Abstract:

Background Hydrogen-rich saline provides a high concentration of hydrogen which selectively reduces levels of hydroxyl radicals and alleviates acute oxidative stress in many models. We investigated the protective effects and mechanisms of three different hydrogen-rich liquid resuscitation preparations on lung injury-induced uncontrolled hemorrhagic shock (UHS) in rats. Materials and methods A UHS rat model was prepared using the method of Capone et al. of arterial bleeding and tail amputation. Healthy male Wistar rats were randomly divided into 7 groups (10/group) to receive: Sham treatment; Ringer’s solution; hydrogen-rich Ringer’s solution (H-Ringer’s solution); hydroxyethyl starch (HES); hydrogen-rich hydroxyethyl starch (H-HES); hypertonic saline/hydroxyethyl starch (HSH); and hydrogen-rich hypertonic saline/hydroxyethyl starch (H-HSH). At 72 hours after successful resuscitation, lung tissue was HE stained to score any pathological changes. We also determined wet-to-dry (W/D) lung weight ratios and lung tissue concentrations of interleukin-6 (IL-6), tumor necrosis factor -α (TNF-α), interleukin -10 (IL-10), and malondialdehyde (MDA), and superoxide dismutase (SOD) and myeloperoxidase (MPO) activities. Results Compared with the Non-H groups, polymorphonuclear neutrophil (PMN) accumulation in alveoli in the H groups was significantly reduced (P value), and capillary leakage and wall edema were ameliorated. Compared with the Sham group, pathologic pulmonary injury scores, W/D ratios, IL-6, TNF-α, IL-10, and MDA concentrations, and MPO activity in the other groups were all increased, whereas SOD activity was decreased (P<0.01). Comparing the H-Ringer’s, H-HES, and H-HSH groups respectively with the Ringer’s, HES, and HSH groups, pathologic pulmonary injury scores, W/D ratios, IL-6, TNF-α, and MDA concentrations, and MPO activity were all reduced, whereas IL-10 concentrations and SOD activity were increased (P<0.01). Conclusions Each hydrogen-rich liquid resuscitation preparation could protect the lung against acute injury secondary to UHS. These mechanisms may be associated with hydrogen inhibiting the release of pro-inflammatory cytokines, promoting anti-inflammatory cytokine release, and reducing oxidative damage.

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https://doi.org/10.1016/j.jss.2014.06.051

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