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The effect of pericardiectomy on maximal oxygen consumption and maximal cardiac output in untrained dogs.

To test the hypothesis that the pericardium limits maximal oxygen consumption by limiting stroke volume and cardiac output, we studied 10 untrained dogs during submaximal and maximal exercise before and after pericardiectomy. Seven additional dogs were studied before and after a sham operation. All dogs were instrumented chronically with aortic and pulmonary artery catheters. Dogs were tested by running on a motor-driven treadmill, 4-6 times before and after pericardiectomy or sham operation. We measured cardiac output (dye dilution), heart rate, and arteriovenous oxygen difference. Oxygen consumption and stroke volume were calculated from these variables. After pericardiectomy, there were significant (P less than 0.01) increases in maximal oxygen consumption, maximal cardiac output, and maximal stroke volume. Maximal oxygen consumption decreased significantly in the sham group. There was no change in maximal heart rate following pericardiectomy, or in maximal cardiac output, heart rate, or stroke volume following sham operation. Both groups of dogs experienced similar significant decreases in hematocrit, arterial and venous oxygen contents, and arteriovenous oxygen difference. Neither pericardiectomy nor sham operation had any effect on oxygen consumption during submaximal exercise. However, the sham group had significant increases in cardiac output and heart rate during submaximal exercise, and the pericardiectomy group demonstrated a trend toward an increased cardiac output during submaximal exercise. These results support the hypothesis that the pericardium limits maximal oxygen consumption by limiting stroke volume and cardiac output during maximal exercise in untrained dogs. Further, these findings suggest that maximal oxygen consumption is limited by the oxygen transport capacity of the cardiovascular system, and not by the oxidative capacity of skeletal muscle in the untrained dog.

Animals↗

Correlation of force-length area with oxygen consumption in ferret papillary muscle.

The ventricular systolic pressure-volume area correlates well with myocardial oxygen consumption. However, in isolated muscle preparations, there are experimental data based on both mechanical and energetic measurements that suggest that the pressure-volume area concept may not obtain. In the present study, force-length area, the analog of pressure-volume area for a linear muscle, was examined in the ferret papillary muscle preparation under a wide range of loading conditions. There were two major findings: first, force-length area is closely correlated with oxygen consumption (r = 0.94-0.98); this correlation is better than those for such other indexes as peak force and force-time integral. Furthermore, this relation of oxygen consumption with force-length area is independent of the mode of contraction (isometric or shortening), while the relations with the other indexes are not. Second, quick release imposed after end-systole during isometric contraction was found to curtail oxygen consumption. The first finding, the optimal correlation of force-length area with oxygen consumption, suggests both that the correlation of pressure-volume area with oxygen consumption on the ventricular level arises from a basic property of cardiac muscle and that force-length area may be the best mechanical index to use in calculating regional oxygen consumption for a ventricular segment. The second finding, however, suggests that the time-varying elastance model, on which the concepts of pressure-volume area and force-length area are based, may not provide a complete description of the mechanical basis of cardiac muscle energetics, especially during the isometric contraction.

Animals↗

Endogenous endothelial nitric oxide synthase-derived nitric oxide is a physiological regulator of myocardial oxygen consumption.

Our objective was to determine the precise role of endothelial nitric oxide synthase (eNOS) as a modulator of cardiac O2 consumption and to further examine the role of nitric oxide (NO) in the control of mitochondrial respiration. Left ventricle O2 consumption in mice with defects in the expression of eNOS [eNOS (-/-)] and inducible NOS [iNOS (-/-)] was measured with a Clark-type O2 electrode. The rate of decreases in O2 concentration was expressed as a percentage of the baseline. Baseline O2 consumption was not significantly different between groups of mice. Bradykinin (10(-4) mol/L) induced significant decreases in O2 consumption in tissues taken from iNOS (-/-) (-28+/-4%), wild-type eNOS (+/+) (-22+/-4%), and heterozygous eNOS(+/-) (-22+/-5%) but not homozygous eNOS (-/-) (-3+/-4%) mice. Responses to bradykinin in iNOS (-/-) and both wild-type and heterozygous eNOS mice were attenuated after NOS blockade with N-nitro-L-arginine methyl ester (L-NAME) (-2+/-5%, -3+/-2%, and -6+/-5%, respectively, P<0.05). In contrast, S-nitroso-N-acetyl-penicillamine (SNAP, 10(-4) mol/L), which releases NO spontaneously, induced decreases in myocardial O2 consumption in all groups of mice, and such responses were not affected by L-NAME. In addition, pretreatment with bacterial endotoxin elicited a reduction in basal O2 consumption in tissues taken from normal but not iNOS (-/-)-deficient mice. Our results indicate that the pivotal role of eNOS in the control of myocardial O2 consumption and modulation of mitochondrial respiration by NO may have an important role in pathological conditions such as endotoxemia in which the production of NO is altered.

Animals↗

Oxygen consumption and transport in stable patients with chronic obstructive pulmonary disease.

We studied the relationship between oxygen consumption and systemic oxygen transport in 30 clinically stable patients with chronic obstructive pulmonary disease (COPD) before and after increasing oxygen transport by passive leg elevation to raise the cardiac output. Results were compared with those observed in 10 patients with silicosis. The effect of leg elevation on oxygen consumption was also studied in 12 normal subjects. Oxygen consumption was measured by a closed circuit system, cardiac output by the direct Fick method, and arterial oxygen content by a cooximeter. Supine oxygen consumption was correlated with oxygen transport in patients with COPD (r = 0.50, p less than 0.01), and with leg elevation transport increased from a mean of 516 +/- 23 (SEM) to 567 +/- 26 ml X min-1 X m-2 and consumption increased from a mean of 136 +/- 3 to 148 +/- 4 ml X min-1 X m-2 (both p less than 0.01). In patients with silicosis, leg elevation raised mean oxygen transport from 620 +/- 40.0 to 745 +/- 54.0 ml X min-1 X m-2 and mean consumption from 161 +/- 6 to 192 +/- 6 ml X min-1 X m-2 (both p less than 0.01). In normal subjects, no change in oxygen consumption was observed with leg elevation (154 +/- 8 to 152 +/- 6 ml X min-1 X m-2).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗

Effect of vasoactive agents on intestinal oxygen consumption and blood flow in dogs.

A comparison study of several vasoconstrictor and vasodilator agents was conducted measuring changes in intestinal blood flow and oxygen consumption during 10-min periods of intra-arterial infusion. Blood flow was measured in a branch of the superior mesenteric artery of anesthetized dogs with an electromagnetic blood flow meter, and the arteriovenous oxygen content difference across the gut segment was determined photometrically. Vasopressin (4 x 10(-3) and 7x 10(-4) U/kg-min) diminished blood flow 60 and 28% and reduced oxygen consumption 54 and 22%, respectively (all P less than 0.001). In a dose which did not lower blood flow, vasopressin still caused a decline in oxygen consumption (P less than 0.01). Epinephrine (5 x 10(-2) mug/kg-min) decreased blood flow 19% (P less than 0.001) but did not reduce oxygen consumption. After beta-adrenergic blockade, however, the same dose of epinephrine decreased blood flow 41% and oxygen consumption 33% (both P less than 0.001). Responses to angiotension II, calcium chloride, and prostaglandin F2alpha resembled effects of vasopressin rather than those of epinephrine, namely decreased blood flow and decreased oxygen consumption. The vasodilator agents, prostaglandin E1, is isoproterenol, and histamine, increased (P less than 0.001) both blood flow (130, 80, and 98%, respectively) and oxygen consumption (98, 64, and 70%, respectively). Vasopressin, angiotensin II, calcium chloride, and prostaglandin F2alpha appear to contract arteriolar and precapillary sphincteric smooth muscle indiscriminately to evoke both intestinal ischemia and hypoxia. Epinephrine is the exceptional constrictor in this case, producing diminished blood flow without a reduction in oxygen uptake.

Animals↗

High K+,Na+-deficient solution inhibits tension, O2 consumption, and ATP synthesis in smooth muscle.

In guinea pig taenia coli, added 45.4 mM K+ induced a sustained contraction, increased the rate of oxygen consumption, and slightly decreased the ATP content. In substituted 154.2 mM K+, Na+-deficient solution, only a transient contraction was induced. Oxygen consumption also showed only a transient increase and ATP content of the muscle rapidly decreased. Such an inhibition of sustained contraction and the decrease in both oxygen consumption and ATP content were recovered when 5.5 mM pyruvate or 50 mM NaCl was added during the 154.2 mM K+-induced contraction. In rabbit aorta, substituted 80 mM K+, 74.2 mM Na+ solution induced a sustained contraction, increase in oxygen consumption, and no change in ATP content. The 80 mM K+ solution without added glucose also induced a sustained contraction followed by a slight increase in oxygen consumption and a slight decrease in ATP content. The 154.2 mM K+, Na+-deficient solution produced similar changes in both oxygen consumption and ATP content as the 80 mM K+, glucose depleted solution. However, the 154.2 mM K+ solution induced only a transient contraction in the vascular smooth muscle. When 100 mM sucrose was hyperosmotically added to the 154.2 mM K+ solution, the suppressed muscle tension increased again, although the ATP content did not increase. From these and the previous results, it is concluded that glucose utilization by the taenia coli is inhibited in the 154.2 mM K+, Na+-deficient solution, and the decreased energy production of the muscle cell does not compensate the increased energy consumption induced by the high concentration of K+. In the aorta, although the Na+-deficient solution also decreases ATP production, it is the cell swelling induced by a high KCI concentration in the medium, not the decrease in energy metabolism, that has a direct inhibitory effect on muscle tension.

Adenosine Triphosphate↗

Effects of thyroid hormones on mitochondrial oxygen consumption in brown adipose tissue and heart from cold-exposed hypothyroid rats.

The present work measured brown adipose tissue and heart mitochondrial oxygen consumption in hypothyroid rats treated with replacement doses of T3, T4 or T4 plus iopanoic acid and kept at 4 degrees C for 24 h. Heart oxygen consumption in normal, untreated hypothyroid and T4-treated hypothyroid rats was unaffected by cold exposure. In rats treated with T4 plus iopanoic acid, rates of oxygen consumption were normal in those maintained at 4 degrees C as well as in those kept at room temperature, despite serum T3 concentration being significantly decreased. The cold-exposed T3-treated hypothyroid rats showed a marked decrease in oxygen consumption (p less than 0.02) and alpha-glycerophosphate dehydrogenase activity, a T3-dependent enzyme. Mitochondrial oxygen consumption in brown fat from normal (p less than 0.01), T4 (p less than 0.02) and T4 plus iopanoic acid-treated (p less than 0.01) rats rose more than twofold in response to cold. In the T3-treated group, oxygen consumption at room temperature was higher (p less than 0.02) than in any other group at similar temperatures. However, the T3-treated group showed no changes in oxygen consumption in response to cold, perhaps because this group reached the maximal response at room temperature. The untreated and the T3-treated hypothyroid rats (both groups devoid of T4) did not survive at 4 degrees C unless T4 or several-fold replacement amounts of T3 were administered. The data demonstrate the crucial role of T4 in thermogenesis during cold exposure.

Adipose Tissue↗

Increased nuclear tri-iodothyronine binding and thyroid hormone-stimulated glucose consumption in mononuclear blood cells from patients with liver cirrhosis.

Nuclear tri-iodothyronine (T3) maximal binding capacity (MBC) and thyroxine- and T3-stimulated cellular oxygen consumption and glucose consumption were examined in mononuclear blood cells from six patients with liver cirrhosis (LC), in six patients with alcoholic hepatitis (AH), and in six healthy control subjects. Serum T3 was decreased in patients with LC. The MBC of T3 was increased significantly (P less than 0.05) in cells from patients with LC compared with patients with AH and controls, whereas the equilibrium association constants did not differ. Unstimulated glucose consumption was slightly increased (P less than 0.05) in cells from patients with AH and LC compared with controls. Thyroid hormone-stimulated glucose consumption was significantly (P less than 0.05) increased in cells from patients with LC compared with controls and patients with AH. Unstimulated oxygen consumption did not differ between the groups, but thyroid hormone-stimulated oxygen consumption was depressed in cells from patients with AC (P less than 0.05) compared with patients with LC and with controls. We conclude that both thyroid hormone-stimulated glucose consumption and T3 nuclear receptor binding in cells from patients with LC are increased, and suggest that the observed changes are responsible for maintenance of euthyroidism in the face of reduced circulating T3.

Adult↗

The effects of oxygen toxicity on the pregnant rat using an apparatus designed to measure oxygen consumption method.

To evaluate the effects of oxygen toxicity in the pregnant rat at high and low concentrations of oxygen, an oxygen-consumption apparatus was devised to measure the consumption of oxygen continuously over long periods. Oxygen consumption, partial oxygen pressure on the skin (tcPo2), and lipid peroxide levels in the serum were measured. There was a close correlation between oxygen consumption and body weight of rats that weighed between 150 g and 450 g. Oxygen consumption during the later stages of pregnancy increased by 1.8 ml/day, an increase of 8%. Oxygen consumption by rats during parturition increased markedly for up to 1 h and then reached and remained at a plateau value until the end of delivery. Exposure of pregnant rats to low concentrations of oxygen resulted in a marked depression in oxygen consumption and tcPo2 during the exposure time. A significant increase in the lipid peroxide level in serum was observed in the mother rat after birth and in the newborn offspring of pregnant rats exposed to 16% oxygen for 3 h.

Animals↗

[Intraoperative oxygen consumption and organ function in liver transplantation].

Liver transplantation has become established as a reasonable and promising treatment option in terminal stages of liver diseases. Since there is no permanent artificial liver support available, primary "non-function" (PNF) of the graft is one of the most threatening complications. Therefore, an early and, if possible, intraoperative assessment of liver function is essential. Pathological changes in total oxygen consumption (VO2) are considered as an early indicator for the occurrence of PNF. Previously, PNF was analyzed using extensive calculations according to the Fick method, but since inauguration of the PhysioFlex anaesthesia device (Dräger, Lübeck, Germany), which is based on a closed anaesthesia circuit, continuous monitoring of oxygen consumption has become possible. The aim of the study was to investigate whether continuous VO2 monitoring using PhysioFlex allows immediate detection of pathological changes in graft function in the very early neohepatic phase of liver tranplantation. Therefore, 51 liver transplants were investigated at the University Hospital of Magdeburg with regard to a correlation between intraoperative VO2 values and ischaemic time periods of the donor organ and the postoperative liver function. A regular course of oxygen consumption was found in uncomplicated transplants and prompt liver function within normal ranges. PNF was not observed in any transplants. Changes in oxygen consumption were caused by early retransplants or by the delayed start of graft-based metabolism intraoperatively and transient diminished liver function found postoperatively, e.g., in pre-existing hepatorenal syndrome. In addition, VO2 indicated precisely the anhepatic and neohepatic phases during the course of liver transplantation. There was no correlation between the course of glucose content of the blood and the metabolic index of glucose and oxygen consumption or between both parameters and initial graft function. Furthermore, the duration of ischaemic time periods was not closely associated with oxygen consumption during the reperfusion phase. However, there was a correlation between intraoperative VO2 and postoperative bilirubin values, while a correlation between VO2 and GLDH as a further relevant parameter of postoperative graft function could not be confirmed, most likely because of the great variance in these values. In conclusion, the results suggest that changes in total oxygen consumption may, in part, be caused by changes in liver metabolism, depending on the various phases of liver transplantation. In addition, oxygen analysis allows monitoring of the critical phases of liver transplantation such as the anhepatic and early neohepatic periods with regard to immediate detection of early changes in graft metabolism. For routine use of this parameter, steady measurement of the mean value displayed on the PhysioFlex for selectable time periods would be helpful in addition to the continuous VO2 analysis, since there is a greater variance in the single VO2 values, which are documented by the anaesthesiologist, than in the online-detected and automatically calculated values of specific periods of transplantation.

Adolescent↗

[An Experimental Study on the diagnosis of high voltage electrical injury by means of biological oxygen consumption measurement].

OBJECTIVE: To investigate the degrees of the degeneration or the necrosis of muscle tissue injured by high voltage electricity as determined by biological oxygen consumption measurement. METHODS: An animal model with high voltage electricity designed in our laboratory was employed in the study. Muscle tissue sized 12 mm x 10 mm x 1 mm at electric burn produced 5 spots of the rabbit injured legs was harvested for the measurement of tissue oxygen consumption for 100s at 2, 8, 14, 24, 48 postburn hours and 5 postburn day. At the same time histological examination was made. RESULTS: One hundred and eighty two pieces of tissue samples were examined. Among them 20 samples with oxygen consumption below 8.7 kpa/100s (43.5%) showed necrosis under LM, while 157 samples with oxygen consumption of 16.9 to 8.78 kpa/100s (84% similar 44%) showed histological necrosis and different degrees of mixed degeneration and normal tissue, and 5 samples with oxygen consumption above 17 kpa/100s (85%) showed normal histological structure. CONCLUSION: The lower the tissue oxygen consumption was, the more severe the tissue degeneration and necrosis were. Oxygen consumption measurement could be valuable in the determination of the degree of tissue injury inflicted by electricity in terms of its convenience, rapidity and accuracy.

Animals↗

Estimate of oxygen consumption and intracellular zinc concentration of human spermatozoa in relation to motility.

AIM: To investigate the human sperm oxygen/energy consumption and zinc content in relation to motility. METHODS: In washed spermatozoa from 67 ejaculates, the oxygen consumption was determined. Following calculation of the total oxygen consumed by the Ideal Gas Law, the energy consumption of spermatozoa was calculated. In addition, the zinc content of the sperm was determined using an atomic absorption spectrometer. The resulting data were correlated to the vitality and motility. RESULTS: The oxygen consumption averaged 0.24 micromol/10(6) sperm x 24h, 0.28 micromol/10(6) live sperm x 24h and 0.85 micromol/10(6) live motile sperm x 24h. Further calculations revealed that sperm motility was the most energy consuming process (164.31 mJ/10(6) motile spermatozoa x 24h), while the oxygen consumption of the total spermatozoa was 46.06 mJ/10(6) spermatozoa x 24h. The correlation of the oxygen/energy consumption and zinc content with motility showed significant negative correlations (r= -0.759; P<0.0001 and r=-0.441; P<0.0001, respectively). However, when correlating sperm energy consumption with the zinc content, a significant positive relation (r=0.323; P=0.01) was observed. CONCLUSION: Poorly motile sperm are actually wasting the available energy. Moreover, our data clearly support the "Geometric Clutch Model" of the axoneme function and demonstrate the importance of the outer dense fibers for the generation of sperm motility, especially progressive motility.

Adult↗

Myocardial protective effect of hypothermia during extracorporeal circulation -- by quantitative measurement of myocardial oxygen consumption -.

OBJECTIVE: To evaluate the effect of systemic temperature on myocardial protection during extracorporeal circulation, we quantitatively evaluated the relationship between myocardial oxygen consumption and rectal temperature. MATERIALS AND METHODS: Myocardial oxygen consumption during cardiac arrest was calculated via blood gas analysis of venous blood samples collected from the coronary sinus. The rectal temperatures of the patients during extracorporeal circulation ranged from 16.0 degrees C to 33.5 degrees C. The patients were classified into three groups according to their rectal temperature: group I (n=10; rectal temperature: 20.3+/-1.80 degrees C), group II (n=24; rectal temperature: 29.4+/-0.97 degrees C), and group III (n=29; rectal temperature: 31.7+/-0.72 degrees C). The myocardial oxygen consumption of each group was then compared. RESULTS: The average of the myocardial oxygen consumption of all cases was 62.5+/-64.0 O(2) ml/min/100 mm(3) left ventricle volume, and the averages of the individual groups were 26.9+/-28.8 in group I, 72.2+/-71.8 in group II, and 69.3+/-62.6 in group III. There was a significant difference in the oxygen consumption between group I and the other two groups. There was a positive correlation between the rectal temperature and myocardial oxygen consumption, as reflected in the following formula: Y=-0.3 x X +1.10 x X(2)-0.02 x X(3) (Y, myocardial oxygen consumption; X, rectal temperature; R(2)=0.533; P<0.0001). CONCLUSION: This study suggested that rectal temperature below 22.5 degrees C is advantageous due to the resultant myocardial protection such hypothermia affords.

Aged↗

[Effect of temperature on the rate of oxygen consumption during the second half of embryonic and early postembryonic development of European pond turtle Emys orbicularis (Reptilia: Emydidae)].

Oxygen consumption by eggs of European pond turtle was determined at two constant incubation temperatures of 25 and 28 degrees C during the second half of embryogenesis. During development at both temperatures, the rate of oxygen consumption initially increased to remain constant during the last quarter of embryogenesis. The difference between the rates of oxygen consumption at these temperatures decreased during the studied period. The coefficient Q10 for the rate of oxygen consumption decreased from 9 to 1.7. At an incubation temperature of 28 degrees C, the changes in the rate of oxygen consumption in response to a short-term temperature decrease to 25 degrees C or increase to 30 degrees C depended on the developmental stage and were most pronounced at the beginning of the studied period. During late embryonic and first 2.5 months of postembryonic development, the rate of oxygen consumption did not significantly differ after such temperature changes. The regulatory mechanisms formed during embryonic development are proposed to maintain the level of oxygen consumption during temperature changes.

Animals↗

Importance of acid-base strategy in reducing myocardial and whole body oxygen consumption during perfusion hypothermia.

During induced hypothermia with cardiopulmonary bypass, acid-base management usually follows one of two strategies: the so-called ectothermic or alpha-stat strategy, in which the pH of the arterial blood increases 0.015 pH units for every degree Celsius decrease in body temperature, or the pH-stat strategy, in which pH remains 7.4 at all temperatures. It has been assumed that oxygen consumption decreases approximately equally during hypothermia with either strategy, although there are biochemical reasons to hypothesize that oxygen consumption would be better maintained with the alpha-stat strategy. We also hypothesized that venous oxygen tension would be lower with the more alkaline alpha-stat strategy than with the pH-stat acid-base strategy, because of the Bohr effect. We tested these hypotheses by placing 10 anesthetized immature domestic pigs on cardiopulmonary bypass. We measured whole body oxygen consumption and myocardial oxygen consumption. Control measurements were made at 37 degrees C. Then the animals were cooled to 27 degrees C and the measurements were repeated. The alpha-stat strategy (pH 7.554 +/- 0.020 at 27 degrees C) was used in five animals and five animals received pH-stat management (pH 7.409 +/- 0.012 at 27 degrees C). Whole body and myocardial oxygen consumption rate decreased in both groups, but more so in the alpha-stat animals than in the pH-stat animals. The unexpectedly high oxygen consumption in the pH-stat animals also resulted in a lower than expected venous oxygen tension. Thus the effect of hypothermia in reducing oxygen consumption was less pronounced with pH-stat acid-base management.

Acid-Base Equilibrium↗

Effect of beta-adrenoceptor stimulation or blockade on regional myocardial function and regional O2 consumption during myocardial ischemia.

The purpose of this study was to determine the effect of beta-adrenoceptor activation and blockade on the relationship between regional myocardial function and regional O2 consumption in ischemic and nonischemic myocardium. Myocardial regional segmental function was assessed in 28 open chest, anesthetized dogs using subepicardial dimension gauges. Ten min after LAD (left anterior descending coronary artery) occlusion, dogs were given i.v. saline, 2 mg/kg propranolol, 0.2 mg/kg pindolol, or 1 microgram/kg/min isoproterenol. Coronary blood flow was determined using radioactive microspheres before LAD occlusion, 10 min after occlusion, and 2 hr after LAD occlusion. Regional O2 consumption was determined using microspectrophotometry. LAD occlusion did not alter any index of myocardial function measured in the nonischemic region, but in the ischemic region, end systolic length (ESL) was increased 20% while shortening was converted to systolic bulging. No agent resulted in an improved ischemic regional function or an altered O2 consumption during LAD occlusion. In the nonischemic region the per cent shortening was increased 60% with isoproterenol compared to control. Propranolol and pindolol both increased the non-schemic regional ratio of per cent shortening vs O2 consumption significantly, suggesting an improved efficiency while isoproterenol lowered this ratio. When per cent shortening was plotted vs regional O2 consumption for all treatments, a significant linear relationship was observed in the nonischemic region. Thus, no drug treatment used in this study significantly improved central ischemic regional function, or O2 consumption, but both beta-adrenoceptor blockers seemed to result in an improved relationship between segmental shortening and O2 consumption in the nonischemic region.

Adrenergic beta-Agonists↗

The relation between sodium transport and oxygen consumption in isolated perfused rat kidney.

A non-filtering isolated perfused rat kidney model was developed to determine renal oxygen consumption in the absence of tubular reabsorption. The oxygen consumption in the absence of filtration was 3.1 +/- 0.8 micron of O2/min/g. This "basal" value was substantially higher than that of 2.0 micron of O2/min/g calculated by extrapolation of a plot of sodium reabsorption vs. oxygen consumption in filtering kidneys. It was also found that ouabain 10(-4) M decreased oxygen consumption in non-filtering kidneys and acetazolamide increased it in a dose dependent fashion. Furosemide did not change "basal" oxygen consumption. In filtering kidneys, the ratio of sodium reabsorbed to oxygen consumed averaged 36.8 muEq of Na/mumole of O2. It is concluded that basal oxygen consumption is not a fixed quantity and can be changed by experimental manipulations thereby changing the relation between transport activity and oxygen consumption.

Acetazolamide↗

Fetal oxygen consumption, umbilical circulation and electrocortical activity transitions in fetal lambs.

Chronically instrumented fetal lambs were employed to test the hypothesis that the high voltage electrocortical activity phase is a state of low fetal oxygen consumption compared with the low voltage electrocortical activity phase. Measurements of umbilical flow (electromagnetic flowmeter) together with oxygen saturations and haemoglobin concentration of umbilical venous and arterial blood were used to calculate oxygen consumption. Significant depression of umbilical flow occurred at the transition from low voltage electrocortical activity to high voltage electrocortical activity; the maximum change averaged 14% 2 min after the onset of the high voltage phase. Significant depressions of oxygen saturation in umbilical venous and arterial blood were found within 5 min of the onset of high voltage electrocortical activity, averaging 2.2% and 5.2% respectively. No depression of oxygen consumption was found during these transient changes in early high voltage electrocortical activity, as the venous-arterial oxygen content difference widened significantly as a consequence of a greater fall in umbilical arterial oxygen content (0.7 ml/dl) than in umbilical venous oxygen content (0.3 ml/dl). Overall, we detected no significant depression of oxygen consumption in high voltage electrocortical activity. However a small but significant depression of oxygen consumption (6%) was found late in the high voltage electrocortical activity phase when the level of oxygen consumption in low voltage electrocortical activity was greater than 7 ml/min per kg. We conclude that the high voltage electrocortical activity in fetal lambs is not associated with a marked depression of oxygen consumption, despite significant transient depressions of umbilical flow and oxygen levels in umbilical venous and arterial blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗