Effects of hydrogen-rich saline treatment on polymicrobial sepsis.
BACKGROUND
Hydrogen has been reported to selectively reduce hydroxyl radicals and peroxynitrite anion in many pathologic processes. This study aimed to test the hypothesis that hydrogen-rich saline (HRS) may ameliorate organ dysfunction in a rat model of polymicrobial sepsis.


METHODS
Sepsis was induced in male Sprague-Dawley rats by cecal ligation and puncture (CLP). Twenty-four rats were equally assigned to Sham group, CLP group, and CLP + HRS group (n = 8). At 0, 6, and 18 h after CLP or sham operation, rats received an intraperitoneal injection of HRS (5 mL/kg) or the same volume of normal saline. Malondialdehyde, superoxide dismutase activities, inflammatory mediators, pulmonary nitric oxide, myeloperoxidase activities, wet-to-dry weight ratio, histologic scores, apoptotic analysis, alanine aminotransferase, creatinine, and blood urea nitrogen were assessed at 24 h after operation. The 7-d survival rate was also recorded.


RESULTS
HRS administration significantly reduced the serum high-mobility group box, alanine aminotransferase, creatinine, and blood urea nitrogen levels; the pulmonary interleukin 6, high-mobility group box, nitric oxide, and malondialdehyde levels; and the wet-to-dry weight ratio, total histologic scores, and terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells, whereas it increased the superoxide dismutase activities 24 h after CLP when compared with the CLP group. However, there was no significant difference in survival rate between the CLP + HRS and CLP groups.


CONCLUSIONS
HRS has potential protective effects against sepsis by decreasing proinflammatory responses, oxidative stress, and apoptosis in a rat model of polymicrobial sepsis.
Department of Anesthesiology and Intensive Care, Jintan Hospital, Jiangsu University, Changzhou, China.
Guo-Min
GM
Li
Mu-Huo
MH
Ji
Xue-Jun
XJ
Sun
Qiu-Ting
QT
Zeng
Mi
M
Tian
Yun-Xia
YX
Fan
Wei-Yan
WY
Li
Ning
N
Li
Jian-Jun
JJ
Yang
D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D015415:Biomarkers / Q000378:metabolism; D002432:Cecum / Q000601:surgery; D060085:Coinfection / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000401:mortality; D006859:Hydrogen / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000378:metabolism; D007274:Injections, Intraperitoneal; D053208:Kaplan-Meier Estimate; D008297:Male; D009102:Multiple Organ Failure / Q000209:etiology / Q000517:prevention & control*; D018384:Oxidative Stress / Q000187:drug effects; D014677:Pharmaceutical Vehicles; D011897:Random Allocation; D051381:Rats; D018805:Sepsis / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000401:mortality; D012965:Sodium Chloride; D016896:Treatment Outcome
D000975:Antioxidants; D015415:Biomarkers; D018836:Inflammation Mediators; D014677:Pharmaceutical Vehicles; D012965:Sodium Chloride; D006859:Hydrogen