Interaction of Mixed‐Function Oxidation with Biosynthetic Processes

Scholz, Roland; Hansen, Werner E.; Thurman, Ronald G.

doi:10.1111/j.1432-1033.1973.tb03034.x

Cited by 283 publications

(62 citation statements)

References 24 publications

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“…Fed rats were anesthetized with sodium pentobarbital (45 mg/kg i.p.). Livers were isolated and perfused with Krebs-Henseleit bicarbonate buffer (pH 7.4, 370C) saturated with 95%02/5%CO2 in a hemoglobin-free, nonrecirculating system at a constant flow rate (36 ml/min) (21). Perfusate was pumped with a rotor pump (Taiyo Scientific Industrial Co., Tokyo, Japan) into the liver via a cannula inserted in the portal vein.…”

Section: Methodsmentioning

confidence: 99%

Roles of endothelin-1 and nitric oxide in the mechanism for ethanol-induced vasoconstriction in rat liver.

Oshita¹,

Takei²,

Kawano³

et al. 1993

J. Clin. Invest.

112

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This study was designed to investigate the mechanism for ethanol-induced hepatic vasoconstriction in isolated perfused rat liver. Upon initiation of ethanol infusion into the portal vein at concentrations ranging from 25 to 100 mM, portal pressure began to increase in a concentration-dependent manner and reached maximal levels in 2-5 min (initial phase), followed by a gradual decrease over the period of ethanol infusion (escape phenomenon). Endothelin-1 antiserum significantly inhibited this ethanol-induced hepatic vasoconstriction by 45-80%. Cessation of infusion of endothelin-1 antiserum was followed by a subsequent increase in portal pressure. On the other hand, when a nitric oxide synthesis inhibitor, NG-monomethyl-L-arginine (L-NMMA), was infused into the portal vein simultaneously with ethanol, the initial phase of the response of portal pressure to ethanol was not altered and the peak values of portal pressure remained unchanged. However, after the peak increase in portal pressure, the rate of decrease was less than in the absence of L-NMMA. Thus, L-NMMA diminished the escape phenomenon and sustained the vasoconstriction. This study supports the hypothesis that two endothelium-derived vasoactive factors, endothelin-1 and nitric oxide, regulate hepatic vascular tone in the presence of ethanol. (J. Clin. Invest.

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Section: Methodsmentioning

confidence: 99%

Roles of endothelin-1 and nitric oxide in the mechanism for ethanol-induced vasoconstriction in rat liver.

Oshita¹,

Takei²,

Kawano³

et al. 1993

J. Clin. Invest.

112

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show abstract

“…The liver perfusion technique employed was virtually identical with the one in [14], except that the position of the liver was inverted (the intestinal aspect up). The venous oxygen tension was continuously monitored with a Clark-type electrode and the portal pressure with a pressure transducer.…”

Section: Liver Perfusionmentioning

confidence: 99%

Regulation of oxygen consumption and microcirculation by α‐sympathetic nerves in isolated perfused rat liver

Beckh

Jungermann

1984

FEBS Letters

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In isolated rat liver perfused at constant flow with erythrocyte-free Krebs-Henseleit bicarbonate buffer containing 5 mM glucose and 2 mM lactate, perivascular stimulation of the hepatic nerves caused a rapid decrease of oxygen uptake, a decrease of the periportal and, after a transient rise, of the perivenous tissue PO, of surface acini, an increase of portal pressure, and an enhancement of glucose output. Furthermore, nerve stimulation changed the intrahepatic distribution of the perfusate drastically. Infusion of trypan blue 20 s after nerve stimulation resulted in a heterogeneous staining of the liver both at the surface and in cross-sections, while it led to a homogeneous distribution in non-stimulated controls. It is concluded that the major component in the mechanism of the nerve-dependent decrease of oxygen uptake is the microcirculatory change rather than a metabolic effect. Oxygen consumptionRat liver Sympathetic nerve Microcirculation Zonal tissue po,

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“…The perfusion fluid was Krebs-Henseleitbicarbonate buffer [44], pH 7.4, saturated with an oxygen/carbon dioxide mixture (95/5). The fluid was pumped from a reservoir through a membrane oxygenator [43] and heater (37 "C) prior to entering the liver via the portal vein. The effluent perfusion fluid was collected via a cannula placed in the vena cava.…”

Section: Non-recirculating Hemoglobin-free Liver Perfusionmentioning

confidence: 99%

Mechanism of the Stimulatory Effect of Fructose on Ethanol Oxidation in Perfused Rat Liver

Scholz

Nohl

1976

Eur J Biochem

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The stimulatory effect of fructose on ethanol oxidation was studied in livers from fasted rats perfused with Krebs-Henseleit-bicarbonate buffer in a non-recirculating system. Two series of experiments were performed : (A) ethanol was infused with stepwise increasing concentrations (0.1 -20 mM) in the presence of 4 mM fructose; (B) fructose was infused with stepwise increasing concentrations (0.5 -10 mM) in the presence of 2 mM ethanol. From measured metabolic rates the following parameters were calculated : energy-rich phosphates consumed for fructose metabolism which were provided from oxidative phosphorylation (A -P) ; reducing equivalents derived from stimulated ethanol utilization which were disposed by mitochondrial oxidation ( A 2H). Under the various conditions studied a linear relationship between these parameters was observed. The ratio d -P/A2H was about 2.0. It is suggested that fructose stimulates ethanol oxidation indirectly by increasing the energy consumption of the liver due to the production of glucose from fructose. Consequently, the rate of oxidative phosphorylation is increased and, therefore, the capacity of the respiratory chain for oxidizing reducing equivalents derived from ethanol is enhanced. The data support the more general hypothesis that the rate of ethanol oxidation depend upon the rate of hepatic energy consumption in a given metabolic state.The rate-controlling factor in ethanol metabolism is still a subject of debate. Previously, it was suggested that the rate of ethanol oxidation is limited by the activity of hepatic alcohol dehydrogenase [l -41. However, this concept has been questioned, since it was observed that the rate of ethanol elimination varied with the metabolic state [5-71 and could be stimulated by various compounds, e.g. pyruvate [l, 6-91, fructose [8 -221, or dinitrophenol [23], and that peroxidatic processes play an important role in ethanol metabolism at high concentrations [24-261. The present concept of rate-control is the following.

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Interaction of Mixed‐Function Oxidation with Biosynthetic Processes

Cited by 283 publications

References 24 publications

Roles of endothelin-1 and nitric oxide in the mechanism for ethanol-induced vasoconstriction in rat liver.

Roles of endothelin-1 and nitric oxide in the mechanism for ethanol-induced vasoconstriction in rat liver.

Regulation of oxygen consumption and microcirculation by α‐sympathetic nerves in isolated perfused rat liver

Mechanism of the Stimulatory Effect of Fructose on Ethanol Oxidation in Perfused Rat Liver

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