Analysis of the metabolic disorder based on the redox theory in the septic patient induced by nitric oxide

Nitric oxide(NO)production in primary cultured rat hepatocytes were observed for 2hours using the NO monitor。These findings were the same as nitrite measured by Griess reagent method。However，after2hours，we would not detected the NO。The attachment of the hepatocytes to the NO monitor affected the measurement.Nitric oxide production and its effect on energy metabolism was investigated in cultured rat hepatocytes obtained from the liver remnant after partial hepatectomy。The hepatocytes obtained from liver remnant after partial hepatectomy(HPH)produced more nitric oxide than hepatocytes obtained from sham operated liver(HS)，following stimulation with IL-1β。In our recent study，IL-1βwas shown to stimulate nitric oxide(NO)production in cultured rat hepatocytes and NO reduced the ketone body ratio(KBR：acetoacetate/b-hydroxybutyrate)。The reduced KBR，reflecting the liver mitochondrial redox state(NAD I D1+ii D1/NADH)，resulted in the inhibition of ATP synthesis。In the present study，KBR in the medium of cultured HPH was lower than that of HS。Furthermore，adenine nucleotides content(ATP，ADP and AMP)was lower in HPH than in HS.These results suggest that following partial hepatectomy，the liver is more susceptible to mitochondrial dysfunction as a result of the nitric oxide produced during infection.The similar results ware observed in hepatocytes obtained from obstructive jaudice rat.In conclusion，hepatocytes in the liver remnant after partial hepatectomy demonstrated increased NO production which was attributed to increased sensitivity to IL-1βNO in turn，cause liver dysfunction after hepatectomy because NO induces hepatic mitochondria dysfunction.

Nitric oxide (NO) production in primary cultured rat hepatocytes were observed for 2 hours using the NO monitor. These findings were the same as nitrite measured by Griess reagent method. However, after 2 hours, we would not detected the NO. The attachment of the hepatocytes to the NO monitor affected the measurement.Nitric oxide production and its effect on energy metabolism was investigated in cultured rat hepatocytes obtained from the liver remnant after partial hepatectomy. The hepatocytes obtained from liver remnant after partial hepatectomy (HPH) produced more nitric oxide than hepatocytes obtained from sham operated liver (HS), following stimulation with IL-1β. In our recent study, IL-1β was shown to stimulate nitric oxide (NO) production in cultured rat hepatocytes and NO reduced the ketone body ratio (KBR : acetoacetate/b-hydroxybutyrate). The reduced KBR, reflecting the liver mitochondrial redox state (NADィイD1+ィエD1/NADH), resulted in the inhibition of ATP synthesis. In the present study, KBR in the medium of cultured HPH was lower than that of HS. Furthermore, adenine nucleotides content (ATP, ADP and AMP) was lower in HPH than in HS. These results suggest that following partial hepatectomy, the liver is more susceptible to mitochondrial dysfunction as a result of the nitric oxide produced during infection. The similar results ware observed in hepatocytes obtained from obstructive jaudice rat.In conclusion, hepatocytes in the liver remnant after partial hepatectomy demonstrated increased NO production which was attributed to increased sensitivity to IL-1βNO in turn, cause liver dysfunction after hepatectomy because NO induces hepatic mitochondria dysfunction.