Emulsified isoflurane preconditioning protects against liver and lung injury in rat model of hemorrhagic shock.
Emulsified isoflurane preconditioning protects against liver and lung injury in rat model of hemorrhagic shock.
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DOI:
10.1016/j.jss.2010.06.037
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发表时间:
2011-12
期刊:
影响因子:
--
通讯作者:
Lei Zhang;Nanfu Luo;Jin Liu;Zeyan Duan;G. Du;Jian Cheng;Haixia Lin;Zhuo Li
中科院分区:
文献类型:
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作者:
Lei Zhang;Nanfu Luo;Jin Liu;Zeyan Duan;G. Du;Jian Cheng;Haixia Lin;Zhuo Li
BACKGROUNDIsoflurane has demonstrated protective effects against ischemia/reperfusion injury in some organs. In this study, using the hemorrhagic shock model, we investigated whether emulsified isoflurane preconditioning protected against liver and lung injury caused by massive surgical blood loss.METHODSMale Sprague-Dawley (SD) rats were randomly divided into five groups: a control group, a hemorrhagic shock (HS) group, an intralipid (IL) group, an isoflurane (Iso) group, and an emulsified isoflurane (E-Iso) group. Saline, intralipid, isoflurane, or emulsified isoflurane were administered over 15 min. Forty-five min after injection, hemorrhage was initiated in the experimental group. Four h after resuscitation alanine aminotransferase (ALT), protein and cellular content in bronchoalveolar lavage fluid (BAL), and the liver and lung histopathology were measured. The malondialdehyde (MDA) and superoxide dismutase (SOD) in the liver and lung mitochondria were tested. The survival was also observed in hemorrhagic shocked rats.RESULTSEmulsified isoflurane enhanced survival and decreased ALT, protein, and cellular content in BAL, liver, and lung apoptosis, and the histologic score. It also decreased MDA and increased SOD activity in mitochondria. In the IL group, liver mitochondrial SOD activity increased, while ALT, liver apoptosis and histological score decreased. In the Iso group liver and lung mitochondrial SOD activity increased, while liver and lung apoptosis decreased.CONCLUSIONEmulsified isoflurane preconditioning has a protective effect against liver and lung injury as well as improving the survival in hemorrhagic shock. The potential mechanisms involved are the inhibition of cell death and improvement of antioxidation in mitochondria.