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PubMed1997

Effects of excitatory amino acids on cerebral oxygen consumption and blood flow in rat.

This investigation tested the importance of excitatory amino acids' effects on regional cerebral O2 consumption and the concomitant changes in cerebral blood flow (rCBF) in isoflurane anesthetized rats. In the glutamate or N-methyl-D-aspartate (NMDA) groups, 10(-2) M glutamate or NMDA was topically applied to the right cortex and the left cortex was used as a control. One mg/kg dizocilpine maleate (MK-801), a non-competitive NMDA receptor antagonist, was administered (iv) to the MK-801 group and saline was given to the control group. Cortical rCBF was determined using 14C-iodoantipyrine and regional O2 extraction was measured microspectrophotometrically. Cerebral O2 consumption increased 77% after glutamate (contralateral cortex: 9.0 +/- 1.1 ml O2/min/100 g, glutamate treated cortex: 15.9 +/- 3.9), while a 46% increase was observed with the same concentration of NMDA (contralateral cortex: 9.8 +/- 2.0, NMDA treated cortex: 14.3 +/- 5.5). After MK-801, the O2 consumption decreased to 37% of the control value (control cortex: 7.0 +/- 1.3, MK-801 treated cortex: 2.6 +/- 3.9). MK-801 significantly decreased cerebral O2 extraction from 7.1 +/- 1.3 ml O2/100 ml (control cortex) to 5.3 +/- 0.6 (MK-801 treated cortex). However, there was no significant difference in cerebral O2 extraction between treated and contralateral cortex in either the glutamate or NMDA groups. The increase in O2 consumption caused by glutamate or NMDA was coupled with increased rCBF. Glutamate increased rCBF from 95 +/- 5 ml/min/100 g (contralateral cortex) to 165 +/- 31 (treated cortex), while NMDA increased rCBF from 114 +/- 12 (contralateral cortex) to 178 +/- 60 (treated cortex). MK-801 decreased O2 consumption with a lesser decrease of rCBF. The rCBF was 48 +/- 9 in the MK-801 treated cortex and 99 +/- 22 in the control cortex. Some substances produced by the activation of NMDA receptors may be related to the coupling of cerebral metabolism and blood flow, since after blockade of NMDA receptors with MK-801, this relationship is uncoupled. These findings suggest that glutamatergic processes have a major effect on cerebral O2 consumption and that this is at least partly due to NMDA receptors.

Animals↗
PubMed2002

The effect of insulin and glucagon on splanchnic oxygen consumption.

UNLABELLED: The purpose of these experiments was to measure the influence of insulin and glucagon on the splanchnic oxygen consumption. Two experiments were performed. METHODS: In one experiment, the influence of hyperinsulinaemia was investigated in six healthy subjects, who were studied during a euglycaemic hyperinsulinaemic clamp. In another experiment, the influence of glucagon was investigated in seven healthy subjects, who were studied twice during a pancreatic islet clamp with either supplementation of insulin and glucagon, or of insulin alone. In both situations the measurements were performed during euglycaemia. Splanchnic oxygen consumption and net substrate balances were studied by the arterio-hepatic venous catheterisation technique and measurement of splanchnic blood flow in all experiments. RESULTS: During the euglycaemic hyperinsulinaemic clamp, the splanchnic blood flow increased significantly and the splanchnic oxygen consumption decreased by about 20%, while the net splanchnic glucose output reversed to a net uptake. In the pancreatic islet clamp experiments there was a significant difference between the net splanchnic glucose outputs whether glucagon and insulin or only insulin was supplemented. In spite of this, the splanchnic oxygen consumption decreased by about 20% in both situations, i.e. independent of glucagon supplementation. In both experiments there was a pronounced inhibition of lipolysis, which led to decreased fatty acids availability to the liver. This resulted in a concomitant decrease in hepatic ketone body formation. This decrease could account for about 30% of the decrease in splanchnic oxygen consumption. CONCLUSION: The reduction in splanchnic oxygen consumption can be explained by decreased ketogenesis, decreased protein synthesis and changes in splanchnic fuel selection, while changes in the rate of gluconeogenesis does not seem to play a significant role.

Adult↗
PubMed1987

Reflectance spectrophotometric measurement of in vivo local oxygen consumption in the cerebral cortex.

A simple method was developed to measure in vivo local oxygen consumption quantitatively in the brain cortex. Reflectance spectra of tissue hemoglobin at the brain's surface were measured for assessment of both local tissue hemoglobin content and its oxygen saturation. Local oxygen consumption was calculated from the spectral changes of tissue hemoglobin during complete cessation of blood flow by compression of the cortical surface in the suprasylvian gyrus with the tip of an optic probe. This procedure was performed without any brain damage and only took approximately 5 s. The calculated local oxygen consumption during this short period of compression remained constant for a few seconds. Then, it decreased rapidly, although the local tissue hemoglobin was not completely deoxygenated. The value of local cerebral oxygen consumption obtained by this method was 3.02 +/- 0.61 mL O2/100 g brain/min; it was not influenced by the change in systemic blood pressure. The effect of pentobarbital on cerebral oxygen consumption was also studied. At the stage of burst and suppression on electrocorticogram, cerebral oxygen consumption decreased significantly (p less than 0.001) to 1.03 +/- 0.07 mL O2/100 g brain/min.

Animals↗
PubMed1993

Glucose- and phorbol myristate acetate-stimulated oxygen consumption and superoxide production in rat peritoneal macrophages is inhibited by dexamethasone.

1. Rat peritoneal macrophages stimulated with phorbol 12-myristate 13-acetate (PMA) (40 nM) show an increase in the rate of oxygen consumption (measured with an O2 electrode) and the production of superoxide (measured by cytochrome c reduction), which are both dependent on the presence of exogenous glucose. There is a 1:1 correlation between the oxygen consumed and the superoxide produced over a range of glucose concentrations (0-10 mM). 2. Preincubation of macrophages with dexamethasone (1 microM) for 3 h significantly decreased the Vmax. for PMA-induced glucose-dependent oxygen consumption (P < 0.001) and glucose-dependent superoxide production (P < 0.001). However, dexamethasone did not significantly change the Km for glucose in either PMA-induced oxygen consumption or superoxide production. Dexamethasone is therefore a non-competitive inhibitor of PMA-stimulated glucose-dependent oxygen consumption (Ki = 0.83 +/- 0.09 microM) and superoxide generation (Ki = 0.87 +/- 0.09 microM). 3. The PMA-induced rate of oxygen consumption by macrophages was decreased at oxygen concentrations below approx. 15 microM. The Km of oxygen for PMA-induced oxygen consumption was 1.28 +/- 0.13 microM (n = 12), and this was not significantly different in the presence of dexamethasone; Km = 1.61 +/- 0.31 microM (n = 12). It is therefore concluded that in vivo macrophage superoxide production is not limited by external oxygen or glucose concentrations, even in hypoxic joints.

Animals↗
PubMed2003

Effects of simultaneous aortocaval occlusion on oxygen consumption in patients.

The effects of simultaneous occlusion of the thoracic aorta and inferior vena cava on oxygen consumption (V O 2) have not yet been reported in humans. Ten patients (all ASA II) needed such simultaneous occlusion to allow hypoxic abdominal perfusion in the treatment of pancreatic cancer. With the development of the PhysioFlex anaesthesia machine for closed-circuit anaesthesia, intra-operative real-time curves of V O 2 became available. Thus, we can continuously measure F I O 2, V E, V O 2, and air consumption. By placing a pulmonary artery catheter, we could also intermittently calculate D O 2 during the several phases of the perfusion procedure. Immediately after the simultaneous aortocaval occlusion started, V O 2 decreased by 35% (68 ml min-1 m-2) and D O 2 decreased below the critical value of 330 ml min-1 m-2. At reperfusion, repayment of the oxygen debt was by a two-stage pattern: a fast repayment stage with an increase of about 65% was followed by a slow repayment stage of 14% increase (values compared to steady state). Oxygen consumption in women was found to be significantly lower than in men (P = 0.02), with significant variation between the sexes during different stages of the procedure. The oxygen debt was not completely repaid by the end of the procedure. We conclude that the significant variation found in oxygen consumption will have consequences while performing low-flow anaesthesia, that additional oxygen supply during the recovery period because of the initially incomplete repayment of oxygen debt may be useful and that studies on oxygen consumption must present gender-specific data because of the gender-dependent variation found in oxygen consumption.

Antineoplastic Agents↗
PubMedDate not supplied

A comparison of three methods of analyzing post-exercise oxygen consumption.

Oxygen consumption after exercise is frequently plotted as a function of time and then the area under the curve (AUC) is calculated. Subsequently, this AUC is further manipulated and thus, differences between these manipulations may impact the interpretation of changes in oxygen consumption after exercise. The purpose of this study was to determine if the method of calculating AUC influences the interpretation of changes in post-exercise oxygen consumption in response to long-term aerobic exercise. Forty-three moderately obese, sedentary participants volunteered to participate in this study (26 women and 17 men). All participants performed verified supervised exercise during the study. Supervised treadmill exercise was initially conducted for 3 d/week at 60 % of heart rate reserve (HRR) for 30 min and progressed to 5 d/week at 75 % of HRR for 45 min across the first 4 months. Pre-exercise, exercise, and post-exercise oxygen consumption was measured at baseline and 9 months. AUC was calculated by three methods; total, incremental, and positive incremental. Descriptive statistics and dependent T-tests were calculated for each method of calculating the AUC. In addition, the intra-individual coefficient of variation was determined for each individual for each AUC method. A pearson product moment correlation was calculated for each method to determine the strength of the relationship between pre- and post-training values. The change in post-exercise oxygen AUC after nine months of training was 5.36+/-10.90 L, 2.17+/-7.61 L, and 1.74+/-9.10 L for the total, incremental, and positive incremental methods, respectively. There was significant change in post-exercise total AUC from baseline to 9-months (5.36 +/- 10.90 L), while there was no significant change in incremental or positive incremental AUC. There was a moderately high correlation (r=0.67, p <0.05) between baseline and 9-months for the total AUC method, while there was no significant correlation for incremental and positive incremental AUC methods. These results suggest that the method used to calculate AUC can lead to a different interpretation of the effects of training on post-exercise oxygen consumption. From this data, it appears that analyzing post exercise oxygen consumption with the total area under the curve method has a greater ability to detect a change from aerobic training, than either the positive or incremental area under the curve methods.

Adaptation, Physiological↗
PubMed1997

Oxygen consumption and ventilation during simulated escape from an offshore oil platform.

Twenty-six male workers from the North Sea offshore oil industry took part in a simulated escape exercise at the Offshore Fire Training Centre. The course was 370 m long and had 19.4 m of vertical ascent and descent using the stairs on simulated offshore structures. Inspired ventilation and oxygen consumption were measured using the P. K. Morgan "Oxylog' and subjects breathed through the apparatus by mouthpiece and one-way valve assembly while wearing a nose clip. On comparison with anthropometric data from larger studies, this sample of the offshore work-force was thought to be representative. The mean duration of the exercise period was 371 s (SD = 24 s, range = 325-424 s). Mean oxygen consumption standing still at the start of the trial was 0.421 min-1 (SD = 0.101 min-1, max. = 0.611 min-1) and mean ventilation 12.351 min-1 (SD = 4.251 min-1, max. = 22.271 min-1). During exercise, the mean oxygen consumption rose to 2.711 min-1 (SD = 0.641 min-1, max = 4.051 min-1) and mean ventilation reached 46.341 min-1 (SD = 15.831 min-1, max = 87.361 min-1) during the fifth minute of exercise. At the end of the exercise period, oxygen consumption returned to resting values after 2 min and ventilation after 3 min. There was no indication of an oxygen debt. Oxygen consumption and ventilation were related to body weight and the maximum figures for ventilation and oxygen consumption were seen in individuals of over the 95th centile for weight who completed the exercise more quickly than other subjects. Draft standards for respiratory protective equipment for use during escape from fire do not specify the breathing volumes identified in this study, and which are considerably higher than those being currently considered. Additionally, the atmospheric conditions near a fire are likely to stimulate ventilation to considerably higher levels than those identified here. Accordingly, such equipment is likely to limit physical performance if a similar intensity of exercise is necessary during an escape. The architecture of offshore installations and protocols for escape from them should be structured to minimize exercise, and stair climbing should be avoided if emergency respirators are to be used. Workers should be trained in the use of escape breathing equipment and instruction should include information regarding its limitations and the need to limit exercise to an appropriate level.

Body Weight↗
PubMed1998

Oxygen consumption and energy state in an in vitro model of rat brain perfused with artificial oxygen carrier.

The present study was performed in order to determine the oxygen consumption of a rat brain perfused with an artificial oxygen carrier. Measurements were performed prior to and 2 or 30 min after an ischemic period of 5 min. In addition, the energy-related metabolites were determined. Basal oxygen consumption and energy state were comparable to in vivo conditions. The tissue concentration of the energy metabolites decreased during ischemia and completely recovered during 30 min of reperfusion. The oxygen consumption was higher in the early phase of reperfusion than under pre-ischemic conditions. However, the oxygen consumption in the later phase of reperfusion was lower than the basal consumption. The data demonstrate that the addition of an artificial oxygen carrier to the perfusate provides sufficient amounts of oxygen to the in vitro preparation and that the measurement of the oxygen consumption during the post-ischemic reperfusion is a more sensitive parameter for the detection of emerging deficits than the measurement of the tissue levels of the energy metabolites.

Adenosine Diphosphate↗
PubMed1997

Oxygen consumption by splanchnic tissues in wethers consuming ad libitum different proportions of bermudagrass and ryegrass-wheat.

Crossbred wethers (n = 18, 7.5 month of age and 31 +/- 0.8 kg) were used in a 23-day experiment to determine effects of ad libitum consumption of diets differing in proportions of coarsely chopped bermudagrass and ryegrass-wheat hay (0, 33, 67 and 100%) on oxygen consumption by splanchnic tissues. Bermudagrass and ryegrass-wheat were 9 and 13% CP and 78 and 71% NDF, respectively. Intake of dry matter (1.03, 0.92, 0.92 and 0.76 kg/d) and digestible energy (13.5, 10.7, 10.6 and 8.2 MJ/d for 0, 33, 67 and 100% bermudagrass, respectively) changed linearly and cubically (P < 0.05) as bermudagrass level increased. Consumption of oxygen by the portal-drained viscera tended to decrease linearly (P = 0.14) with increasing bermudagrass (182, 154, 156 and 137 mM/h), and hepatic oxygen consumption decreased linearly (P < 0.05) and changed cubically (P = 0.07; 150, 113, 116 and 103 mM/h for 0, 33, 67 and 100% bermudagrass, respectively). Splanchnic tissue energy consumption expressed as a percentage of digestible energy intake increased linearly (P = 0.08) with increasing bermudagrass (24.0, 27.6, 28.6 and 33.2% for 0, 33, 67 and 100% bermudagrass, respectively). In conclusion, the level rather than presence alone of different grass sources consumed ad libitum affected energy use by the splanchnic bed, and as a percentage of digestible energy intake splanchnic bed energy consumption increased with increasing dietary bermudagrass level and decreasing digestible energy intake.

Animal Nutritional Physiological Phenomena↗
PubMed1974

Nonequilibrium thermodynamic analysis of the coupling between active sodium transport and oxygen consumption.

Sodium transport and oxygen consumption have been simultaneously studied in the short-circuited toad skin. A constant stoichiometric ratio was observed in each skin under control condition (NaCl-Ringer's solution bathing both sides of the skin) and after block of sodium transport by ouabain. During alterations of sodium transport by removal and addition of K to the internal solution the stoichiometric ratio is constant although having a value higher than that observed in other untreated skins. The coupling between active sodium transport and oxygen consumption was studied after a theoretical nonequilibrium thermodynamic model. Studies were made of the influence of Na chemical potential difference across the skin on the rates of Na transport and oxygen consumption. A linear relationship was observed between the rates of Na transport and oxygen consumption and the Na chemical potential difference. Assuming the Onsager relationship to be valid, the three phenomenological coefficients which describe the system were evaluated. Transient increases in the rate of sodium transport and oxygen consumption were observed after a transitory block of sodium transport by removal of Na from the external solution. Cyanide blocks completely the rate of oxygen consumption in less than 2 min and the short-circuit current measured after that time decays exponentially with time, suggesting a depletion of ATP from a single compartment.

Animals↗
PubMed1989

Exchange of oxygen across the epicardial surface distorts estimates of myocardial oxygen consumption.

The rate of oxygen consumption of isolated, Langendorff-circulated, saline-perfused hearts of guinea pigs, rats, and rabbits was measured using the classical Fick Principle method. The heart was suspended in a glass chamber the oxygen partial pressure, PO2, of which could be varied. The measured rate of oxygen consumption was found to vary inversely with the ambient (heart chamber) PO2. This result prevailed whether the chamber was filled with air, saline, or oil, and whether the pericardium was present or the heart was wrapped in Saran. The effect varied inversely with heart size both within and across species. It is concluded that the epicardial surface is permeable to oxygen which will diffuse either into or out of the heart as the PO2 gradient dictates. In either case the classically measured rate of oxygen consumption will be in error. The error can be large in studies of cardiac basal metabolism. A simple model is developed to describe the observed rate of oxygen consumption as classically measured. The measured rate is partitioned into two components: the true rate of oxygen consumption of the heart, and the rate of loss of oxygen by diffusive exchange across the epicardial surface. The latter component is proportional to the gradient of oxygen partial pressure from myocardium to environment and to the diffusive oxygen conductance of myocardial tissue. Application of the model allows the true rate of oxygen consumption of the heart to be recovered from measured values which may be considerably in error.

Animals↗
PubMed2006

Oxygen consumption and osmoregulatory capacity in Neomysis integer reduce competition for resources among mysid shrimp in a temperate estuary.

Results of field surveys and laboratory measurements of oxygen consumption and body fluid osmolality at different salinities in the mysids Neomysis integer, Mesopodopsis slabberi, and Rhopalophthalmus mediterraneus from the Guadalquivir estuary (southwest Spain) were used to test the hypothesis that osmotic stress (oxygen consumption vs. isosmotic points) was lowest at salinities that field distributions suggest are optimal. The three species showed overlapping spatial distributions within the estuary but clear segregation along the salinity gradient: N. integer, M. slabberi, and R. mediterraneus displayed maximal densities at lower, intermediate, and higher salinities, respectively. Adults of N. integer were extremely efficient hyperregulators (isosmotic point 30 per thousand) over the full salinity range tested (3 per thousand-32 per thousand), and their oxygen consumption rates were independent of salinity; adults of M. slabberi were strong hyper- and hyporegulators at salinities between 7 per thousand and 29 per thousand (isosmotic point, 21 per thousand) and showed higher oxygen consumptions at the lowest salinity (6 per thousand); adults of R. mediterraneus hyperregulated at salinities between 19 per thousand and seawater (isosmotic point, 36 per thousand), with the lowest oxygen consumption at salinity around their isosmotic point (35 per thousand). Thus, the osmoregulation capabilities of M. slabberi and R. mediterraneus seem to determine the salinity ranges in which most of their adults live, but this is not so for adults of N. integer. Moreover, maximal field densities of M. slabberi (males and females) and R. mediterraneus (males) occur at the same salinities as the lowest oxygen consumption. In contrast, field distribution of N. integer was clearly biased toward the lower end of the salinity ranges within which it osmoregulated. We hypothesize that the greater euryhalinity of N. integer makes it possible for this species to avoid competition with R. mediterraneus by inhabiting the more stressful oligohaline zone.

Animals↗
PubMed1990

Effect of hyper- and hypovolaemia on regional myocardial oxygen consumption.

STUDY OBJECTIVE - The purpose of the investigation was to study the effect of preload on coronary blood flow and myocardial oxygen consumption in subendocardial and subepicardial regions of left ventricular free wall. DESIGN - Ventricular volume in anaesthetised open chest dogs was altered over a range of 20% to produce hypovolaemia (10-15% exsanguination) or hypervolaemia (colloid infusion), allowing measurements of regional blood flow and oxygen consumption with varying preloads. beta Adrenergic blockade was used to limit changes in inotropy, and heart rate was kept constant by pacing at 150 beats.min-1. SUBJECTS - 9 mongrel dogs of either sex weighing 24.9 (SEM 4.1) kg were studied. MEASUREMENTS and RESULTS - Left ventricular volume was calculated from ultrasonic measurements of long and short axis end diastolic diameters and wall thickness. Regional myocardial blood flow was estimated using radioactive microspheres, and oxygen consumption in each region was determined from microspectrophotometric measurements of oxygen saturations in small arteries and veins. Hypervolaemia increased subepicardial blood flow from 66.8(6.9) (normovolaemic) to 114.1(13.5) ml.min-1.100 g-1, and regional oxygen consumption from 4.08(0.57) to 6.44(1.08) ml.min-1.100 g-1. Values in the subendocardium were similar, except for oxygen consumption, which increased less than in the subepicardium. Left ventricular end diastolic volume, pressure, and output were each increased in hypervolaemia, but not dP/dt and systolic aortic pressure. Hypovolaemia reduced blood pressures without reducing end diastolic volume. CONCLUSIONS - Augmented flow work produced by increased preload (even in the absence of changes in pressure work) increases myocardial oxygen supply equally in the subepicardium and the subendocardium, while oxygen extraction and consumption are preferentially augmented in the subepicardium.

Animals↗
PubMed1985

Oxygen consumption in mice (I strain) after feeding.

To determine if excess heat production can account for the lower fat accumulation in I strain mice, oxygen consumption, a measure of energy expenditure, was measured in I mice and C57BL mice (a control strain) to determine basal metabolic rate (BMR) and resting metabolic rate (RMR) and response to food consumption and acute cold exposure. Oxygen consumption was higher in the I strain than in the C57BL mice only after the dark cycle (feeding period). No difference between I and C57BL mice in spontaneous activity was found during the dark or light cycle. Body temperature was also not different in I and C57BL mice. Oxygen consumption in response to norepinephrine was similar in the two strains. These results indicate oxygen consumption is greater in I than C57BL mice only in response to feeding. Differences in glucose utilization by I and C57BL mice, including a lower glucose tolerance curve, greater deposition of glucose to muscle glycogen and lactate production in I mice also indicate differences in nutrient processing. Higher oxygen consumption after feeding in I mice than in C57BL mice indicates inefficient food utilization and accounts for their lower ability to store energy as fat.

Animals↗
PubMed1997

Jejunal glucose uptake and oxygen consumption in turkey poults selected for rapid growth.

Two lines of turkey poults, one selected for rapid growth at 16 wk of age (F line) and the other a randombred control line (RBC2) were used to investigate the effect of selection for rapid growth on jejunal O2 consumption and glucose transport as well as whole-body O2 consumption. All trials used unsexed poults and were designed as a randomized complete block with day and line as independent variables. In Trial 1, 120 turkey poults, fed a standard starter ration (25.5% CP), were used to examine the effect of selection on feed intake, body weight gain, and efficiency from hatching (Day 0) to 13 d of age. At Day 14, 36 of 60 birds from each line were killed to measure intestinal length and weight and jejunal O2 consumption after 18 h of feed deprivation. Compared with the RBC2 line, the F line had relatively shorter but heavier small intestinal segments when adjusted by 18 h feed-deprived body weight (FBW; P < 0.001). The F line consumed more O2 over the entire jejunum adjusted to FBW than RBC2 line (43.8 vs 34.6 nmol O2/min.g FBW; P < 0.001). Jejunal ouabain- and cycloheximide-sensitive O2 consumption were greater (P < 0.05) in the F line. In Trial 2, 16 14-d-old poults from each line were used to measure in vitro jejunal glucose transport rate. There was no difference in glucose transport of the jejunum (nanomoles per minute per gram of FBW) between the lines. In Trial 3, 20 poults from each line were used to measure whole-body O2 consumption at 7 to 10 d of age. The F and RBC2 lines had similar whole-body O2 consumption rate per gram of FBW. These data suggest that selection of turkeys for rapid growth at 16 wk of age did not increase efficiency of jejunal glucose uptake in 14-d-old turkey poults.

Aging↗
PubMed1983

Hepatic perfusion and splanchnic oxygen consumption in patients postinjury.

Hepatic dysfunction following injury is felt to be due to hepatic ischemia. To test this hypothesis we measured hepatic blood flow (HBF) and splanchnic oxygen delivery and consumption in nine multiply injured patients. HBF, measured by indocyanine green clearance, was 0.4 +/- 0.1 L/min/m2 12 hours after injury. It steadily increased to 1.3 +/- 0.1 L/min/m2 by 1 week after injury. Changes in cardiac output were similar and were due largely to changes in HBF. Hepatic hypoperfusion was correlated with subsequent increases in serum bilirubin. High oxygen consumption was associated with high HBF and oxygen delivery, and splanchnic oxygen consumption became a large fraction (range, 21-67%) of total body oxygen consumption. Although splanchnic oxygen delivery was diminished with low HBF, splanchnic oxygen consumption remained normal (37 +/- 2 ml/min/m2) due to increased oxygen extraction. We conclude that hepatic blood flow is markedly reduced after injury. Reduced HBF is correlated with liver dysfunction although normal splanchnic oxygen consumption is maintained.

Accidents, Traffic↗
PubMed2000

Reduced oxygen consumption precedes the drop in body core temperature caused by hemorrhage in rats.

This study examines the early time course in core temperature change and oxygen consumption at 4 levels of hemorrhage. Chronically instrumented rats were acclimatized to a respirometry chamber for 30 min. The rats were briefly (10 min) removed from the chamber for a fixed volume hemorrhage of 0 mL/kg (sham), 8 mL/kg, 16 mL/kg, 24 mL/kg, or 32 mL/kg. Rats were then returned to the chamber, and oxygen consumption and body core temperature were monitored for the next 2 h. Oxygen consumption (control 1.26 mL O2/g/h) fell significantly 5 min after hemorrhage in all but the sham and 8 mL/kg hemorrhage groups, with the decrease proportional to the hemorrhage volume. The 32 mL/kg hemorrhage group showed the greatest decrease, to 0.47 mL O2/g/h. Body core temperature (control 37.5 degrees C) fell more gradually, declining to 35.6 degrees C 110 min after the 24 mL/kg hemorrhage, and to 33.2 degrees C at 6 h after the 32 mL/kg hemorrhage. In the 16 mL/kg hemorrhage group, oxygen consumption fell significantly by 5 min after hemorrhage, but a drop in body temperature was not seen until 25 min after hemorrhage. The data from this study indicate that the drop in core temperature does not cause the observed decrease in oxygen consumption. In fact, the timing and magnitude of the drop in oxygen consumption indicate that the reduced metabolic rate may mediate the hemorrhage-induced drop in body core temperature in conscious rats.

Animals↗
PubMed2002

Impaired regulation of renal oxygen consumption in spontaneously hypertensive rats.

Abnormalities of nitric oxide (NO) and oxygen radical synthesis and of oxygen consumption have been described in the spontaneously hypertensive rat (SHR) and may contribute to the pathogenesis of hypertension. NO plays a role in the regulation of renal oxygen consumption in normal kidney, so the response of renal cortical oxygen consumption to stimulators of NO production before and after the addition of the superoxide scavenging agent tempol (4-hydroxy-2,2,6,6-tetramethyl piperidine-1-oxyl) was studied. Baseline cortical oxygen consumption was similar in SHR and Wistar-Kyoto (WKY) rats (SHR: 600 +/- 55 nmol O(2)/min per g, WKY: 611 +/- 51 nmol O(2)/min per g, P > 0.05). Addition of bradykinin, enalaprilat, and amlodipine decreased oxygen consumption significantly less in SHR than WKY (SHR: bradykinin -13.9 +/- 1.9%, enalaprilat -15.3 +/- 1.6%, amlodipine -11.9 +/- 0.7%; WKY: bradykinin -22.8 +/- 1.0%, enalaprilat -24.1 +/- 2.0%, amlodipine -20.7 +/- 2.3%; P < 0.05), consistent with less NO effect in SHR. Addition of tempol reversed the defects in responsiveness to enalaprilat and amlodipine, suggesting that inactivation of NO by superoxide contributes to decreased NO availability. The response to an NO donor was similar in both groups and was unaffected by the addition of tempol. These results demonstrate that NO availability in the kidney is decreased in SHR, resulting in increased oxygen consumption. This effect is due to enhanced production of superoxide in SHR. By lowering intrarenal oxygen levels, reduced NO may contribute to susceptibility to injury and renal fibrosis. Increasing NO production, decreasing oxidant stress, or both might prevent these changes by improving renal oxygenation.

Amlodipine↗