Published online Feb 4, 2018. doi: 10.5492/wjccm.v7.i1.1
Peer-review started: September 17, 2017
First decision: November 27, 2017
Revised: December 3, 2017
Accepted: December 14, 2017
Article in press: December 14, 2017
Published online: February 4, 2018
Processing time: 138 Days and 21.2 Hours
To evaluate the effects of mineralocorticoid receptor (MR) antagonists on mortality and inflammatory responses after hemorrhagic shock (HS) in rats.
One hundred and two male Sprague–Dawley rats were randomly assigned to one of the following three groups: Control, spironolactone (SPL), and eplerenone (EP) groups. HS was induced by the removal of blood. One half of rats were evaluated to determine mortality, hemodynamics, plasma tumor necrosis factor-alpha (TNF-α) concentrations, and arterial blood gas at 8 h after HS recovery. In the remainder of rats, the expression levels of genes encoding cytokines were evaluated in liver tissue samples at 1 h after HS recovery.
The survival rates 8 h after HS recovery were 71%, 94%, and 82% in the control, SPL, and EP groups, respectively. There were no significant differences in survival rates among the three groups (P = 0.219). Furthermore, there were no significant differences in gene expression levels in the liver or plasma TNF-α concentrations among the three groups (P = 0.888).
Pretreatment with MR antagonists did not improve mortality or cytokine responses in the liver after HS recovery in rats.
Core tip: Mineralocorticoid receptor (MR) antagonists have anti-inflammatory effects in models of ischemic and reperfusion injury, suggesting potential clinical value in patients with hemorrhagic shock. However, our findings indicate that pretreatment with MR antagonists does not improve mortality rates or cytokine responses in the liver after recovery from hemorrhagic shock in rats.