Godoy, L. C. [1] ; Negri, E. M. [1] ; Pontieri, V. [1] ; Moretti, A. I. [1] ; Fernandes, T. R. [1] ; Soriano, F. G. [1] ; Velasco, I. T. [1] ; Souza, H. P. [1]
Total Authors: 10
Affiliation:
[1] Univ Sao Paulo, Dept Clin Med LIM51, Fac Med, Disciplina Emergencias Clin, BR-01246903 Sao Paulo - Brazil
Total Affiliations: 1
Document type: Journal article
Source: Brazilian Journal of Medical and Biological Research; v. 42, n. 10, p. 892-901, OCT 2009.
Web of Science Citations: 5
Abstract

Shock and resuscitation render patients more susceptible to acute lung injury due to an exacerbated immune response to subsequent inflammatory stimuli. To study the role of innate immunity in this situation, we investigated acute lung injury in an experimental model of ischemia-reperfusion (I-R) followed by an early challenge with live bacteria. Conscious rats (N = 8 in each group) were submitted to controlled hemorrhage and resuscitated with isotonic saline (SS, 0.9% NaCl) or hypertonic saline (HS, 7.5% NaCl) solution, followed by intratracheal or intraperitoneal inoculation of Escherichia coli. After infection, toll-like receptor (TLR) 2 and 4 mRNA expression was monitored by RT-PCR in infected tissues. Plasma levels of tumor necrosis factor α and interleukins 6 and 10 were determined by ELISA. All animals showed similar hemodynamic variables, with mean arterial pressure decreasing to nearly 40 mmHg after bleeding. HS or SS used as resuscitation fluid yielded equal hemodynamic results. Intratracheal E. coli inoculation per se induced a marked neutrophil infiltration in septa and inside the alveoli, while intraperitoneal inoculation-associated neutrophils and edema were restricted to the interseptal space. Previous I-R enhanced lung neutrophil infiltration upon bacterial challenge when SS was used as reperfusion fluid, whereas neutrophil influx was unchanged in HS-treated animals. No difference in TLR expression or cytokine secretion was detected between groups receiving HS or SS. We conclude that HS is effective in reducing the early inflammatory response to infection after I-R, and that this phenomenon is achieved by modulation of factors other than expression of innate immunity components. (AU)