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Objective: To study the effect of high dose Vitamin C, administered intravenously, on treating implanted hepatoma in rats. Methods: Rats implanted with hepatoma were treated with high-dose Vitamin C 2.83g/kg or 5.65g/kg intravenously and compared to a "model" (control) group. The liver function (A/G, ALT, AST, and GGT), tumor volume and weight, and cancer necrotic grades were determined. Results: The A/G of rats with 2.83g/ kg Vitamin C treatment was greater than that of the model rats (P<0.05), ALT was less than that of the model rats (P<0.01), GGT was less than that of the model rats (P<0.05). The ALT of rats with 5.65g/kg Vitamin C treatment was less than that of the model rats (P<0.05). The cancer necrosis rate of rats with 2.83g/kg Vitamin C treatment was more than that of model rats (P<0.05). Previously reported data indicates that 2.83g Vitamin C /kg body weight delivered intravenously to rats is equivalent to a dose of 30g intravenous Vitamin C /60kg in humans. Conclusion: These results demonstrate that the intravenous administration of Vitamin C at levels of 2.83g/kg Vitamin C can accelerate hepatoma Walker256 cell death and protect the liver function in implanted hepatoma rats. [ABSTRACT FROM AUTHOR]

Cardiomyopathy is a common complication associated with increased mortality in sepsis, but lacks specific therapy. Here, using genetic and pharmacological approaches, we explored the therapeutic effect of α 2A -adrenergic receptor (AR) blockade on septic cardiomyopathy. CLP-induced septic rats were treated with BRL44408 (α 2A -AR antagonist), prazosin (α 1 -AR antagonist) and/or reserpine. CLP-induced cardiomyopathy, indicated by reduced dP/dt and increased cardiac troponin I phosphorylation, was attenuated by BRL44408, this was associated with reduced cardiac TNF-α and endothelial VCAM-1 expression, cardiomyocyte apoptosis and related signal molecule phosphorylation. BRL44408 increased cardiac norepinephrine (NE) concentration in CLP rats. Pretreatment with reserpine that exhausts cardiac NE without affecting the circulating NE concentration or with prazosin partially abolished the cardioprotection of BRL44408 and reversed its inhibitory effects on myocardial TNF-α, apoptosis and related signal molecule phosphorylation, but not on VCAM-1 expression in septic rats. These effects of BRL44408 were confirmed by α 2A -AR gene deletion in septic mice. Furthermore, α 2 -AR agonist not only enhanced LPS-induced TNF-α and VCAM-1 expression in cardiac endothelial cells that express α 2A -AR, but also enhanced LPS-induced cardiac dysfunction in isolated rat hearts. Our data indicate that α 2A -AR blockade attenuates septic cardiomyopathy by promoting cardiac NE release that activates myocardial α 1 -AR and suppressing cardiac endothelial activation.