Metabolic response to ambient temperature and hypoxia in sinoaortic-denervated rats

1994 ◽  
Vol 266 (2) ◽  
pp. R387-R391 ◽  
Author(s):  
T. Matsuoka ◽  
A. Dotta ◽  
J. P. Mortola
Keyword(s):  
Significant Contribution ◽  
Metabolic Response ◽  
Acute Hypoxia ◽  
Co2 Production ◽  
Adult Rats ◽  
Arterial Pco2 ◽  
Open Flow ◽  
Ambient Temperatures ◽  
Colonic Temperature ◽  
Arterial Po2

We tested the hypothesis that the sinoaortic afferents may contribute to normoxic thermogenesis and to the magnitude of the hypometabolic response to hypoxia. Adult rats were either sinoaortic denervated (SAX; n = 20) or sham operated (Sham; n = 20). A few days after the operation, gaseous metabolism [O2 uptake (VO2) and CO2 production (VCO2)] was measured with an open-flow system at ambient temperatures (Tamb) of 20, 25, 30, and 35 degrees C as the animal was resting awake. At thermoneutrality (Tamb 30 degrees C) or higher Tamb there was no difference in VO2 or VCO2. Below thermoneutrality, metabolic rate was significantly lower in SAX than in Sham animals (-14 and -16% at 20 and 25 degrees C, respectively). Colonic temperature and arterial PO2 were also slightly less, whereas arterial PCO2 and pH, mean arterial pressure, and heart rate did not differ significantly between the two groups. Exposure to acute hypoxia (10% inspired O2, 20-30 min) at Tamb 20 and 25 degrees C significantly reduced VO2 in both groups to a similar value; hence, at either Tamb, the metabolic drop during hypoxia in Sham animals was larger than that in SAX animals. Hypercapnia (5% CO2 breathing) did not change VO2 in either group. We conclude that in the rat at Tamb slightly below thermoneutrality, the sinoaortic afferents 1) provide a small but significant contribution to normoxic thermogenesis and 2) are not required for the manifestation of the drop in metabolism during hypoxia.

Metabolic-ventilatory interaction in conscious rats: effect of hypoxia and ambient temperature

1994 ◽  
Vol 76 (4) ◽  
pp. 1594-1599 ◽  
Author(s):  
C. Saiki ◽  
T. Matsuoka ◽  
J. P. Mortola
Keyword(s):  
Blood Pressure ◽  
Metabolic Rate ◽  
Ambient Temperature ◽  
Blood Gases ◽  
Male Rats ◽  
Co2 Production ◽  
O2 Consumption ◽  
Arterial Pco2 ◽  
Open Flow ◽  
Arterial Po2

Previous studies have indicated that the hypometabolic response to hypoxia depends on ambient temperature (Ta), being more pronounced in the cold. If metabolic rate were an important contributor to the level of ventilation (VE), the magnitude of the hyperpneic response to hypoxia should also depend on Ta. We tested this hypothesis on adult conscious male rats. In normoxia, a drop in Ta from 25 to 10 degrees C increased O2 consumption and CO2 production (VO2 and VCO2, respectively, measured by an open-flow technique) and VE (measured with the barometric method) by 80 and 60%, respectively, with no changes in blood gases. At both Ta, hypoxia (10% inspired O2, 33–35 Torr arterial PO2) induced the same degree of hyperventilation, i.e., the same drop in arterial PCO2 (about -13 Torr). The hyperventilation at 25 degrees C Ta was achieved exclusively by an increase in VE, whereas at 10 degrees C Ta the hyperpnea was minimal (+15%) and accompanied by a drop (-30%) in VO2 and VCO2. Diaphragmatic electromyograms confirmed the VE results. Changes in blood pressure were similar at both Ta. Addition of 3% CO2 to the inspired air further increased VE, indicating that the hypoxic rat was not breathing at its maximal VE at either Ta. We conclude that, in the rat, changes in metabolic rate play an important role in the VE response to hypoxia and that Ta influences the response because of its effect on the degree of hypoxic hypometabolism.

Effect of 2,4-dinitrophenol on the hypometabolic response to hypoxia of conscious adult rats

1997 ◽  
Vol 83 (2) ◽  
pp. 537-542 ◽  
Author(s):  
Chikako Saiki ◽  
Jacopo P. Mortola
Keyword(s):  
Body Temperature ◽  
Oxidative Phosphorylation ◽  
Acute Hypoxia ◽  
Mammalian Species ◽  
Metabolic Effect ◽  
Adult Rats ◽  
Open Flow ◽  
Pharmacological Stimulation ◽  
Before And After ◽  
Mitochondrial Uncoupler

Saiki, Chikako, and Jacopo P. Mortola. Effect of 2,4-dinitrophenol on the hypometabolic response to hypoxia of conscious adult rats. J. Appl. Physiol. 83(2): 537–542, 1997.—During acute hypoxia, a hypometabolic response is commonly observed in many newborn and adult mammalian species. We hypothesized that, if hypoxic hypometabolism were entirely a regulated response with no limitation in O2availability, pharmacological uncoupling of the oxidative phosphorylation should raise O2consumption (V˙o 2) by similar amounts in hypoxia and normoxia. Metabolic, ventilatory, and cardiovascular measurements were collected from conscious rats in air and in hypoxia, both before and after intravenous injection of the mitochondrial uncoupler 2,4-dinitrophenol (DNP). In hypoxia (10% O2 breathing, 60% arterial O2 saturation),V˙o 2, as measured by an open-flow technique, was less than in normoxia (∼80%). Successive DNP injections (6 mg/kg, 4 times) progressively increasedV˙o 2 in both normoxia and hypoxia by similar amounts. Body temperature slightly increased in normoxia, whereas it did not change in hypoxia. The DNP-stimulatedV˙o 2 during hypoxia could even exceed the control normoxic value. A single DNP injection (17 mg/kg iv) had a similar metabolic effect; it also resulted in hypotension and a drop in systemic vascular resistance. We conclude that pharmacological stimulation ofV˙o 2 counteracts theV˙o 2 drop determined by hypoxia and stimulates V˙o 2not dissimilarly from normoxia. Hypoxic hypometabolism is likely to reflect a regulated process of depression of thermogenesis, with no limitation in cellular O2availability.

Effect of hypoxia on metabolic rate in awake ponies

1994 ◽  
Vol 76 (6) ◽  
pp. 2380-2385 ◽  
Author(s):  
M. J. Korducki ◽  
H. V. Forster ◽  
T. F. Lowry ◽  
M. M. Forster
Keyword(s):  
Metabolic Rate ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Pulmonary Ventilation ◽  
Time Dependent ◽  
Hypoxic Hypoxia ◽  
Arterial Pco2 ◽  
Breathing Room ◽  
Arterial Po2 ◽  
Transient Failure

To determine the effect of hypoxia on metabolic rate (VO2) of ponies, on 2 days we studied ponies that were breathing room air for 1 h followed by 5 h of either hypoxic hypoxia (fractional concn of inspired O2 = 0.126) or 5 h of CO hypoxia. Control arterial PO2 was 103 +/- 1.2 Torr, and at 5 min and 5 h of hypoxic hypoxia, arterial PO2 was 53.1 +/- 1.8 and 41.0 +/- 1.8 Torr, respectively. There was a time-dependent hypocapnia and alkalosis during hypoxic hypoxia. During CO hypoxia, carboxyhemoglobin increased to 25% after 30 min and remained constant thereafter. With increased carboxyhemoglobin, arterial PCO2 was 1.3 Torr above (P < 0.05) and 1.5 Torr (P < 0.05) below control levels after 30 min and 3 h, respectively. There were no significant (P > 0.10) changes in VO2 during either hypoxic or CO hypoxia. However, in 50% of the ponies, VO2, pulmonary ventilation, and rectal temperature increased and shivering was evident after 30 min of hypoxia. Peak values of pulmonary ventilation, VO2, and shivering occurred at approximately 2 h with a subsequent return toward control levels. We conclude that, in contrast to smaller mammals, acute hypoxia does not depress VO2 of ponies. The hypermetabolism and hyperthermia during chronic hypoxia in some ponies may reflect a transient failure in thermoregulation.

Effects of hypoxia and ambient temperature on gaseous metabolism of newborn rats

1992 ◽  
Vol 263 (2) ◽  
pp. R267-R272 ◽  
Author(s):  
J. P. Mortola ◽  
A. Dotta
Keyword(s):  
Heat Dissipation ◽  
Metabolic Response ◽  
Whole Body ◽  
Newborn Rats ◽  
Open Flow ◽  
Ambient Temperatures ◽  
Limited Effectiveness ◽  
Old Rats ◽  
Per Se ◽  
Maintain Body Temperature

Whole body metabolic rate was measured by open-flow respirometry in 2-day-old rats at ambient temperatures (Ta) between 40 and 15 degrees C, changed at a rate of 0.5 degrees C/min, during normoxia or hypoxia (10% inspired O2). In normoxia, the thermoneutral range was found to be very narrow, at around 33 degrees C, suggesting a limited effectiveness in the mechanisms controlling heat dissipation. At lower or higher Ta, metabolism was at first increased; this increase could be maintained for at least 30 min at 30 and 35 degrees C, i.e., slightly below or above thermoneutrality, but it was not maintained at lower Ta. The metabolic response to Ta was not sufficient to maintain body temperature (Tb). In hypoxia, at all Ta, oxygen consumption (VO2) was consistently less than in normoxia and was linearly related to Ta (Q10 approximately 1.4). The rat's specific heat was 4 J.g-1.degrees C-1, and the time constant of passive heat exchange was 2.2 +/- 0.5 min; from these values it was calculated that the normoxic VO2 of the 2-day-old rat could be per se sufficient to maintain Tb of 35-36 degrees C at Ta of 33 degrees C, while at lower Ta the metabolic response could not be adequate to maintain Tb. In hypoxia, Tb was directly dependent on Ta.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise performance with added dead space in chronic airflow obstruction

1984 ◽  
Vol 56 (4) ◽  
pp. 1020-1026 ◽  
Author(s):  
S. E. Brown ◽  
R. R. King ◽  
S. M. Temerlin ◽  
D. W. Stansbury ◽  
C. K. Mahutte ◽  
...  
Keyword(s):  
Exercise Capacity ◽  
Dead Space ◽  
Exercise Performance ◽  
Airflow Obstruction ◽  
Co2 Production ◽  
Base Line ◽  
Arterial Pco2 ◽  
Maximum Exercise ◽  
Ventilatory Mechanics ◽  
Arterial Po2

Individuals with chronic airflow obstruction (CAO) are thought to have limited exercise tolerance primarily because of impaired ventilatory mechanics. We studied the effects of added external dead space (DS) on exercise capacity [maximum O2 consumption (VO2max)], maximum exercise ventilation (VEmax), and blood gases (arterial PO2, PCO2, pH) in 22 patients with CAO [forced expired volume at 1 s (FEV1) = 0.96 +/- 0.41 liter]. Maximum exercise testing (Emax) was performed by incremental cycle ergometry. Patients exercised at base line (BL) and with DS (0.25 liter if FEV1 less than 0.8, and 0.50 liter if FEV1 greater than 0.8 liter), in random-order single-blind fashion. DS resulted in a 12.2% increase in VEmax (P less than 0.001); tidal volume increased (P less than 0.025) while respiratory frequency was unchanged. The VO2max and maximum CO2 production decreased (P less than 0.001) with DS. Arterial PCO2 at rest and at exhaustion increased with DS (P less than 0.001). The pH and arterial PO2 showed small declines at rest and at Emax. Thus, at the lower maximum work load achieved with DS, the patients ventilated more and tolerated a higher arterial PCO2 and a lower arterial PO2 and pH before stopping from dyspnea as compared with the BL exercise run. In contrast, the VO2max of nine normal control subjects was unaffected by the addition of DS. Although VEmax can be increased in CAO patients with DS, this increase is not sufficient to prevent further CO2 retention or a decrease in exercise capacity. We conclude that exercise performance is limited primarily by impaired ventilatory mechanics in CAO.

Body temperature and rate of O2 consumption in Chinese pangolins

1986 ◽  
Vol 250 (3) ◽  
pp. R377-R382 ◽  
Author(s):  
M. E. Heath ◽  
H. T. Hammel
Keyword(s):  
New York ◽  
Metabolic Response ◽  
Co2 Production ◽  
O2 Consumption ◽  
Metabolic Rates ◽  
Short Term ◽  
Ambient Temperatures ◽  
Lower Critical Temperature ◽  
Manis Pentadactyla ◽  
The Relationship

Body temperatures and rates of O2 consumption and CO2 production were measured in four Chinese pangolins (Manis pentadactyla) during short-term exposures (2-4 h) to ambient temperatures (Ta) of 10-34 degrees C. At Ta less than 27 degrees C the pangolins curled into a sphere. At Ta greater than 28 degrees C the animals laid on their backs with their soft abdominal skin exposed. Rectal temperatures between 33.4 and 35.5 degrees C were recorded from animals exposed to Ta of 10-32 degrees C. At Ta greater than or equal to 32 degrees C the animals appeared to be markedly heat stressed, rate of breathing was elevated, and core temperature rose somewhat. Resting metabolic rates averaged 3.06 ml O2 X kg-1 X min-1. This is significantly lower than would be predicted from the relationship between body mass and metabolic rate established by Kleiber (The Fire of Life: an Introduction to Animal Energetics. New York: Wiley, 1975) for other eutherian mammals. The magnitude of the metabolic response to Ta below the lower critical temperature was inversely correlated to the mass of the pangolin, the slope being greatest for the smallest animals. Respiratory quotients of 0.85-1.0 were observed.

Role of nitric oxide in hypoxic hypometabolism in rats

1999 ◽  
Vol 87 (1) ◽  
pp. 104-110 ◽  
Author(s):  
Henry Gautier ◽  
Cristina Murariu
Keyword(s):  
Nitric Oxide ◽  
Ventilatory Response ◽  
No Synthase ◽  
Adult Rats ◽  
Ambient Temperatures ◽  
Thermal Changes ◽  
Synthase Inhibitor ◽  
Colonic Temperature ◽  
Ventilatory Response To Hypoxia

Because it has been recently suggested that nitric oxide (NO) may mediate the effects of hypoxia on body temperature and ventilation, the present study was designed to assess more completely the effects of a neuronal NO synthase inhibitor (7-nitroindazole, 25 mg/kg ip), at ambient temperature of 26 and 15°C, on the ventilatory (V˙), metabolic (O2 consumption), and thermal changes (colonic and tail temperatures) induced by ambient hypoxia (fractional inspired O2 of 11%) or CO hypoxia (fractional inspired CO of 0.07%) in intact, unanesthetized adult rats. At both ambient temperatures, 7-nitroindazole decreased oxygen consumption, colonic temperature, andV˙ in normoxia. The drug reduced ambient or CO hypoxia-induced hypometabolism and ventilatory response, but the hypothermia persisted. It is concluded that NO arising from neural NO synthase plays an important role in the control of metabolism andV˙ in normoxia. As well, it mediates, in part, the hypometabolic and the ventilatory response to hypoxia. The results are consistent with the notion that central nervous system hypoxia resets the thermoregulatory set point by decreasing brain NO.

Effect of acute hypoxia on phosphate excretion in rats

1994 ◽  
Vol 266 (2) ◽  
pp. R578-R583
Author(s):  
Y. Mimura ◽  
F. G. Knox
Keyword(s):  
Acute Hypoxia ◽  
Fractional Excretion ◽  
Respiratory Alkalosis ◽  
Renal Handling ◽  
Arterial Pco2 ◽  
Phosphate Excretion ◽  
Fractional Excretion Of Phosphate ◽  
Spontaneously Breathing ◽  
Arterial Po2 ◽  
Hypoxic Group

This study evaluated the effect of acute hypoxia on renal handling of phosphate in rats in the presence and absence of parathyroid hormone (PTH). Hypoxia causes respiratory alkalosis in spontaneously breathing humans and animals. Respiratory alkalosis has been reported to induce a blunted phosphaturic response to PTH. In this study, to avoid the confounding effect of hypocapnia accompanying the hypoxia on phosphate excretion, the rats were ventilated mechanically, and arterial PCO2 levels were controlled. Rats were divided into two main groups depending on the arterial PO2 levels: a hypoxic group (n = 16) and a normoxic group (n = 18). Hypoxia was produced by ventilating with 10% oxygen, and hypocapnia was produced by hyperventilation. In response to PTH, the hypoxic rats without hypocapnia showed a greater increase in fractional excretion of phosphate (FEPi; 37.7 +/- 2.6%, mean +/- SE) compared with normoxic rats (27.4 +/- 2.5%, P < 0.02). During hypocapnia, there was no difference in FEPi between hypoxic and normoxic groups (21.2 +/- 1.5 and 19.5 +/- 1.2%, respectively), and both groups showed a significantly blunted phosphaturic response to PTH compared with normocapnia (P < 0.05 and P < 0.01, respectively). Urinary adenosine 3',5'-cyclic monophosphate (cAMP) increased similarly after PTH infusion between each group. To test whether the phosphaturic effect of PTH in hypoxia and the blunted phosphaturic effect of PTH in hypocapnia are due to steps beyond the generation of cAMP, the phosphaturic response to cAMP infusion was evaluated in 1) hypoxic and normocapnic rats (n = 6), 2) normoxic and normocapnic (control) rats (n = 6), and 3) normoxic and hypocapnic rats (n = 7).(ABSTRACT TRUNCATED AT 250 WORDS)

Interaction between CO2 production and ventilation in the hypoxic kitten

1993 ◽  
Vol 74 (2) ◽  
pp. 905-910 ◽  
Author(s):  
J. P. Mortola ◽  
T. Matsuoka
Keyword(s):  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Co2 Production ◽  
Depressant Effect ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Parallel Increase ◽  
Shallow Breathing

We hypothesized that in the hypoxic newborn the drop in metabolic rate, and particularly in CO2 production (VCO2), contributes to the magnitude of the ventilatory response. Experiments were performed on unanesthetized newborn kittens in a warm [28–30 degrees C ambient temperature (Ta)] or cold (20 degrees C) environment. Breathing pattern and gaseous metabolism were measured by the barometric technique and the inflow-outflow O2 and CO2 difference, respectively. At 30 degrees C, hypoxia (10% O2) decreased VCO2 and induced rapid and shallow breathing, with little effect on minute ventilation (VE). Normoxic exposure to 20 degrees C determined a parallel increase in VE and metabolism; at this Ta, hypoxia decreased VCO2 more than at the higher Ta, and the drop in tidal volume (VT) was also proportionally larger; hence, at 20 degrees C, hypoxic VE was markedly below the normoxic values. Despite these changes in breathing pattern, at neither Ta during hypoxia did arterial PCO2 increase above the normoxic value; in fact, arterial PCO2 at 20 degrees C was slightly decreased because of the important drop in VCO2. Exposure to hypoxia with a CO2 load (inspired CO2 = 1, 3, or 5%) did not abolish the hypometabolic response; the hypoxic depressant effect on VT was either unchanged (by 1% CO2), completely offset (by 3% CO2), or reversed (by 5% CO2), with parallel effects on VE. The results are consistent with the hypothesis that in the newborn the level of CO2, by controlling VT, could represent a link between the metabolic and ventilatory responses to acute hypoxia.

ACTH secretion and ventilation increase at similar arterial PO2 in conscious rats

1989 ◽  
Vol 66 (5) ◽  
pp. 2245-2250 ◽  
Author(s):  
L. Jacobson ◽  
M. F. Dallman
Keyword(s):  
Acute Hypoxia ◽  
Exposure Period ◽  
Plasma Corticosterone ◽  
Acth Secretion ◽  
Arterial Pco2 ◽  
System Activity ◽  
Conscious Rats ◽  
Arterial Ph ◽  
Arterial Po2 ◽  
Adrenocortical System

To compare the arterial PO2 (PaO2) at which adrenocorticotropic hormone (ACTH) secretion and ventilation are stimulated, conscious rats with chronic femoral arterial catheters were exposed for 50 min to 21, 18, 15, 12, or 9% O2. Decreases in arterial PCO2 (PaCO2) and increases in arterial pH and adrenocortical system activity occurred consistently throughout the exposure period in rats exposed to 9 or 12% O2. In contrast, changes in PaCO2 or pH were only transient or delayed, plasma ACTH did not change, and plasma corticosterone only increased after 20 min in rats exposed to 15 or 18% O2 relative to those breathing 21% O2. Omitting the large blood sample at 20 min for ACTH eliminated the increase in corticosterone in the 15% O2 group. Overall, ACTH increased, and PaCO2 decreased, below PaO2 of approximately 60 Torr. We conclude that ACTH secretion increases at a similar PaO2 as hyperventilation-induced decreases in PaCO2 and thus represents a primary physiological response to acute hypoxia; hemodynamic stimuli may also interact with hypoxia to augment adrenocortical system activity.

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