Hyperbaric oxygen protects against lipopolysaccharide-stimulated oxidative stress and mortality in rats
Introduction
Septic shock is a serious progressive failure of the circulation with a high mortality rate of 30–90% (Rangel-Frausto et al., 1995). Lipopolysaccharide evokes a septic shock-like state characterized by fever, hypotension, vasohyporeactivity to vasoactive agents, myocardial dysfunction, hypoglycemia, and multiple organ failure. It has become clear that lipopolysaccharide does not injure host tissues directly, but acts through a variety of inflammatory mediators, such as tumor necrosis factor alpha (TNF-α), interleukins, and nitric oxide (NO) (Chorinchath et al., 1996, Zhao et al., 1997). However, recent studies using antibodies to inflammatory mediators do not show reduced mortality in patients with septic shock (Fukumoto et al., 1996, Volman et al., 2002b). Notably, lipopolysaccharide also increases production of reactive oxygen species such as superoxide anions (Tsao et al., 2003, Victor and De La Fuente, 2003). Recently, pretreatment with hyperbaric oxygen has shown some beneficial effects on lipopolysaccharide-induced sepsis shock (Sunakawa and Yusa, 1997, Pedoto et al., 2003), but the underlying protective mechanism remains to be examined.
Hyperbaric oxygen therapy provides 100% inhaled oxygen at increased atmospheric pressure. It is used as an adjuvant therapy for many disorders, including several types of inflammatory conditions and ischemic tissue injury (Tibbles and Edelsberg, 1996, Nighoghossian and Trouillas, 1997). Hyperbaric oxygen successfully protects mice with aerobic septicemia and significantly prolongs survival of the infected host through its antibacterial activity (Ross and McAllister, 1965). Luongo and coworkers have reported that hyperbaric oxygen significantly decreases symptoms, reduces TNF-α and NO levels, and improves survival of animals shocked by zymosan, a nonbacterial and nonendotoxic agent (Luongo et al., 1998). Recently, in vitro studies show that hyperbaric oxygen inhibits the endotoxin lipopolysaccharide-induced proinflammatory cytokines in monocyte-macrophages (Benson et al., 2003). Furthermore, the beneficial effect of hyperbaric oxygen is mediated by increased superoxide dismutase and glutathione peroxidase activities in experimental acute necrotizing pancreatitis (Yasar et al., 2003). In this study, we investigated the relevance of the reduction of TNF-α, NO, and superoxide anion formation to improvement of vasohyporeactivity and mortality after hyperbaric oxygen treatment in endotoxic rats.
Section snippets
Materials
Eight- to ten-week-old male Wistar–Kyoto rats weighing 230–280 g were obtained from the National Animal Breeding and Research Center, Taipei, Taiwan. All reagents were obtained from Sigma Chemicals (St. Louis, MO) unless otherwise specified. The main reagents used include lipopolysaccharide from Escherichia coli, serotype 0127:B8, and aminoguanidine. Drugs and chemicals were dissolved in sterile normal saline for experimental use.
Hyperbaric oxygen treatment and experimental protocol
Animals were anaesthetized with pentobarbital sodium (50 mg/kg
Effect of hyperbaric oxygen and aminoguanidine treatment on TNF-α and NOx release
Plasma TNF-α and NOx concentrations for the five rat groups are shown in Fig. 1. Significant increases in plasma TNF-α (from 0.8±1.3 to 780±87 pg/ml; P<0.05) at 2 h and NOx (from 31.2±1.3 to 435±16 μM; P<0.05) at 9 h were noted in lipopolysaccharide-treated rats compared with the control group. In lipopolysaccharide-treated rats, administration of aminoguanidine significantly decreased plasma TNF-α production by 54% (P<0.05) and NOx by 46% (P<0.05), and exposure to hyperbaric oxygen
Discussion
Previous studies have shown that hyperbaric oxygen has beneficial effects on experimental acute necrotizing pancreatitis and zymosan-induced shock models (Luongo et al., 1998, Pedoto et al., 2003, Yasar et al., 2003). Our study further demonstrated that TNF-α and NOx release, vascular superoxide anion production, hypovasoreactivity and survival rate in lipopolysaccharide-treated rats were improved by serial exposure to hyperbaric oxygen (2 ATA). The effects of aminoguanidine, an inhibitor of
Acknowledgments
This work was supported by NSC 91-2314-B-016-036 Grants from National Science Council and C.Y. Foundation for Advancement of Education, Sciences and Medicine, Taiwan.
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