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PubMed1982

Myocardium in hypertrophy: oxygen consumption by isolated cardiac myocytes and working hearts from spontaneously hypertensive rats.

Oxygen consumption was measured on suspensions of calcium tolerant myocytes obtained from hearts of Spontaneously Hypertensive Rats (SHR) and normotensive Wistar Kyoto Rats (WKY). Oxygen consumptions of the isolated cells were not significantly different from each other either in the presence or absence of added calcium (1.5 mM). Additionally, there was excellent agreement between the oxygen consumption of the isolated cells and estimates of basal oxygen consumption between work and myocardial oxygen utilization in isolated perfused working hearts. At any given workload there was no significant difference in oxygen consumption between SHR hearts and WKY hearts. The mechanical performance of the SHR hearts was lower compared to that of the WKY hearts at low preloads. At high preloads and high afterloads the SHR hearts developed higher pressures than did hearts obtained from WKY rats. The data suggest that: (1) basal oxygen consumption of the two hearts are similar and (b) the contractile defects in the SHR heart are not the result of hypoxia.

Animals↗
PubMed1993

Relationship between cyclic-AMP content, regional myocardial function and O2 consumption in experimental left ventricular hypertrophy: effect of negative inotropes.

The aim of this study was to examine the hypothesis that negative inotropic agents that lower myocyte cyclic-AMP by different means would have similar effects on local myocardial segment work and O2 consumption in control hearts, but that this response would differ in left ventricular hypertrophy (LVH) induced by aortic valve stenosis. Open chest anesthesized LVH and control dogs were studied before and during esmolol (100 micrograms/kg/min) and acetylcholine (100 micrograms/kg/min) infusion. Regional work was calculated as the integrated product of instantaneous force (miniature transducer) and shortening (sonomicrometry) per min. Regional O2 consumption was calculated from blood flow (radioactive microspheres) and O2 saturation of small frozen vessels (microspectrophotometry). Cyclic-AMP level was determined with a competitive binding assay using 3H-cyclic-AMP and was found to be 731 +/- 90 (mean +/- S.D.) pmol/g in control and 711 +/- 163 in LVH. There were similar decreases in cyclic-AMP levels in control hearts with acetylcholine (365 +/- 135) and the beta adrenergic blocker (430 +/- 95). In LVH, esmolol lowered cyclic-AMP (383 +/- 39), but acetylcholine did not (689 +/- 105). In control animals, regional O2 consumption (7.7 +/- 0.6, 5.6 +/- 0.4 and 5.6 +/- 0.5 ml O2/min/100 g, control, acetylcholine, esmolol, respectively) and segment work (878 +/- 82, 546 +/- 80, 627 +/- 66 g*mm/min) fell to similar levels with these agents. Similar decreases were found in LVH with esmolol for O2 consumption (7.1 +/- 1.2, 5.1 +/- 1.0, baseline, esmolol) and segment work (895 +/- 140, 427 +/- 65). Acetylcholine had no significant effect on segment work (800 +/- 201), but did lower regional O2 consumption (4.0 +/- 0.7) in LVH dogs. It is concluded that there is a strong relationship between the level of cyclic-AMP and myocardial function and O2 consumption in control hearts. The action of acetylcholine is altered in LVH leading to an uncoupling between regional cyclic-AMP, function and metabolism.

Analysis of Variance↗
PubMed1989

Oxygen consumption and guanosine diphosphate binding by fetal brown adipose tissue in diabetic pregnancy.

Oxygen consumption and 3H-guanosine diphosphate (GDP) binding were determined in brown adipocytes and mitochondria from 28-day gestation fetuses of alloxan-diabetic rabbit does and saline-injected controls. Maternal diabetes was classified as severe or mild determined by whether maternal blood glucose values were greater or less than 200 mg/dL, respectively, at death. Basal oxygen consumption and adipocyte diameters did not vary among groups. A significant reduction in maximal norepinephrine (NE) stimulated O2 consumption by fetal brown adipose tissue (BAT) cells was seen in offspring of severely diabetic pregnancies when compared with control values (248 +/- 53 +/- v482 +/- 32 microL O2/10(6) cells/h; P less than .005). In contrast, a significant increase in maximal NE-stimulated O2 consumption by fetal BAT cells occurred in offspring of mild diabetic pregnancies (807 +/- 60, P less than .001 v controls). A highly significant inverse correlation between serum glucose levels and maximal O2 consumption by fetal BAT was observed in fetuses from mild and severe diabetic pregnancies (r = -.98, P less than .005), and there was no correlation between these two parameters in offspring of normal pregnancies. A significant inverse correlation was observed between maximal O2 consumption by fetal BAT cells and serum insulin levels in offspring of both control and diabetic pregnancy (r = -.74; P less than .02). Tissue cytochrome oxidase activity was lower in offspring of severely affected diabetic does, indicating a reduction in BAT mitochondrial content compared with controls. BAT mitochondria from fetuses of severely diabetic does exhibited reduced 3H-GDP capacity, which was 2.5-fold lower than controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue, Brown↗
PubMed1988

Enhancement of the oxygen consumption in the hippocampal slices of the guinea pig induced by glutamate and its related substances.

The effects of glutamate (Glu), kainate (Ka), and N-methyl-D-aspartate (NMDA) on the oxygen consumption of the hippocampal slices of the guinea pig were investigated. The oxygen consumption of slices at resting state was 8.43 mumol/g protein/min. Bath application of Ka (1 x 10(-8) to 1 x 10(-6) M), NMDA (1 x 10(-8) M to 1 x 10(-4) M), and Glu (1 x 10(-5) M to 5 x 10(-4) M) enhanced the oxygen consumption dose-dependently in the similar tendency although the effective doses varied for the different excitants. Subsequently the consumption was maximal at approximately 140% of the resting level. The enhancement of the oxygen consumption due to NMDA and Glu was antagonized by DL-2-amino-5-phosphonovaleric acid (APV) for NMDA and by glutamic acid diethylester (GDEE) and Joro spider toxin (JSTX) for Glu. From these results it was suggested that the increase of the oxygen consumption observed here must reflect the neuronal activation induced by these excitants.

Action Potentials↗
PubMed1983

Oxygen consumption of hypothalamic tissue slices after varying incubation periods.

In order to quantitate possible time-related changes in the viability of rat hypothalamic tissue slices, tissue oxygen consumption was measured after incubation periods ranging from 0-4 hours. There were no significant differences in mean tissue oxygen consumption between the various incubation periods; nor was there any trend indicating that oxygen consumption gradually decreases over time. Moreover, no regional differences were observed among the various rostral hypothalamic slices. One obvious trend, however, was that during the first two hours of each experiment, tissue oxygen consumption decreased briefly and then returned to normal higher levels. The exact occurrence of this transitory decrease varied from experiment to experiment; but the subsequent recovery in oxygen consumption was always complete by two hours of incubation. This initial transient decrease in tissue oxygen consumption may reflect the initial period of electrophysiological inactivity reported in several in vitro studies.

Animals↗
PubMed1995

The effects of endotoxin on oxygen consumption of various cell types in vitro: an EPR oximetry study.

We have studied the effects of bacterial endotoxin on the oxygen consumption of a variety of target cells, and found that the rate of utilization of oxygen by treated cells was decreased in a time- and dose-dependent manner. Precise EPR measurement of oxygen concentrations enabled us to demonstrate that this effect was linked to mitochondrial dysfunction and was particular to each cell type. Such detailed knowledge on oxygen utilization by viable whole cells and the varied effects of endotoxin are as yet undocumented. Oxygen consumption was shown to decrease quite markedly in CHO cells and kidney cells from the cortex region. Cells from the kidney medulla region had lower baseline consumption and were stimulated to increased levels of oxygen consumption on addition of similar doses of endotoxin. Macrophages exhibited a dual response in that in addition to inhibiting mitochondrial oxygen consumption, endotoxin pretreatment primed these cells to exhibit an enhanced oxidative burst on stimulation with Zymosan. These results show that endotoxin has a direct effect on normal cellular oxygen consumption and is an important parameter that must be considered when following the early effects on cells and tissues during the septic syndrome.

Animals↗
PubMed2006

Rapid hydrogen sulfide consumption by Tetrahymena pyriformis and its implications for the origin of mitochondria.

Although sulfide is typically regarded as toxic to eukaryotic cells, it is avidly consumed by Tetrahymena pyriformis. That was observed only when the sulfide concentration was kept below 1 microM. Previously concentrations that were too high had been tested. A new device (Sulfidostat) was used to measure sulfide consumption in steady-state concentrations as low as 10(-12)M. The technique was validated non-biologically by slowly injecting AgNO(3) into buffer and using Ag(2)S precipitation to mimic sulfide consumption, confirming that rates of sulfide consumption could be measured independently of sulfide concentrations. With T. pyriformis, sulfide consumption was 0.25 micromol (gprotein)(-1)s(-1) in 0.5 microM sulfide. Sulfide consumption required O(2) and was inhibited by HCN or by too much sulfide. When cells were separated into fractions, sulfide consumption occurred in the particulate (mitochondrial) fraction. Unexpectedly, the soluble cytosolic fraction slowly produced sulfide even when aerated. The observations are consistent with the conjecture that mitochondria evolved from sulfidotrophic symbionts in a sulfidogenic host cell.

Animals↗
PubMed2004

Insulin-like growth factor 1 improves the relationship between systemic oxygen consumption and delivery in piglets after cardiopulmonary bypass.

OBJECTIVE: We sought to assess the effects of insulin-like growth factor 1 on the balance between systemic oxygen consumption and oxygen delivery after cardiopulmonary bypass in piglets. METHODS: Twelve piglets weighing 4.5 to 8.3 kg undergoing hypothermic (28 degrees C) cardiopulmonary bypass for 70 to 120 minutes with 40 minutes of aortic crossclamping were studied before and during the first 6 hours after cardiopulmonary bypass. Oxygen consumption was continuously measured by an indirect calorimeter, Deltatrac II MBM-200 Metabolic Monitor (Datex Division Instrumentarium, Helsinki, Finland). Oxygen delivery and cardiac output were calculated from oxygen consumption and the arterial and mixed venous oxygen contents sampled before and every 30 minutes after cardiopulmonary bypass. Oxygen extraction ratio was derived by the ratio of oxygen consumption to oxygen delivery. Arterial blood lactate was measured before and every 30 minutes after cardiopulmonary bypass. Six animals were randomly assigned to receive an intravenous infusion of insulinlike growth factor 1 at 1.2 mg/h from 1 to 6 hours after cardiopulmonary bypass; the remaining 6 served as a control group. RESULTS: Relative to the control group, intravenous infusion of insulin-like growth factor 1 significantly reduced oxygen consumption (P =.02) and increased cardiac output (P =.016) and oxygen delivery (P =.049) during the first 6 hours after surgery with hypothermic cardiopulmonary bypass. As a result, oxygen extraction was significantly decreased (P =.012). CONCLUSIONS: Intravenous infusion of insulin-like growth factor 1 improved oxygen transport by reducing oxygen consumption as well as increasing cardiac output and oxygen delivery during the first 6 hours after cardiopulmonary bypass in piglets. This may have important clinical implications for the care of critically ill children after surgery with cardiopulmonary bypass.

Age Factors↗
PubMed2005

Assumed oxygen consumption frequently results in large errors in the determination of cardiac output.

OBJECTIVE: We sought to investigate the differences in assumed and measured oxygen consumption values for the determination of cardiac output by using the Fick principle in a pediatric population with congenital heart disease. METHODS: The patient population consisted of 143 patients with a mean age of 11.3 years (age range, 2 days to 23.8 years) undergoing cardiac catheterization during general anesthesia and with mechanical ventilation. Oxygen consumption was measured with a standard commercial analyzing system (Deltatrac II; Datex, Engström, Helsinki, Finland). Assumed oxygen consumption values were calculated according to the formulas of Krovetz and Goldbloom and LaFarge and Miettinen. Comparisons between measurements and assumptions were performed by Bland-Altman plots. Two-sided paired t tests were used to assess a difference of the assumed and measured values. RESULTS: The range of measured oxygen consumption values was between 55.2 and 249 mL . min -1 . m -2 . The Krovetz-Goldbloom formula led to systematically larger values compared with the measured values (P = .0001; mean difference of -53.3 mL . min -1 . m -2 ; 95% confidence interval, -56.7 to -49.8 mL . min -1 . m -2 ). The use of the LaFarge-Miettinen formula tends to overestimate oxygen consumption (P = .0037; mean difference of -15.9 mL . min -1 . m -2 ; 95% confidence interval, -26.5 to -5.4 mL . min -1 . m -2 ). A similarly poor agreement was found when analyzing a subgroup of 25 patients with Fontan-type circulation. CONCLUSION: The use of assumed instead of measured oxygen consumption values introduces large errors in the determination of cardiac output.

Adolescent↗
PubMed2003

Paranatal oxygen consumption and respiratory frequency in the Laysan Albatross.

The oxygen consumption and respiratory frequency of Laysan Albatross eggs were measured during the different phases of pipping (paranatal period) and in hatchlings. The initial phase of pipping--penetration of the aircell of the egg by the embryonic beak--coincided with the beginning of pulmonary ventilation, the embryo rebreathing aircell gas, but it did not result in a statistically significant increase in oxygen consumption. The second phase of pipping--star-fracture of the shell (external pipping)--was the shortest (25 h) of the three phases of pipping, and it did not result in a significant increase in either oxygen consumption or respiratory frequency. The longest phase of pipping (65 h)--the pip-hole phase--represented 54% of the total duration of pipping, and it was accompanied by significant increases in oxygen consumption and respiratory frequency. When the eggs hatched, the oxygen consumption increased further but respiratory frequency diminished significantly. It was calculated that the paranatal period, which represented 7.9% of the total incubation period of the egg, accounted for 37.2% of the total oxygen consumption of the egg.

Analysis of Variance↗
PubMed2006

Impact of zinc and nickel on oxygen consumption of benthic microbial communities assessed with microsensors.

In this study, the effect of zinc and nickel on oxygen consumption in sediments was determined using oxygen microsensors. Sediments from the southwest lagoon of New Caledonia, in the vicinity of the city of Nouméa, were incubated nearby in situ conditions and exposed to Zn and Ni concentrations of 20 and 60 mg l(-1). The depth distribution of oxygen consumption was estimated from the steady-state oxygen microprofiles, and the effects of metal were compared on the distributions before and after spiking. In most cases, metal had a strong effect on oxygen consumption at the surface. After 6 h exposure, oxygen consumption was only 10-40% of the initial value. However, the strong decrease in oxygen consumption observed at the sediment surface was counterbalanced by an increase of oxygen consumption deeper in the sediment. This is probably due to (i) a downward migration of aerobic microbial microorganisms living at the surface in order to escape the toxic effect of metal or/and (ii) a switch of the facultative aerobes from the low efficiency fermentation mode to the high-energy aerobic respiration mode.

Environmental Monitoring↗
PubMed2004

Intermediates of Krebs cycle correct the depression of the whole body oxygen consumption and lethal cooling in barbiturate poisoning in rat.

Rats poisoned with one LD50 of thiopental or amytal are shown to increase oxygen consumption when intraperitoneally given sucinate, malate, citrate, alpha-ketoglutarate, dimethylsuccinate or glutamate (the Krebs cycle intermediates or their precursors) but not when given glucose, pyruvate, acetate, benzoate or nicotinate (energy substrates of other metabolic stages etc). Survival was increased with succinate or malate from control groups, which ranged from 30-83% to 87-100%. These effects were unrelated to respiratory depression or hypoxia as judged by little or no effect of succinate on ventilation indices and by the lack of effect of oxygen administration. Body cooling of comatose rats at ambient temperature approximately 19 degrees C became slower with succinate, the rate of cooling correlated well with oxygen consumption decrease. Succinate had no potency to modify oxygen consumption and body temperature in intact rats. A condition for antidote effect of the Krebs intermediate was sufficiently high dosage (5 mmol/kg), further dose increase made no odds. Repeated dosing of succinate had more marked protective effect, than a single one, to oxygen consumption and tended to promote the attenuation of lethal effect of barbiturates. These data suggest that suppression of whole body oxygen consumption with barbiturate overdose could be an important contributor to both body cooling and mortality. Intermediates of Krebs cycle, not only succinate, may have a pronounced therapeutic effect under the proper treatment regimen. Availability of Krebs cycle intermediates may be a limiting factor for the whole body oxygen consumption in barbiturate coma, its role in brain needs further elucidation.

Amobarbital↗
PubMed1997

Beneficial effects of a Ca2+ sensitizer, MCI-154, on the myocardial oxygen consumption-cardiac output relation in patients with left ventricular dysfunction after myocardial infarction: comparison with dobutamine and phosphodiesterase inhibitor.

Although conventional inotropic agents such as catecholamines increase myocardial oxygen consumption, a newly developed inotropic agent, a Ca2+ sensitizer, may be able to increase cardiac output with less myocardial oxygen consumption. By using right-side heart catheterization, we assessed the ratio of the increase in myocardial oxygen consumption per unit increase in cardiac output during beta-adrenergic receptor stimulation (dobutamine, n = 15), phosphodiesterase inhibition (E-1020, n = 10), and Ca2+ sensitization (MCI-154, n = 17) in patients with coronary artery disease. Dobutamine increased cardiac output and myocardial oxygen consumption. E-1020 increased cardiac output but did not change myocardial oxygen consumption. MCI-154 increased cardiac output and decreased myocardial oxygen consumption. The oxygen cost of increasing cardiac output with dobutamine and with E-1020 was different from that with dextran infusion (n = 18); in contrast, the oxygen cost with MCI-154 was significantly smaller. Thus a newly developed Ca2+ sensitizer, MCI-154, may be beneficial for the treatment of heart failure.

Cardiac Output↗
PubMed2003

Oxygen consumption rates and oxygen concentration in molt-4 cells and their mtDNA depleted (rho0) mutants.

Respiratory deficient cell lines are being increasingly used to elucidate the role of mitochondria and to understand the pathophysiology of mitochondrial genetic disease. We have investigated the oxygen consumption rates and oxygen concentration in wild-type (WT) and mitochondrial DNA (mtDNA) depleted (rho(0)) Molt-4 cells. Wild-type Molt-4 cells have moderate oxygen consumption rates, which were significantly reduced in the rho(0) cells. PCMB (p-chloromercurobenzoate) inhibited the oxygen consumption rates in both WT and rho(0) cells, whereas potassium cyanide decreased the oxygen consumption rates only in WT Molt-4 cells. Menadione sodium bisulfite (MSB) increased the oxygen consumption rates in both cell lines, whereas CCCP (carbonyl cyanide m-chlorophenylhydrazone) stimulated the oxygen consumption rates only in WT Molt-4 cells. Superoxide radical adducts were observed in both WT and rho(0) cells when stimulated with MSB. The formation of this adduct was inhibited by PCMB but not by potassium cyanide. These results suggest that the reactive oxygen species (ROS) induced by MSB were at least in part produced via a mitochondrial independent pathway. An oxygen gradient between the extra- and intracellular compartments was observed in WT Molt-4 cells, which further increased when cells were stimulated by CCCP and MSB. The results are consistent with our earlier findings suggesting that such oxygen gradients may be a general phenomenon found in most or all cell systems under appropriate conditions.

Benzoates↗
PubMed2001

Potential role of eNOS in the therapeutic control of myocardial oxygen consumption by ACE inhibitors and amlodipine.

OBJECTIVES: Our aim was to investigate the potential therapeutic role of endothelial nitric oxide synthase (eNOS) in the modulation of cardiac O(2) consumption induced by the angiotensin converting enzyme (ACE) inhibitor ramiprilat and amlodipine. METHODS: Three different groups of mice were used; wild type, wild type in the presence of N-nitro-L-arginine methyl ester (L-NAME, 10(-4) mol/l) or genetically altered mice lacking the eNOS gene (eNOS -/-). Myocardial O(2) consumption was measured using a Clark-type O(2) electrode in an air-tight stirred bath. Concentration-response curves to ramiprilat (RAM), amlodipine (AMLO), diltiazem (DIL), carbachol (CCL), substance P (SP) and S-nitroso-N-acetyl-penicillamine (SNAP) were performed. The rate of decrease in O(2) concentration was expressed as a percentage of the baseline. RESULTS: Baseline O(2) consumption was not different between the three groups of mice. In tissues from wild type mice, RAM (10(-5) mol/l), AMLO (10(-5) mol/l), DIL (10(-4) mol/l), CCL (10(-4) mol/l), SP (10(-7) mol/l) and SNAP (10(-4) mol/l) reduced myocardial O(2) consumption by -32+/-4, -27+/-10, -20+/-6, -25+/-2, -22+/-4 and -42+/-4%, respectively. The responses to RAM, AMLO, CCL and SP were absent in tissues taken from eNOS -/- mice (-7.1+/-4.3, -5.0+/-6.0, -5.2+/-5.1 and -0.4+/-0.2%, respectively). In addition, L-NAME significantly (P<0.05) inhibited the reduction in O(2) consumption induced by RAM (-9.8+/-4.4%), AMLO (-1.0+/-6.0%), CCL (-8.8+/-3.7%) and SP (-6.6+/-4.9%) in cardiac tissues from wild type mice. In contrast, NO-independent responses to the calcium channel antagonist, DIL, and responses to the NO donor, SNAP, were not affected in cardiac tissues taken from eNOS -/- (DIL: -20+/-4%; SNAP: -46+/-6%) or L-NAME-treated (DIL: -17+/-2%; SNAP: -33+/-5%) mice. CONCLUSIONS: These results suggest that endogenous endothelial NO synthase derived NO serves an important role in the regulation of myocardial O(2) consumption. This action may contribute to the therapeutic action of ACE inhibitors and amlodipine.

Amlodipine↗
PubMed2001

Inhibition of oxygen consumption by pentachlorophenol and tetrachloroguaiacol in rainbow trout (Oncorhynchus mykiss).

Rainbow trout (Oncorhynchus mykiss) were exposed for 24 h to concentrations representing 100, 50 and 25% of the 96 h-LC50 of pentachlorophenol (PCP) or tetrachloroguaiacol (TCG), and their oxygen consumption, cardiac output, heart rate and stroke volume were measured at regular intervals. Oxygen consumption either remained stable at basal levels (PCP), or increased to 130% of basal levels (TCG) when fish were exposed to the 96 h-LC50 of each chemical. However, oxygen consumption decreased to about 50-60% of basal levels when fish were exposed to concentrations of PCP or TCG representing 50 and 25% of the 96 h-LC50. This decrease in oxygen consumption did not appear to affect cardiac function since cardiac output, heart rate and stroke volume remained stable. PCP is best known for its capacity to uncouple oxidative phosphorylation and increase oxygen consumption. However, this study showed that it can also decrease oxygen consumption, and that the effects of PCP and TCG on fish metabolism are similar.

Animals↗
PubMed2000

Role of the etiology of cardiomyopathies on exercise capacity and oxygen consumption in patients with severe congestive heart failure.

Peak oxygen consumption is of great importance for the decision of heart transplantation in congestive heart failure. Moreover, the level of exercise capacity seems to depend on the etiology of congestive heart failure. This study compared 14 heart failure patients with idiopathic dilated cardiomyopathy (group 1) to 14 heart failure patients with cardiomyopathy due to ischemic heart disease (group 2), matched for sex (13 male, one female in each group), age +/-10 years, left ventricular ejection fraction +/-5% and pulmonary artery mean pressure +/-5 mm Hg, to assess exercise capacity and oxygen consumption independently of the age, sex and the level of left ventricular dysfunction. Right ventricular function was also assessed. No difference existed in terms of right ventricular parameters. Maximal exercise parameters were significantly higher in group 1 than in group 2. Peak oxygen consumption was statistically higher in group 1 than in group 2. In the whole population, a significant correlation was found between peak oxygen consumption and right ventricular ejection fraction (r=0. 44, P<0.02) but not between peak oxygen consumption and left ventricular ejection fraction. For similar levels of left ventricular dysfunction, exercise capacity and oxygen consumption appear to be better in idiopathic dilated cardiomyopathy than in ischemic cardiomyopathy, thereby suggesting that functional tolerance of left ventricular dysfunction might depend on the etiology of severe congestive heart failure.

Cardiomyopathies↗
PubMed1997

Propranolol blocks the stimulatory effects of naloxone on ventilation and oxygen consumption in hamsters.

The purposes of these studies were: 1) to determine the effects of various doses of propranolol, a nonspecific beta-adrenergic antagonist, on ventilation, oxygen consumption, and body temperature in hamsters, and 2) to test the hypothesis that in hamsters the stimulatory effects of naloxone, an opioid receptor antagonist, on ventilation and oxygen consumption occur, at least in part, through the release of catecholamines that act via beta-adrenergic receptors. Propranolol, a non-specific beta adrenergic receptor antagonist, at a 20 mg/kg depressed body temperature, oxygen consumption, tidal volume, and ventilation relative to saline. The lower dose of 10 mg/kg had only transitory effects on tidal volume at 60 min and ventilation at 30 min post-injection-Naloxone (1 mg/kg) relative to saline stimulated ventilation and oxygen consumption. These effects were blocked by propranolol pretreatment. The results of these experiments demonstrate that in the hamster, 1) body temperature, oxygen consumption, and ventilation appear to be modulated by beta-adrenergic receptors, and 2) the stimulatory effects of naloxone on oxygen consumption and ventilation may occur through the interaction of endogenous opioids and beta-adrenergic receptor systems.

Adrenergic beta-Antagonists↗