[Show abstract][Hide abstract] ABSTRACT: Hydrogen is a major component of interstellar space and the fuel that sustains the stars. However, it is seldom regarded as a therapeutic gas. A recent study provided evidence that hydrogen inhalation exerted antioxidant and anti-apoptotic effects and protected the brain against ischemia-reperfusion injury by selectively reducing hydroxyl radical and peroxynitrite. It has been known that the mechanisms underlying the brain injury after acute carbon monoxide poisoning are interwoven with multiple factors including oxidative stress, free radicals, and neuronal nitric oxide synthase as well as abnormal inflammatory responses. Studies have shown that free radical scavengers can improve the neural damage. Based on the findings abovementioned, we hypothesize that hydrogen therapy may be an effective, simple, economic and novel strategy in the treatment of acute carbon monoxide poisoning.
Full-text · Article · Mar 2010 · Medical Hypotheses
[Show abstract][Hide abstract] ABSTRACT: The objectives were to investigate the potential beneficial effects and molecular mechanisms of heparin and low-molecular-weight heparin (LMWH) on acute lung injury (ALI).
Forty-eight rabbits were randomized into four groups: normal control group (Group A), lipopolysaccharide (LPS) group (Group B), LPS + heparin group (Group C), and LPS + LMWH group (Group D). The rabbit ALI model was established by intravenous (IV) injection with LPS. Alveolar-arterial O2 difference (P(A-a)O2), serum tumor necrosis factor alpha (TNF-alpha), circulating p38 mitogen-activated protein kinase (p38 MAPK) levels, lung nuclear factor (NF)-kappaB levels, and lung dry/wet (D/W) ratio were measured, and the lung injury scores were calculated.
Lipopolysaccharide caused significant increases in P(A-a)O2, serum TNF-alpha, expression of p38 MAPK in polymorphonuclear neutrophils (PMNs), the lung injury scores, and nuclear factor-kappaB (NF-kappaB) activity in the lung tissue and caused a decrease in lung D/W ratio. A positive linear correlation was found between p38 MAPK and TNF-alpha at 1, 2, 4, and 6 hours (r = 0.68, 0.92, 0.93, and 0.93, respectively) and between NF-kappaB and p38 MAPK and TNF-alpha at 6 hours (r = 0.94 and 0.83, respectively). IV heparin or LMWH given after LPS treatment attenuated these changes in inflammatory response, oxygenation, p38 MAPK expression, and NF-kappaB activation.
The anti-inflammatory mechanisms of heparin in ALI may be inhibiting p38 MAPK and NF-kappaB activities, and then TNF-alpha overexpression, thus alleviating the inflammatory reaction.
Preview · Article · Aug 2008 · Academic Emergency Medicine