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PubMed1995

Assumed oxygen consumption based on calculation from dye dilution cardiac output: an improved formula.

This study was performed because of observed differences between dye dilution cardiac output and the Fick cardiac output, calculated from estimated oxygen consumption according to LaFarge and Miettinen, and to find a better formula for assumed oxygen consumption. In 250 patients who underwent left and right heart catheterization, the oxygen consumption VO2 (ml.min-1) was calculated using Fick's principle. Either pulmonary or systemic flow, as measured by dye dilution, was used in combination with the concordant arteriovenous oxygen concentration difference. In 130 patients, who matched the age of the LaFarge and Miettinen population, the obtained values of oxygen consumption VO2(dd) were compared with the estimated oxygen consumption values VO2(lfm), found using the LaFarge and Miettinen formulae. The VO2(lfm) was significantly lower than VO2(dd); -21.8 +/- 29.3 ml.min-1 (mean +/- SD), P < 0.001, 95% confidence interval (95% CI) -26.9 to -16.7, limits of agreement (LA) -80.4 to 36.9. A new regression formula for the assumed oxygen consumption VO2(ass) was derived in 250 patients by stepwise multiple regression analysis. The VO2(dd) was used as a dependent variable, and body surface area BSA (m2). Sex (0 for female, 1 for male), Age (years), Heart rate (min-1) and the presence of a left to right shunt as independent variables. The best fitting formula is expressed as: VO2(ass) = (157.3 x BSA + 10.0 x Sex - 10.5 x In Age + 4.8) ml.min-1, where ln Age = the natural logarithm of the age. This formula was validated prospectively in 60 patients. A non-significant difference between VO2(ass) and VO2(dd) was found; mean 2.0 +/- 23.4 ml.min-1, P = 0.771, 95% Cl = -4.0 to +8.0, LA -44.7 to +48.7. In conclusion, assumed oxygen consumption values, using our new formula, are in better agreement with the actual values than those found according to LaFarge and Miettinen's formulae.

Adolescent↗
PubMed1995

Pancuronium does not decrease oxygen consumption during hypothermic or normothermic cardiopulmonary bypass.

Muscle relaxation reportedly reduces systemic oxygen consumption 30% during hypothermic cardiopulmonary bypass. A potential mechanism is inhibition of hypothermia-induced subclinical muscle tone ("microshivering"). Accordingly, we tested the hypothesis that pancuronium administration would decrease systemic oxygen consumption during hypothermic cardiopulmonary bypass, but not during normothermic bypass. We studied 20 patients undergoing normothermic cardiopulmonary bypass at a nasopharyngeal temperature of 37.6 +/- 0.8 degrees C (mean +/- SD) and 15 patients undergoing hypothermic bypass at a nasopharyngeal temperature of 28.2 +/- 1.2 degrees C. Oxygen consumption during bypass was determined, using the Fick principle, before and after administration of pancuronium 0.15 mg/kg. Morphometric characteristics and anesthetic management were similar in the two groups. Oxygen consumption averaged 93 +/- 28 mL.min-1.m-2 in the normothermic patients and 43 +/- 10 mL.min-1.m-2 in the hypothermic group. Administration of pancuronium decreased oxygen consumption only 2% in the normothermic patients. However, muscle relaxation also decreased oxygen consumption only 2% in the hypothermic patients. We were thus unable to confirm our hypothesis because muscle relaxation induced by administration of pancuronium did not significantly reduce oxygen consumption in either group.

Aged↗
PubMed1990

Low-dose halothane anesthesia does not affect the hemodynamic estimation of myocardial oxygen consumption in dogs.

The accuracy of the product of systolic blood pressure and heart rate as a correlate of myocardial oxygen consumption has been questioned in anesthetized patients, suggesting that anesthesia alters the relationship between myocardial oxygen consumption and the hemodynamics. This relationship was reexamined in the awake state and during 0.95% end-tidal halothane anesthesia in seven chronically instrumented dogs. Measurements of myocardial oxygen consumption were compared with two indices, the systolic pressure rate product and the pressure work index. The latter is a weighted combination of the systolic pressure rate product and external cardiac work. A wide range in myocardial oxygen consumption (3.0-38.2 ml O2.min-1.100g-1) and hemodynamic states (range in pressure rate 4,100-40,700 mmHg/min and range in pressure work 3.7-37.0 ml O2.min-1.100g-1) was achieved with infusions of norepinephrine, nitroglycerin, neosynephrine, nitroprusside, and isoproterenol. Both the pressure rate product and the pressure work index correlated closely with myocardial oxygen consumption not only when the animals were awake but also during anesthesia. For each animal best-fit regression analysis for the awake and the anesthetized data did not reveal any significant change in the slope or y-intercept. Pooled data analysis that only permitted a change in slope with the addition of anesthesia (intercept unchanged) revealed a 17% decrease (P less than 0.05 on t test) in the slope constant when the pressure rate product was applied and no change in slope when the pressure work index was used to estimate myocardial oxygen consumption. It was concluded that myocardial oxygen consumption can be estimated during 0.95% halothane anesthesia by either index but that the pressure work index performs better than the systolic pressure rate product.

Anesthesia↗
PubMed1999

Brief vibrotactile stimulation does not increase cortical oxygen consumption when measured by single inhalation of positron emitting oxygen.

Vibrotactile stimulation of the hand elicits no increase in oxygen consumption commensurate with the increase in blood flow measured in human sensory cortex. To test the hypothesis that previous failures to detect a proportionate increase in oxygen consumption could be an artefact of the sequential bolus, or three-step, method used to measure this parameter in the human brain in vivo, the authors compared the measurements with the results of a novel single bolus, or one-step, method of measuring oxygen consumption. The time of completion of the three-step method was 40 to 50 minutes, whereas the one-step method lasted only 3 minutes. The baseline whole-brain oxygen consumption averaged 185 +/- 32 micromol hg(-1) min(-1) by the three-step method and 153 +/- 15 micromol hg(-1) min(-1) by the one-step method. Vibrotactile stimulation did not elicit a significant increase in oxygen consumption measured by either method. This finding rejects the hypothesis that failure to detect an increase of oxygen consumption could be an artefact caused by limitations of the method used previously. Conversely, it also rejects the hypothesis that observations of an increase of oxygen consumption by the new method are artefacts caused by limitations of the one-step method.

Blood Flow Velocity↗
PubMed2005

Beyond flux: total corneal oxygen consumption as an index of corneal oxygenation during contact lens wear.

PURPOSE: The purpose of this study is to compute total corneal oxygen consumption during contact lens wear and consider the concept as an index for describing corneal oxygenation during contact lens wear as opposed to flux, partial pressure, or Dk/t. METHOD: Estimates of total corneal oxygen consumption were generated using a previously described eight-layer model based on oxygen diffusion equations and using contemporary estimates of tear and corneal layer thicknesses. Relative consumption, expressed as %Q (percentage of normal consumption without contact lens wear), was also calculated for daily wear and continuous wear modes, thereby providing an index of the chronic hypoxic effect of contact lens wear. RESULTS: Corneal oxygen consumption is calculated to converge to the same value of 44.8 nL/cm/sec above a Dk/t of approximately 20 and 300 x 10(-9) (cm/sec)(mL0(2)/mL/mm Hg) for the open and closed eye scenarios, respectively. Lenses with Dk/t values of 15 and 50 x 10(-9) (cm/sec)(mL0(2)/mL/mm Hg) allow about 96% of normal long-term total oxygen consumption without a contact lens in place for daily wear and continuous wear, respectively. CONCLUSION.: Total corneal oxygen consumption is based on physical parameters, represents a direct index of corneal oxygen metabolism and thus cellular energy (ATP) production, allows direct comparison between two lenses or a lens and nonlens-wearing state, and eliminates the ambiguity of other measures, thereby providing an attractive means of describing corneal oxygenation.

Contact Lenses↗
PubMed1984

Influence of fatty acids on energy metabolism. 1. Stimulation of oxygen consumption, ketogenesis and CO2 production following addition of octanoate and oleate in perfused rat liver.

Changes in metabolic rates (oxygen consumption, ketogenesis, 14CO2 production from labelled fatty acids, glycolysis) following the addition of octanoate or oleate were studied in isolated livers from fed and starved rats perfused with Krebs-Henseleit bicarbonate buffer in a non-recirculating system. The following results were obtained. The infusion of fatty acids caused a large increase in the rate of oxygen consumption. The effect was greater with octanoate than with oleate and was half-maximal with fatty acid concentrations (free plus albumin bound) around 0.1 mM. The effects of oleate were only partially suppressed when the perfusate contained albumin concentrations near the physiological range. When fatty acids were oxidized at high rates, the glycolytic rate was diminished by 50%. The increase in oxygen consumption could not be explained fully by the increased ATP demand for fatty acid metabolism or by a compensation for the diminished extramitochondrial ATP generation. In the presence of phenylalkyl oxirane carboxylic acid, an inhibitor of the transport of long-chain acyl-CoA derivates into the mitochondria, ketogenesis and 14CO2 production from labelled oleate were strongly inhibited, whereas the increase in oxygen consumption was only slightly affected. In the presence of antimycin A, the increase in oxygen consumption due to fatty acids was totally abolished. Following pretreatment of rats with ciprofibrate (induction of enzymes for peroxisomal beta-oxidation of long-chain fatty acids), ketogenesis (but not 14CO2 production) from oleate was enhanced threefold. The increase in oxygen consumption, however, was not affected. In conclusion, the increase in hepatic oxygen consumption due to addition of fatty acids reflects a mitochondrial process; it is, in part, independent of the ATP demand of the cell. An uncoupling-like effect of fatty acids on the respiratory chain and its possible physiological significance in ketogenesis are discussed.

Adenosine Triphosphate↗
PubMed2004

Oxygen consumption in a hollow fiber bioartificial liver--revisited.

Oxygen consumption dynamics in a hollow fiber, hepatocyte-loaded bioartificial liver are investigated both theoretically and experimentally. The theoretical model is based upon the Krogh cylinder, which approximates the bioreactor as a collection of cylindrical elements comprised of an inner fiber lumen for media perfusion, the fiber wall through which oxygen can diffuse, and an annular region of hepatocytes surrounding the fiber. The primary non-dimensional parameters that describe the system are: (i) the Peclet number, Pe, which is the ratio of convective oxygen transport through the lumen to diffusive oxygen transport to the fiber walls; (ii) the hepatocyte saturation parameter, theta, which is the ratio of the inlet oxygen partial pressure to the Michaelis-Menten half-rate oxygen partial pressure; (iii) the Thiele modulus, phi2, which is the ratio of oxygen consumption rate to oxygen diffusion rate in the hepatocyte annulus; (iv) the hepatocyte permeability ratio, beta31, which is the ratio of oxygen permeability in the hepatocyte cell mass to oxygen permeability in the perfusing lumen medium; and (v) the hepatocyte annular thickness, rho3, which is the ratio of the exterior hepatocyte annular radius to the fiber lumen radius. Only Pe and theta are easily manipulated operating variables. phi2, beta31, and rho3 are engineering design parameters that are set when a bioreactor is fabricated. The model results are expressed as the effective hepatocyte utilization ratio, Vratio, which is the ratio of the observed oxygen consumption rate to the intrinsic hepatocyte oxygen consumption rate. Large regions of Vratio > 0.9, which is deemed an acceptable effective hepatocyte utilization are found for parameter values consistent with standard hollow fiber cartridges used in bioartificial liver fabrication. The extent of the Vratio > 0.9 region increases to a plateau with increasing Pe, increases with increasing theta, decreases with increasing phi2, increases with increasing beta31, and decreases with increasing rho3. The theoretical results indicate that Vratio > 0.9 is found whenever the experimentally observed fractional oxygen consumption from the perfusing medium, is less than 0.25. Combination of the theoretical and experimental results indicate that intrinsic, per cell oxygen consumption in the hollow fiber system may decrease as hepatocyte cell density increases and that this decrease may be due to lower intrinsic oxygen requirements in denser suspensions and not due to diffusion limitations in oxygen transport in the hollow fiber system as might be expected from two-dimensional, monolayer culture oxygen consumption measurements.

Animals↗
PubMed1980

Oxygen consumption and phosphate efflux in mammalian non-myelinated nerve fibres.

1. A comparison has been made between the efflux of labelled phosphate from the non-myelinated fibres of the desheathed rabbit vagus nerve at 37 degrees C and the corresponding O2 consumption at rest and during activity, and during a variety of experimental interventions. 2. The resting rate constant of phosphate efflux was 2.61 X 10(-3) min-1: electrical stimulation (10 sec-1, 3 min) produced an extra fractional loss of 6.75 X 10(-6) impulse-1. 3. The corresponding resting O2 consumption was 0.484 m-mole x kg-1 impulse-1. 4. Ouabain (100 microM) produced a sustained depression (of about 40%) of the resting O2 consumption, accompanied by a transient fall (of about 14%) in the rate constant of phosphate efflux. 5. Na salicylate (10 mM) or Na arsenate (1 mM) produced a much larger increase in phosphate efflux than in resting O2 consumption. 6. Changing the external phosphate concentration (between 0.02 and 2 mM), addition of acetylcholine (1.7 mM), and addition of lanthanum (20 microM)--all of which are known to affect markedly the phosphate efflux in rabbit non-myelinated fibres--had little or no effect on the resting O2 consumption or, where tested, on the extra O2 consumption with electrical stimulation. 7. Changing the external Ca concentration (between 0.09 and 9 mM) had only minor effects on the O2 consumption (resting and stimulated) and on the rate constant of resting phosphate efflux. 8. It is concluded that although changes in metabolism of the nerve produce changes in the phosphate efflux expected on the basis of the concomitant changes in the internal concentration of inorganic phosphate, the converse is not true; and increases and decreases in the rate constant of phosphate efflux do not necessarily signal the corresponding metabolic changes.

Animals↗
PubMed1988

Benzodiazepines inhibit transport-related oxygen consumption in thick ascending limb.

Specific binding sites for benzodiazepines (BZD) have been identified in several nonneuronal tissues including the kidney where they are localized predominantly to the tubular epithelium of the thick ascending limb of Henle's loop (TALH). The physiological function of these nonneuronal (peripheral) BZD-binding sites is undefined, but it has been suggested that they may represent receptors for putative endogenous ligands that may modulate cell function. In the current study, we examined the in vitro effects of diazepam and Ro5-4864, a specific peripheral BZD-receptor agonist, on the oxygen consumption of medullary TALH tubule suspensions of rabbit kidney. Maximal inhibition of total oxygen consumption was achieved at a dose of 5 X 10(-4) M of either agent. On average, diazepam and Ro5-4864 reduced total oxygen consumption by 41 and 44%, respectively. The predominant inhibition was in the ouabain-sensitive component of oxygen consumption, which suggests that BZDs inhibit active sodium-chloride transport in the TALH. To assess whether this inhibition depends on sodium uptake, TALH tubules were pretreated with amphotericin B (2 X 10(-6) M) to enhance sodium uptake and stimulate basal oxygen consumption; subsequent addition of Ro5-4864 (5 X 10(-4) M) still reduced oxygen consumption to a residual value that was not different from that in TALH tubules treated with Ro5-4864 but without pretreatment with amphotericin B. This suggests that BZD inhibition of transport-related oxygen consumption is not caused by diminution of sodium uptake into cells and thus appears to be distinct from the effect of furosemide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Oxygen consumption by rat liver: effects of taurocholate and sulfobromophthalein transport, glucagon, and cation substitution.

The proportion of total hepatic energy utilized for bile formation and transport of taurocholate (TC) and conjugated sulfobromophthalein (cBSP) has not been defined previously. To study this question we have measured changes in oxygen consumption by the isolated perfused rat liver and freshly isolated hepatocytes occurring in response to TC and cBSP administration, cation substitution, and glucagon infusion. The basal rates of bile formation and oxygen consumption varied considerably among different livers, and there was little or no relationship between these two variables. Administration of either TC or cBSP to the perfused liver elicited a marked choleresis but failed to alter steady-state oxygen consumption even at maximal rates of TC or cBSP transport. Similarly, incubation of hepatocytes with TC or cBSP did not alter oxygen consumption. In contrast, inhibition of Na-K-ATPase by removal of sodium and/or potassium from the medium reduced oxygen consumption by perfused rat liver and isolated hepatocytes by 27-37%, and glucagon administration increased oxygen consumption in both systems by 31-40%. These findings indicate that the oxygen requirement for bile formation and even maximal rates of TC and cBSP transport is small compared with that for the metabolic changes induced by glucagon or for hepatic Na-K-ATPase activity. This is in contrast to other epithelial tissues, such as kidney and rectal gland, in which oxygen utilization for transepithelial solute and water transport constitutes a large fraction of both total and Na-K-ATPase-dependent oxygen consumption.

Animals↗
PubMed2005

Estimating oxygen consumption rates of arteriolar walls under physiological conditions in rat skeletal muscle.

To examine the effects of vascular tone reduction on O2 consumption of the vascular wall, we determined the O2 consumption rates of arteriolar walls under normal conditions and during vasodilation induced by topical application of papaverine. A phosphorescence quenching technique was used to quantify intra- and perivascular PO2 in rat cremaster arterioles with different branching orders. Then, the measured radial PO2 gradients and a theoretical model were used to estimate the O2 consumption rates of the arteriolar walls. The vascular O2 consumption rates of functional arterioles were >100 times greater than those observed in in vitro experiments. The vascular O2 consumption rate was highest in first-order (1A) arterioles, which are located upstream, and sequentially decreased downstream in 2A and 3A arterioles under normal conditions. During papaverine-induced vasodilation, on the other hand, the O2 consumption rates of the vascular walls decreased to similar levels, suggesting that the high O2 consumption rates of 1A arterioles under normal conditions depend in part on the workload of the vascular smooth muscle. These results strongly support the hypothesis that arteriolar walls consume a significant amount of O2 compared with the surrounding tissue. Furthermore, the reduction of vascular tone of arteriolar walls may facilitate an efficient supply of O2 to the surrounding tissue.

Animals↗
PubMed1986

Substrate support of medullary thick ascending limb oxygen consumption.

The oxygen consumption of medullary thick ascending limb tubule suspensions was measured in the presence and absence of exogenous glucose. In the absence of exogenous glucose, the control oxygen consumption decreased 15%. Under identical conditions, the nystatin-stimulated oxygen consumption was inhibited 36%, indicating that oxidation of endogenous substrates could not meet the ATP demand of the fully stimulated Na+-K+-ATPase. Addition of inhibitors of fatty acid oxidation (bromooctanoate and tetradecylglycidic acid) further inhibited oxygen consumption, revealing that endogenous fats are oxidized in control and nystatin-stimulated states. Inhibition of endogenous carbohydrate (2-deoxy-D-glucose present) or amino acid (aminooxyacetate present) oxidation suppressed the nystatin response. In the presence of 10 mM glucose, only aminooxyacetate inhibited the nystatin-stimulated oxygen consumption, suggesting that the involvement of the malate-aspartate shuttle in redox balance during increased glycolytic flux. Addition of fatty acids or acetoacetate increased the control, nystatin-stimulated and uncoupler-stimulated oxygen consumption of tubules suspended in 10 mM glucose, indicating that these tubules oxidize exogenous fatty acids and ketones and oxidation of exogenous glucose alone may not meet all the energy demands of the tissue. Conversely, the addition of organic acids failed to enhance control oxygen consumption, possibly due to the absence of transport systems for these compounds in the medullary thick ascending limb tubules.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Oxygen consumption and oxidant stress in surviving nephrons.

We investigated the effects of reduction of renal mass on rates of oxygen consumption, sodium transport, and indexes of oxidant stress in surviving nephrons. Rates of oxygen consumption in surviving nephrons were elevated by more than twofold compared with nephrons in intact kidneys in rats on standard protein intakes. Absolute rates of sodium reabsorption (TNa) in the surviving nephrons were increased with a lower ratio of TNa to oxygen consumption. To determine oxidant stress, we measured malondialdehyde (MDA) in the kidney and urine and the glutathione redox ratio in kidney tissue. MDA per nephron was increased in the subtotally nephrectomized model and was accompanied by increased absolute and fractional urinary excretion of MDA but not by an increase in kidney MDA per milligram protein. The glutathione redox ratios were similar. Since increased dietary protein intake worsens renal injury, we studied the effects of dietary protein manipulation (30 vs. 6%) on oxygen consumption, MDA levels, and the glutathione redox ratio. The kidneys of subtotally nephrectomized animals maintained on 30% protein diets exhibited increased rates of oxygen consumption. Increased dietary protein intake led to increased MDA per nephron, increased urinary excretion of MDA, and increased MDA per milligram protein in subtotally nephrectomized animals, and markedly increased the glutathione redox ratio. We conclude that, despite increased oxygen consumption, surviving nephrons compared with intact nephrons in rats on standard protein intake demonstrate no evidence of oxidant stress. Increased urinary clearance of MDA may provide a mechanism that prevents the buildup of lipid peroxidation. Subjecting the remnant nephron to increased protein increases oxygen consumption and imposes oxidant stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Endothelial nitric oxide synthase plays an essential role in regulation of renal oxygen consumption by NO.

Nitric oxide (NO) regulates renal O2 consumption, but the source of NO mediating this effect is unclear. We explored the effects of renal NO production on O2 consumption using renal cortex from mice deficient (-/-) in endothelial (e) nitric oxide synthase (NOS). O2 consumption was determined polarographically in slices of cortex from control and eNOS-/- mice. NO production was stimulated by bradykinin (BK) or ramiprilat (Ram) in the presence or absence of an NOS inhibitor. Basal O2 consumption was higher in eNOS-/- mice than in heterozygous controls (919 +/- 46 vs. 1,211 +/- 133 nmol O(2). min(-1). g(-1); P < 0.05). BK and Ram decreased O2 consumption significantly less in eNOS-/- mice [eNOS-/-: BK -19.0 +/- 2.8%, Ram -20.5 +/- 3.3% at 10(-4) M; control: BK -29.5 +/- 2.5%, Ram -34 +/- 1.6% at 10(-4) M]. The NO synthesis inhibitor nitro-L-arginine methyl ester (L-NAME) attenuated this decrease in control but not eNOS-/- mice. An NO donor inhibited O2 consumption similarly in both groups independent of the presence of L-NAME. These results demonstrate that NO production by eNOS is responsible for regulation of renal O2 consumption in mouse kidney.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1979

Oxygen consumption by chick embryos exposed to mechanical (shaking) stress.

Stage 34 (8-day) and 41 (15-day) chick embryos (Gallus gallus; in ovo) were exposed (3 min) to two separate amounts of mechanical (shaking) stress. Oxygen consumption determinations, following a temperature equilibration period (60 min), were made on entire, intact eggs using a Warburg apparatus equipped with 130-ml flasks modified to hold the egg. Shaking at 300 excursions per minute (epm) resulted in depressed O2 consumption by stages 34 and 41. Only stage 34 embryos had markedly depressed O2 consumption values when shaken at 100 epm. When exposed to 300 epm and reincubated for either 1, 2, or 4 hr prior to O2 consumption determinations stage 34 embryos, following an early return to control levels exhibited a marked fall in O2 consumption by 4 h reincubation. The stage 41 embryos, on the other hand, demonstrated a gradual rise to control O2 consumption levels by 4 h reincubation. Oxygen consumption has now been shown for the first time in an embryonic system (at two distinct developmental stages) to be functionally impaired by mechanically induced stress.

Animals↗
PubMedDate not supplied

Oxygen consumption in aortic tissue from rabbits with diet-induced atherosclerosis.

The inner parts of the arterial wall depend upon diffusion for nutrition and oxygenation. During the atherosclerotic process, increased intimal thickness leads to impaired diffusion, and at the same time the oxygen requirements increase. On this basis it has been suggested that the balance between the supply and demand of oxygen in the arterial wall may be important for the fate of the initiated lesion. In the first part of the present study, the oxygen consumption was measured during perfusion in aortic intima-media segments from cholesterol-fed rabbits. The results indicated that the oxygen consumption per DNA increased with increasing degree of atherosclerotic involvement up to a certain level. For more diseased aortas, however, the oxygen consumption decreased again. In the second part of the study, the oxygen consumption was measured in foam cell and smooth muscle cell fractions isolated from rabbit aortic intima-media. These measurements indicated that the oxygen consumption of isolated foam cells was three times higher than that of isolated smooth muscle cells. It is proposed in the study that the increased oxygen consumption of the less diseased aortas reflected an increased proportion of foam cells in the arterial wall. As the lesions grow and the number of foam cells in the intima increases, the available diffusion capacity for oxygen and nutrients to deeper parts of the lesion may become insufficient, leading to the observed decrease in cellular oxygen consumption of the more diseased samples. Hypoxic cell damage and further tissue reactions may occur and the healing of the initiated lesion may be endangered.

Animals↗
PubMed1997

ACE inhibitors promote nitric oxide accumulation to modulate myocardial oxygen consumption.

BACKGROUND: ACE inhibitors potentiate kinin-nitric oxide (NO)-dependent coronary vascular dilation, and NO can modulate myocardial oxygen consumption. Whether ACE inhibitors also affect myocardial O2 consumption has not been established. METHODS AND RESULTS: Production of nitrite, a metabolite of NO in aqueous solution, in coronary microvessels and O2 consumption in myocardium were quantified with the use of in vitro tissue preparations, the Greiss reaction, and a Clark-type O2 electrode. In coronary microvessels, kininogen (the precursor of kinin; 10 micrograms/mL) and three ACE inhibitors (captopril, enalaprilat, or ramiprilat; 10(-8) mol/L) increased nitrite production from 76 +/- 6 to 173 +/- 15, 123 +/- 12, 125 +/- 12, and 153 +/- 12 pmol/mg, respectively (all P < .05). In myocardium, kininogen (10 micrograms/mL) and captopril, enalaprilat, or ramiprilat (10(-4) mol/L) reduced cardiac O2 consumption by 41 +/- 2%, 19 +/- 3%, 25 +/- 2%, and 35 +/- 2%, respectively. The changes in both nitrite release and O2 consumption in vitro were blocked by N omega-nitro-L-arginine methyl ester or N omega-nitro-L-arginine, inhibitors of endogenous NO formation. The effects were also blocked by HOE 140, which blocks the bradykinin B2-kinin receptor, and serine protease inhibitors, which inhibit local kinin formation. CONCLUSIONS: Our data indicate that stimulation of local kinin formation by use of a precursor for kinin formation or inhibition of kinin degradation by use of ACE inhibitors increases NO formation and is important in the control of cardiac O2 consumption. Vasodilation and control of myocardial O2 consumption by NO may contribute importantly to the therapeutic actions of ACE inhibitors in cardiac disease states.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Rat atrial natriuretic peptides inhibit oxygen consumption by rat kidney.

The inhibitory effect of high and low molecular weight native and synthetic rat atrial peptides on oxygen consumption in isolated rat kidney mitochondria and slices was measured. Oxygen consumption by mitochondria was measured in the presence of succinate and/or adenosine diphosphate, furosemide, and low and high molecular weight native and synthetic rat atrial peptides. After the addition of succinate, adenosine diphosphate limiting respiration (State 4) increased in the presence of low, but not high, molecular weight native rat atrial peptides. Furosemide caused a significant decrease in State 4 respiration (p less than 0.001). Angiotensin II and arginine vasopressin did not alter State 4 respiration. The rate of oxygen consumption after the addition of saturating adenosine diphosphate in the presence of saturating succinate (State 3 respiration) was reduced by low and high molecular weight native rat atrial peptides. Furosemide completely blocked oxygen consumption after the addition of adenosine diphosphate. Oxygen consumption was unchanged by trypsin treated (natriuretically inactive) low molecular weight rat atrial peptides and ventricular protein extracts of high and low molecular weight native rat atrial peptides. Synthetic and low molecular weight native rat atrial peptides had similar effects on mitochondrial oxygen consumption. Low molecular weight native and synthetic rat atrial peptides decreased the adenosine diphosphate to oxygen ratio, and these peptides, as well as furosemide, also induced mitochondrial swelling; none of the other rat atrial peptide combinations nor angiotensin II produced this effect. In kidney slices, basal oxygen consumption (without substrates) was stimulated by succinate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗