Protective Effects of Hydrogen-Rich Saline on Rats with Smoke Inhalation Injury.

Xing Chen,Qi Liu,Dawei Wang,Qun Liu,Yongjian Zhao,Yun Shi,Shihai Feng

doi:10.1155/2015/106836

Abstract

Objective. To explore the protective effects of hydrogen-rich saline on rats with smoke inhalation injury. Methods. 36 healthy male Sprague-Dawley rats were randomly divided into 3 groups (n = 12 per group): sham group (S), inhalation injury plus normal saline treatment group (I+NS), and inhalation injury plus hydrogen-rich saline treatment group (I+HS). 30 min after injury, normal saline and hydrogen-rich saline were injected intraperitoneally (5 mL/kg) in I+NS group and I+HS group, respectively. All rats were euthanized and blood and organ specimens were collected for determination 24 h after inhalation injury. Results. Tumor necrosis factor-alpha (TNF-α) levels, malondialdehyde (MDA) concentrations, nuclear factor kappa B (NF-κB) p65 expression, and apoptosis index (AI) in I+HS group were significantly decreased (P < 0.05), while superoxide dismutase (SOD) activities were increased compared with those in I+NS group; and a marked improvement in alveolar structure was also found after hydrogen-rich saline treatment. Conclusions. Hydrogen-rich saline treatment exerts protective effects in acute lung injury induced by inhalation injury, at least in part through the activation of anti-inflammatory and antioxidant pathways and inhibition of apoptosis.

Highlights

Inhalation injury, when accompanied by multiple organ injury, is caused by heat and smoke respiratory damage and contributes to being the leading cause of death in intensive care units, with a mortality that has remained in the range of 10%–20% [1].Airway damage is an important pathological change in the process of inhalation injury
Rats in injury plus normal saline treatment group (I+NS) group showed a significant increase in lung MDA activity and a significant decrease in superoxide dismutase (SOD) activity compared with those in S group (P < 0.01)
TNF-α levels in injury plus hydrogen-rich saline treatment group (I+HS) group decreased significantly compared with the I+NS group (P < 0.05) (Figure 1(c))

Summary

Introduction

Inhalation injury, when accompanied by multiple organ injury, is caused by heat and (or) smoke respiratory damage and contributes to being the leading cause of death in intensive care units, with a mortality that has remained in the range of 10%–20% [1]. Airway damage is an important pathological change in the process of inhalation injury. Due to the physiological structure, severe airway damage is mostly caused by smoke inhalation injury. The chemicals in the smoke can cause bronchitis and lead to the airway mucosa membrane hyperemia, edema, and hemorrhage and even mucosal erosion, necrotic damage, and ulceration and eventually result in dysfunctional ventilation function in the lung. The release of oxygen free radicals, inflammation, and stress are important factors in inhalation injury. In the early stages of inhalation injury, the release of oxygen free radicals can directly cause the damage of the airway epithelium [2]

Results

Discussion

Conclusion