O2 dependence of insulin stimulation of glucose uptake by perfused rat liver: effects of carboxyhaemoglobin and haematocrit

Livers from fed male rats were perfused in a non-recirculating system with undiluted rat blood containing 14 mM glucose. In these experiments there was a substantial uptake of glucose which was stimulated by insulin. Perfusion with blood containing carboxyhaemoglobin at a concentration of 40% of total haemoglobin lowered O2 consumption and abolished hepatic glucose uptake in control and insulin-infused livers, respectively. In experiments with rat erythrocytes resuspended in buffer to haematocrit values of 38 and 22%, O2 consumption and control and insulin-stimulated rates of glucose uptake were similar to corresponding perfusions with undiluted blood and blood containing carboxyhaemoglobin. It is concluded that serum factors are of relatively small importance and that hepatic glucose uptake is dictated by O2 supply.     

Effects of haematocrit value and glucagon on the metabolism of perfused rat liver

Liver from adult male rats were perfused in situ for 30 min with either undiluted, defibrinated rat blood (haematocrit value 38%) or the same blood diluted with buffer to give a haematocrit of 20%. Perfusion with diluted blood lowered the PO2 of the effluent perfusate but this was insufficient to prevent the fall in O2 consumption due to the reduction in haematocrit. Glucagon (5 X 10(-9) M) increased hepatic O2 consumption with whole blood but not with diluted blood. perfusate K+ was increased by perfusion with diluted blood and glucagon. Bile flow was depressed and biliary K+ increased by glucagon but only in experiments with whole blood. Perfusate glucose was raised by lowering of hepatic O2 consumption but the hormonal stimulation of glucose output was the same at both haematocrits. Net ketogenesis was increased with perfusion with diluted blood and by glucagon. In the absence of glucagon there was a net secretion of triacylglycerols which was depressed by lowering of the haematocrit. Glucagon inhibited triacylglycerol secretion and the effect was greater with whole blood so that there was net uptake. While effects of glucagon were obtained during perfusion at a lower haematocrit, it would appear that whole blood was the medium that allowed their fullest expression.     

Impaired sensitivity to insulin of rat livers perfused with blood of diminished haematocrit.

1. In livers from fed rats perfused with homologous whole blood of a haematocrit value of 37%, insulin decreased the perfusate concentrations of glucose and amino acids, production of ketone bodies (3-hydroxybutyrate + acetoacetate) and increased bile flow. 2. Perfusion with blood diluted with buffer to a haematocrit value of 17% decreased hepatic O2 consumption by 40-50%. Perfusate concentrations of glucose and lactate, the rate of ketogenesis and the ratios [lactate]/[pyruvate] and [3-hydroxybutyrate]/[acetoacetate] were all increased. 3. In livers perfused with blood of diminished haematocrit, effects of insulin on perfusate glucose an amino acids, ketogenesis and bile flow were abolished.     

3-isobutylmethylxanthine inhibits hepatic urea synthesis: protection by agmatine

We previously showed that agmatine stimulated hepatic ureagenesis. In this study, we sought to determine whether the action of agmatine is mediated via cAMP signaling. A pilot experiment demonstrated that the phosphodiesterase inhibitor, 3-isobutylmethylxanthine (IBMX), inhibited urea synthesis albeit increased [cAMP]. Thus, we hypothesized that IBMX inhibits hepatic urea synthesis independent of [cAMP]. We further theorized that agmatine would negate the IBMX action and improve ureagenesis. Experiments were carried out with isolated mitochondria and (15)NH(4)Cl to trace [(15)N]citrulline production or [5-(15)N]glutamine and a rat liver perfusion system to trace ureagenesis. The results demonstrate that IBMX induced the following: (i) inhibition of the mitochondrial respiratory chain and diminished O(2) consumption during liver perfusion; (ii) depletion of the phosphorylation potential and overall hepatic energetic capacity; (iii) inhibition of [(15)N]citrulline synthesis; and (iv) inhibition of urea output in liver perfusion with little effect on [N-acetylglutamate]. The results indicate that IBMX directly and specifically inhibited complex I of the respiratory chain and carbamoyl-phosphate synthase-I (CPS-I), with an EC(50) about 0.6 mm despite a significant elevation of hepatic [cAMP]. Perfusion of agmatine with IBMX stimulated O(2) consumption, restored hepatic phosphorylation potential, and significantly stimulated ureagenesis. The action of agmatine may signify a cascade effect initiated by increased oxidative phosphorylation and greater ATP synthesis. In addition, agmatine may prevent IBMX from binding to one or more active site(s) of CPS-I and thus protect against inhibition of CPS-I. Together, the data may suggest a new experimental application of IBMX in studies of CPS-I malfunction and the use of agmatine as intervention therapy.     

Acetaldehyde-dependent oxidation of glutathione catalyzed by rat liver cytosol

We have identified a novel reaction in which acetaldehyde promotes rat hepatic cytosolic catalysis of O2 consumption coupled with glutathione oxidation without apparent release of activated forms of O2. Acetaldehyde is not consumed in the reaction. The reaction (O2 consumption or oxidized glutathione production) is saturable with respect to varying glutathione (K'm congruent to 20-45 microM) but not at high acetaldehyde concentrations. However, activity in the range of acetaldehyde found in liver from alcohol metabolism (10-100 microM) appeared to be saturable (K'm congruent to 25-50 microM). Since neither acetaldehyde-dependent glutathione loss nor O2 consumption is detectable in guinea pig hepatic cytosol or hepatic cytosol from selenium-deficient rats, we propose that acetaldehyde interacts with glutathione peroxidase, converting the enzyme into a glutathione oxidase.     

Muscle oxygen extraction and perfusion heterogeneity during continuous and intermittent static exercise.

The purpose of this study was to compare the effects of intermittent and continuous static exercise on muscle perfusion, perfusion heterogeneity, and oxygen extraction. Perfusion and oxygen uptake of quadriceps femoris muscle were measured in 10 healthy men by using positron emission tomography and [(15)O]H(2)O and [(15)O]O(2) first during intermittent static exercise [10% of maximal static force (MSF)] and thereafter during continuous static exercise at the same tension-time level (5% static; 5% of MSF). In 4 of these subjects, perfusion was measured during continuous static exercise with 10% of MSF (10% continuous) instead of the second [(15)O]O(2) measurement. Muscle oxygen consumption was similar during intermittent and 5% continuous, but muscle perfusion was significantly higher during 5% continuous. Consequently, muscle oxygen extraction fraction was lower during 5% continuous. Perfusion was also more heterogeneous during 5% continuous. When exercise intensity was doubled during continuous static exercise (from 5% continuous to 10% continuous), muscle perfusion increased markedly. These results suggest that continuous, low-intensity static exercise decreases muscle oxygen extraction and increases muscle perfusion and its heterogeneity compared with intermittent static exercise at the same relative exercise intensity.     

Effects of pent-4-enoate on cellular redox state, glycolysis and fatty acid oxidation in isolated perfused rat heart

The metabolic effects of pent-4-enoate were studied in beating and potassium-arrested perfused rat hearts. The addition of 0.8mm-pent-4-enoate to the fluid used to perfuse a potassium-arrested heart resulted in a 70% increase in the O(2) consumption and a 66% decrease in the glycolytic flux as measured in terms of the de-tritiation of [3-(3)H]glucose, although the proportion of the O(2) consumption attributable to glucose oxidation decreased from an initial 30% to 10%. The pent-4-enoate-induced increase in O(2) consumption was only 15% in the beating heart. In the potassium-arrested heart, pent-4-enoate stimulated palmitate oxidation by more than 100% when measured in terms of the production of (14)CO(2) from [1-(14)C]palmitate, but in the beating heart palmitate oxidation was inhibited. Perfusion of the heart with pent-4-enoate had no effect on the proportion of pyruvate dehydrogenase found in the active form, in spite of large changes in the CoASH and acetyl-CoA concentrations and changes in their concentration ratios. The effects of pent-4-enoate on the cellular redox state were dependent on the ATP consumption of the heart. In the beating heart, pent-4-enoate caused a rapid mitochondrial NAD(+) reduction that subsequently faded out, so that the final state was more oxidized than the initial state. The arrested heart, however, remained in a more reduced state than initially, even after the partial re-oxidation that followed the initial rapid NAD(+) reduction. The ability of pent-4-enoate to increase or decrease fatty acid oxidation can be explained on the basis of the differential effects of pent-4-enoate on the concentration of citric acid-cycle intermediates under conditions of high or low ATP consumption of the myocardial cell. The proportion of the fatty acids in the fuel consumed by the heart is probably primarily determined by the regulatory mechanisms of glycolysis. When pent-4-enoate causes an increase in the citric acid-cycle intermediates, feedback inhibition of glycolysis results in an increase in the oxidation of fatty acids.     

Characterization of insulin uptake into subcellular fractions of perfused rat liver using two different iodinated tracers

The binding and uptake of insulin in perfused rat liver has been investigated with specifically labelled 125I-A14-tyrosyl insulin as a tracer and compared with a commercially available iodo-insulin preparation. The commercial preparation did not show saturation uptake kinetics and the clearance from the perfusate remained low and constant throughout a wide concentration range. A14 labelled insulin showed saturation kinetics and high clearance at low carrier concentration, falling rapidly with increasing carrier concentration and reaching a steady state value of 1 ml/min. These results emphasize the importance of using specifically labelled insulin in physiological and biochemical studies of hepatic insulin metabolism. Perfusion with A14 tyrosine-labelled insulin at 4 degrees C showed apparent saturation with binding to the plasma membrane fraction. Perfusion at 37 degrees C also showed apparent saturation with uptake predominantly to the ligandosome fraction. These results implicate the plasma membrane-ligandosome pathway in the hepatic uptake of insulin at both physiological and pharmacological concentrations of the hormone.     

Blood carboxyhaemoglobin,plasma thiocyanate,and cigarette consumption: implications for epidemiological studies in smokers.

Carboxyhaemoglobin and plasma thiocyanate concentrations were found to be significantly correlated with self-reported daily cigarette consumption in 360 smokers (r = 0.416 and 0.412 respectively; p less than 0.001). The extent to which inhalation patterns affected the intake of cigarette smoke constituents was determined from the partial correlation between carboxyhaemoglobin and plasma thiocyanate concentrations after the number of cigarettes smoke per day had been allowed for (r = 0.48). Thus 23% of the variation in carboxyhaemoglobin and thiocyanate concentrations was accounted for by the was a cigarette was smoked and a further 21% by the number smoked a day. Furthermore, the relation between carboxyhaemoglobin or plasma thiocyanate and daily cigarette consumption was not linear but reached an asymptote at consumption rates above 25 cigarettes a day. These results suggest that by itself daily cigarette consumption will not identify those smokers most at risk and will also underestimate and dose-response relationship between smoking and selected diseases.     

Increased hemoglobin O2 affinity does not improve O2 consumption in hypoxemia

We perfused an isolated rabbit hindlimb preparation with suspensions of human erythrocytes (RBC) having different O2 affinities. Our objective was to compare the effect of changes in P50, the PO2 at which hemoglobin is 50% saturated, on tissue O2 consumption during severe hypoxemia. A high-affinity (HA) group (n = 9) was perfused with RBC incubated in NaCNO (P50 = 21.4 +/- 1.9 Torr). This was compared with a low-affinity (LA) group (n = 9) perfused with rejuvenated RBC (P50 = 31.1 +/- 1.8 Torr). The arterial PO2 of the perfusate was decreased to approximately 24 Torr in both preparations. Perfusion flow and hemoglobin concentration were maintained constant. During hypoxemia arterial O2 saturation and total O2 transport (TO2) were greater in the HA than the LA group (P less than 0.05). O2 consumption and effluent venous PO2 decreased with hypoxemia in both groups to similar levels. Consequently, the LA group showed a greater O2 extraction ratio than the HA group (P less than 0.05). The ratio of phosphocreatine to inorganic phosphate, measured with 31P magnetic resonance spectroscopy, decreased at a comparable rate in both groups. As shown by a mathematical model of peripheral O2 transport, these experimental results can be explained on the basis of peripheral limitation to O2 diffusion. We conclude that increased hemoglobin affinity does not appreciably improve tissue oxygenation in hypoxemia, since the increase in TO2 is offset by diffusion limitation at the tissues.     

Simulation of oxygen carrier mediated oxygen transport to C3A hepatoma cells housed within a hollow fiber bioreactor

A priori knowledge of the dissolved oxygen (O2) concentration profile within a hepatic hollow fiber (HF) bioreactor is important in developing an effective bioartificial liver assist device (BLAD). O2 provision is limiting within HF bioreactors and we hypothesize that supplementing a hepatic HF bioreactor's circulating media with bovine red blood cells (bRBCs), which function as an O2 carrier, will improve oxygenation. The dissolved O2 concentration profile within a single HF (lumen, membrane, and representative extra capillary space (ECS)) was modeled with the finite element method, and compared to experimentally measured data obtained on an actual HF bioreactor with the same dimensions housing C3A hepatoma cells. Our results (experimental and modeling) indicate bRBC supplementation of the circulating media leads to an increase in O2 consumed by C3A cells. Under certain experimental conditions (pO2,IN) = 95 mmHg, Q = 8.30 mL/min), the addition of bRBCs at 5% of the average in vivo human red blood cell concentration (% hRBC) results in approximately 50% increase in the O2 consumption rate (OCR). By simply adjusting the operating conditions (pO2,IN) = 25 mmHg, Q = 1.77 mL/min) and increasing bRBC concentration to 25% hRBC the OCR increase is approximately 10-fold. However, the improved O2 concentration profile experienced by the C3A cells could not duplicate the full range of in vivo O2 tensions (25-70 mmHg) typically experienced within the liver sinusoid with this particular HF bioreactor. Nonetheless, we demonstrate that the O2 transport model accurately predicts O2 consumption within a HF bioreactor, thus setting up the modeling framework for improving the design of future hepatic HF bioreactors.     

Rapid stimulation of hepatic oxygen consumption by 3,5-di-iodo-L-thyronine.

Tri-iodothyronine (T3) and thyroxine (T4) as well as 3,5-di-iodothyronine (T2) stimulated O2 consumption by isolated perfused livers from hypothyroid rats at a concentration as low as 1 pM by about 30% within 90 min. Application of T2 resulted in a faster stimulation than with application of T3 or T4. Inhibition of iodothyronine monodeiodinase by propylthiouracil, thereby blocking the degradation of T4 to T3 and of T3 to T2, demonstrated that only T2 is the active hormone for the rapid stimulation of hepatic O2 consumption: T3 and T4 lost all of their stimulative activity, whereas T2 was as potent as in the absence of propylthiouracil. Perfusion experiments with thyroid-hormone analogues confirmed the specificity of the T2 effect. The nucleus is unlikely to contribute to the rapid T2 effect, as can be deduced from perfusion experiments with cycloheximide and lack of induction of malic enzyme by T2. In conclusion, a new scheme of regulation of mitochondrial activity is proposed: T2 acts rapidly and directly via a mitochondrial pathway, whereas T3 exerts its long-term action indirectly by induction of specific enzymes.     

Hepatic oxygen and lactate extraction during stagnant hypoxia

As O2 delivery falls, tissues must extract increasing amounts of O2 from blood to maintain a normal O2 consumption. Below a critical delivery threshold, increases in O2 extraction cannot compensate for the falling delivery, and O2 uptake falls in a supply-dependent fashion. Numerous studies have identified a critical delivery in whole animals, but the regional contributions to the critical O2 delivery are less fully understood. In the present study, we explored the limits of O2 extraction in the isolated liver, seeking to determine 1) the normal relationship between O2 consumption and delivery in the liver and 2) the relationship of hepatic lactate extraction to the drop in hepatic O2 consumption at low O2 deliveries. To answer these questions, using support dogs as a source for oxygenated metabolically stable blood, we studied eight pump-perfused canine livers. By lowering the blood flow in a model of stagnant hypoxia, we explored the relationship between O2 consumption and delivery over the entire physiological range of O2 delivery. The critical O2 delivery was 28 +/- 5 (SD) ml.kg-1.min-1; the livers extracted 68 +/- 9% of the delivered O2 before reaching supply dependence. This suggests that the liver has an O2 extraction capacity quite similar to the body as a whole and not different from other tissues that have been isolated. At high blood flows, the livers extracted approximately 10% of the lactate delivered by the blood, but the arteriovenous lactate differences were small. At low blood flows, however, the livers changed from lactate consumption to production. The O2 delivery coinciding with the dropoff in lactate extraction did not differ significantly from the critical O2 delivery. We conclude that reductions in lactate uptake by the liver do not precede the transition to O2 supply dependence.     

Macrophages as a major source of oxygen radicals in the hyperoxic newborn rat lung

The lungs of newborn rats exposed to 60% O(2) for 14 d were found to have a greatly increased cyanide-insensitive O(2) consumption, reflecting increased reactive oxygen species (ROS) formation. Exposure of the lung to hyperoxia is known to increase the production of ROS by mitochondria. We hypothesized that macrophages may also be a major contributor to this increase. Newborn rat pups were exposed to either air or 60% O(2) for 14 d and received either intraperitoneal gadolinium chloride (GdCl(3)) to abrogate macrophage influx, or inert vehicle. Lung homogenates were equilibrated in either 21% or 100% O(2) and total and cyanide-insensitive O(2) consumption, as well as nitric oxide accumulation were measured polarographically. Citrate synthase, a marker of mitochondrial mass, and nitrotyrosine, a marker of peroxynitrite formation, were quantified by Western blot. In addition to increased macrophage numbers, the lungs of 60% O(2)-exposed animals had greatly increased cyanide-insensitive O(2) consumption (p <.05 compared to air controls) and immunoreactive nitrotyrosine (p <.05), which were all completely abrogated by treatment with GdCl(3). Exposure to 60% O(2) for 14 d had no effect on peroxynitrite-independent nitric oxide release or mitochondrial mass. We conclude that increased ROS in the lungs of newborn rats exposed to 60% O(2) for 14 d was likely to be caused, in significant part, by the presence of increased numbers of macrophages.     

Hepatic dysoxia commences during O2 supply dependence.

Hepatic O2 consumption (VO2) remains relatively constant (O2 supply independent) as O2 delivery (DO2) progressively decreases, until a critical DO2 (DO2c) is reached below which hepatic VO2 also decreases (O2 supply dependence). Whether this decrease in VO2 represents an adaptive reduction in O2 demand or a manifestation of tissue dysoxia, i.e., O2 supply that is inadequate to support O2 demand, is unknown. We tested the hypothesis that the decrease in hepatic VO2 during O2 supply dependence represents dysoxia by evaluating hepatic mitochondrial NAD redox state during O2 supply independence and dependence induced by progressive hemorrhage in six pentobarbital-anesthetized dogs. Hepatic mitochondrial NAD redox state was estimated by measuring hepatic venous beta-hydroxybutyrate-to-acetoacetate ratio (beta OHB/AcAc). The value of DO2c was 5.02 +/- 1.64 (SD) ml.100 g-1.min-1. The beta-hydroxybutyrate-to-acetoacetate ratio was constant until a DO2 value (3.03 +/- 1.08 ml.100 g-1.min-1) was reached (P = 0.05 vs. DO2c) and then increased linearly. Peak liver lactate extraction ratio was 15.2 +/- 14.1%, occurring at a DO2 of 5.48 +/- 2.54 ml.100 g-1.min-1 (P = NS vs. DO2c). Our data support the hypothesis that the decrease in VO2 during O2 supply dependence represents tissue dysoxia.     

Oxygen consumption in perfused skeletal muscle. Effect of perfusion with aged, fresh and aged-rejuvenated erythrocytes on oxygen consumption, tissue metabolites and inhibition of glucose utilization by acetoacetate.

1. O2 consumption, glucose metabolism and the energy status of skeletal muscle were compared in isolated rat hindquarters perfused with aged (21--35 days), fresh and aged-rejuvenated human erythrocytes. 2. The age of the erythrocytes did not affect O2 consumption, glucose utilization or lactate release either at rest or during exercise. The concentrations of ATP, phosphocreatine and lactate within the muscle were also unaffected by the use of aged erythrocytes. 3. Perfusion with acetoacetate did not inhibit glucose utilization; but, it caused a marked increase in the tissue concentration of citrate in the soleus, a slow-twitch red muscle, and a smaller increase in the gastrocnemius, which contains fast-twitch red and white fibres. Results were similar in hindquarters perfused with aged and aged-rejuvenated erythrocytes. 4. These findings suggest that perfusion with aged human erythrocytes does not cause major alterations in the metabolic performance of the isolated rat hindquarter.     

Low-O(2) affinity erythrocytes improve performance of ischemic myocardium.

O(2) transport and O(2) diffusion interact in providing O(2) to tissue, but the extent to which diffusion may be critical in the heart is unclear. If O(2) diffusion limits mitochondrial oxygenation, a change in blood O(2) affinity at constant total O(2) transport should alter cardiac O(2) consumption (VO(2)) and function. To test this hypothesis, we perfused isolated isovolumically working rabbit hearts with erythrocytes at physiological blood-gas values and P(50) (PO(2) required to half-saturate hemoglobin) values at pH of 7.4 of 17 +/- 1 Torr (2,3-bisphosphoglycerate depletion) and 33 +/- 5 Torr (inositol hexaphosphate incorporation). When perfused at 40 and 20% of normal coronary flow, mean VO(2) decreased from the control value by 37 and 46% (P < 0.001), and function, expressed as cardiac work, decreased by 38 and 52%, respectively (P < 0.001). Perfusion at higher P(50) during low-flow ischemia improved VO(2) by 20% (P < 0.001) and function by 36% (P < 0.02). There was also modest improvement at basal flow (P < 0.02 and P < 0.002, respectively). The improvement in VO(2) and function due to the P(50) increase demonstrates the importance of O(2) diffusion in this cardiac ischemia model.     

Down-Regulation of AMPA Glutamate Receptors Reduces Cerebrocortical Metabolic Response to Stimulation

We tested the hypothesis that chronic stimulation of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate) glutamate receptors with an agonist causes down-regulation of the receptor protein and a decrement in basal and/or stimulated cerebral O2 consumption. Male Wistar rats were intradurally infused with 10 microM AMPA by an osmotic pump at a rate of 1 microl/h for 6 days. As a result, the specific binding of (S)-[3H]-5-fluorowillardiine to AMPA receptors in the cerebral cortex decreased 46% from 2.7 +/- 0.3 to 1.5 +/- 0.6 (density units). Under isoflurane anesthesia and after topical stimulation to the right cerebral cortex with 10(-3) M AMPA, cerebral blood flow (14C-iodoantipyrine method) and O2 consumption (cryomicrospectrophotometrically determined) were determined in control and down-regulated rats. Down-regulation of AMPA receptors did not alter basal O2 consumption. In control, after agonist stimulation, the O2 consumption in the ipsilateral cortex increased by 34%, (4.7 +/- 0.5 ml O2 x min(-1) x 100 g(-1) compared to 3.5 +/- 0.4 in the contralateral cortex). In the down-regulated rats, the O2 consumption did not significantly increase (4.0 +/- 1.5 ml O2 x min(-1) x 100 g(-1) compared to 3.3 +/- 1.7 in the contralateral cortex) after AMPA. In conclusion, following chronic simulation, AMPA receptors underwent down-regulation, but such down-regulation did not alter basal cerebrocortical blood flow or O2 consumption. AMPA down-regulation reduced the agonist stimulated increase in cortical O2 consumption.     

Interpreting the carboxyhaemoglobin concentration in fetal cord blood

We calculated the fetal-to-maternal carboxyhaemoglobin concentration ratio in 19 mother-infant pairs at the time of term delivery. Mothers, who had a less than 10% drop in their carboxyhaemoglobin concentration during labour, had an average ratio of 1.40 +/- 0.19. For mothers whose carboxyhaemoglobin concentrations dropped by 10% or more during labour, the average fetal-to-maternal carboxyhaemoglobin concentration ratio was 1.83 +/- 0.48. There was a strong correlation (r = 0.82) between the percent change in maternal carboxyhaemoglobin concentration during labour and the fetal-to-maternal carboxyhaemoglobin concentration ratio at the time of delivery. We conclude that increased CO elimination during labour may be accompanied by rapid changes in the maternal carboxyhaemoglobin concentration, leading to a spuriously high fetal-to-maternal carboxyhemoglobin concentration ratio at the time of delivery.     

盐度与体重对台湾罗非鱼耗氧率的影响

在盐度为淡水、7、14、2 1、2 8和 35的条件下 ,测定了 3个体重组 (1.5 7～ 4.87g ,7.0 7～ 18.2 3g和31.5 0～ 5 2 .41g)的台湾红罗非鱼的耗氧率 ,方差分析表明 ,盐度对台湾红罗非鱼的耗氧率有极显著的影响(P <0 .0 1) .体重范围为 1.5 7～ 18.2 4g时 ,盐度 7实验组的耗氧率最高 ,分别为 0 .41mgO2 ·g-1·h-1(1.5 7～ 4.78g)和 0 .34mgO2 ·g-1·h-1(7.0 7～ 18.2 3g) ,体重范围为 31.5 0～ 5 2 .41g时 ,耗氧率最高值出现在盐度 35组 ,为 0 .30mgO2 ·g-1·h-1.耗氧率最低值也因体重范围的不同而出现在不同的盐度 ,体重范围为1.5 7～ 4.78g时 ,盐度 14组的耗氧率最低 ,为 0 .2 8mgO2 ·g-1·h-1,体重范围在 7.0 7～ 5 2 .41g时 ,耗氧率的最低值均出现在盐度 2 1组 ,其中体重范围 7.0 7～ 18.2 3g的最低值为 0 .2 2mgO2 ·g-1·h ,而体重范围31 5 0～ 5 2 .41g的最低耗氧率为 0 .13mgO2 ·g-1·h-1.协方差分析表明 ,盐度和体重对台湾红罗非鱼的耗氧率存在极显著的交互作用 (P <0 .0 1) .