An Analysis of Scaphognathite Pumping Performance in the Crayfish Orconectes virilis: Compensatory Changes to Acute and Chronic Hypoxic Exposure

1983 ◽  
Vol 56 (3) ◽  
pp. 309-318 ◽  
Author(s):  
Warren W. Burggren ◽  
Brian R. McMahon
Keyword(s):  
Hypoxic Exposure ◽  
Orconectes Virilis

Respiratory Responses to Long-Term Hypoxic Stress in the Crayfish Orconectes virilis

1974 ◽  
Vol 60 (1) ◽  
pp. 195-206 ◽  
Author(s):  
B. R. McMAHON ◽  
W. W. BURGGREN ◽  
J. L. WILKENS
Keyword(s):  
Oxygen Consumption ◽  
Hypoxic Exposure ◽  
Experimental Chamber ◽  
Orconectes Virilis ◽  
Oxygen Utilization ◽  
Experimental Conditions ◽  
Acclimation Period ◽  
Pumping Rates ◽  
Irrigation Volume

1. Changes in the rate and force of scaphognathite beating, irrigation volume, oxygen utilization, oxygen consumption and heart rate during acclimation in response to the experimental conditions and in response to long-term hypoxic exposure have been measured in the crayfish Orconectes virilis. 2. Immediately following placement in the experimental chamber the animals exhibited very high levels of respiratory and circulatory performance. These levels decreased slowly and stable minimal performance levels could be measured only after 2-3 days. A 3-day acclimation period under normoxic conditions thus routinely preceded hypoxic experiments to ensure measurement of unmasked hypoxic responses. 3. Two responses to hypoxia were routinely observed: an initial hyperirrigation response maintained oxygen consumption by increased branchial water flow. This response was not maintained, but oxygen consumption remained at pre-hypoxic levels while pumping rates decreased. 4. Possible mechanisms of acclimation to hypoxia are discussed.

ВЛИЯНИЕ ОБЕДНЕННОГО ДЕЙТЕРИЕМ ПИТЬЕВОГО РАЦИОНА НА ФУНКЦИОНАЛЬНОЕ СОСТОЯНИЕ ЦЕНТРАЛЬНОЙ НЕРВНОЙ СИСТЕМЫ ЖИВОТНЫХ В УСЛОВИИ ГИПОКСИИ

2020 ◽  
Vol 65 (6) ◽  
pp. 1196-1202
Author(s):  
С.В. Козин ◽  
◽  
А.А. Кравцов ◽  
Э.И. Злищева ◽  
Л.В. Шурыгина ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Control Level ◽  
Learning Ability ◽  
Hypoxic Exposure ◽  
Amnestic Effect ◽  
Hypoxia With Hypercapnia ◽  
Antiamnestic Effect ◽  
The Central Nervous System ◽  
Deuterium Depleted Water

The effects of prolonged (42 days) addition of deuterium-depleted water into rat’s diet on the functional state of the central nervous system in normal conditions and under conditions of normobaric hypoxia with hypercapnia were studied. It was also established that the use of deuterium-depleted water both in normal conditions and after exposure to oxidative stress contributes to a significant reduction in the emotional anxiety of animals. Prolonged use of deuterium-depleted water before hypoxic exposure (amnestic effect) helps to maintain learning and memory at the control level, i.e. it has a pronounced protective antiamnestic effect. In normal conditions, deuterium-depleted water does not affect the learning ability of animals.

scholarly journals Hypoxic Exposure Increases Energy Expenditure by Increasing Carbohydrate Oxidation in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Yeram Park ◽  
Deunsol Hwang ◽  
Hun-Young Park ◽  
Jisu Kim ◽  
Kiwon Lim
Keyword(s):  
Glucose Metabolism ◽  
Energy Expenditure ◽  
Pyruvate Dehydrogenase ◽  
Hypoxic Condition ◽  
Open Circuit ◽  
Pyruvate Dehydrogenase Kinase ◽  
Hypoxic Exposure ◽  
Control Group ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

Aims. Hypoxic exposure improves glucose metabolism. We investigated to validate the hypothesis that carbohydrate (CHO) oxidation could increase in mice exposed to severe hypoxic conditions. Methods. Seven-week-old male ICR mice (n=16) were randomly divided into two groups: the control group (CON) was kept in normoxic condition (fraction of inspired O2=21%) and the hypoxia group (HYP) was exposed to hypoxic condition (fraction of inspired O2=12%, ≈altitude of 4,300 m). The CON group was pair-fed with the HYP group. After 3 weeks of hypoxic exposure, we measured respiratory metabolism (energy expenditure and substrate utilization) at normoxic conditions for 24 hours using an open-circuit calorimetry system. In addition, we investigated changes in carbohydrate mechanism-related protein expression, including hexokinase 2 (HK2), pyruvate dehydrogenase (PDH), pyruvate dehydrogenase kinase 4 (PDK4), and regulator of the genes involved in energy metabolism (peroxisome proliferator-activated receptor gamma coactivator 1-alpha, PGC1α) in soleus muscle. Results. Energy expenditure (EE) and CHO oxidation over 24 hours were higher in the HYP group by approximately 15% and 34% (p<0.001), respectively. Fat oxidation was approximately 29% lower in the HYP group than the CON group (p<0.01). Body weight gains were significantly lower in the HYP group than in the CON group (CON vs. HYP; 1.9±0.9 vs. −0.3±0.9; p<0.001). Hypoxic exposure for 3 weeks significantly reduced body fat by approximately 42% (p<0.001). PDH and PGC1α protein levels were significantly higher in the HYP group (p<0.05). Additionally, HK2 was approximately 21% higher in the HYP group. Conclusions. Hypoxic exposure might significantly enhance CHO oxidation by increasing the expression of PDH and HK2. This investigation can be useful for patients with impaired glucose metabolism, such as those with type 2 diabetes.

Brain adaptation to chronic hypobaric hypoxia in rats

1992 ◽  
Vol 72 (6) ◽  
pp. 2238-2243 ◽  
Author(s):  
J. C. LaManna ◽  
L. M. Vendel ◽  
R. M. Farrell
Keyword(s):  
Blood Flow ◽  
Motor Cortex ◽  
Microvessel Density ◽  
Hypobaric Hypoxia ◽  
Regional Blood Flow ◽  
Oxygen Availability ◽  
Sensory Cortex ◽  
Hypoxic Exposure ◽  
Normal Brain ◽  
Tissue Po2

Rats were exposed to hypobaric hypoxia (0.5 atm) for up to 3 wk. Hypoxic rats failed to gain weight but maintained normal brain water and ion content. Blood hematocrit was increased by 48% to a level of 71% after 3 wk of hypoxia compared with littermate controls. Brain blood flow was increased by an average of 38% in rats exposed to 15 min of 10% normobaric oxygen and by 23% after 3 h but was not different from normobaric normoxic rats after 3 wk of hypoxia. Sucrose space, as a measure of brain plasma volume, was not changed under any hypoxic conditions. The mean brain microvessel density was increased by 76% in the frontopolar cerebral cortex, 46% in the frontal motor cortex, 54% in the frontal sensory cortex, 65% in the parietal motor cortex, 68% in the parietal sensory cortex, 68% in the hippocampal CA1 region, 57% in the hippocampal CA3 region, 26% in the striatum, and 56% in the cerebellum. The results indicate that hypoxia elicits three main responses that affect brain oxygen availability. The acute effect of hypoxia is an increase in regional blood flow, which returns to control levels on continued hypoxic exposure. Longer-term effects of continued moderate hypoxic exposure are erythropoiesis and a decrease in intercapillary distance as a result of angiogenesis. The rise in hematocrit and the increase in microvessel density together increase oxygen availability to the brain to within normal limits, although this does not imply that tissue PO2 is restored to normal.

Mechanisms of lung polyamine accumulation in chronic hypoxic pulmonary hypertension

1990 ◽  
Vol 259 (6) ◽  
pp. L351-L358 ◽  
Author(s):  
R. T. Shiao ◽  
H. B. Kostenbauder ◽  
J. W. Olson ◽  
M. N. Gillespie
Keyword(s):  
Ventricular Hypertrophy ◽  
Chronic Hypoxia ◽  
Pulmonary Arterial Pressure ◽  
Hypoxic Exposure ◽  
Maximal Velocity ◽  
Pulmonary Vascular Remodeling ◽  
Hypoxic Environment ◽  
Elevated Activity ◽  
Pulmonary Arterial ◽  
Rate Limiting

Chronic hypoxia causes polyamine-dependent hypertensive pulmonary vascular remodeling (J. E. Atkinson. J. W. Olson, R. J. Altierre, and M. N. Gillespie, J. Appl. Physiol. 62: 1562–1568, 1987), but mechanisms by which lung polyamine contents are elevated have not been established. This study measured polyamine contents, biosynthetic activities, and transport in lungs of rats exposed to hypobaric hypoxia (simulated altitude: 4,570 m) for 4–14 days. Hypoxia increased lung contents of spermidine and spermine within 40 h and of putrescine within 4 days. These changes preceded hypoxia-induced increases in pulmonary arterial pressure and development of right ventricular hypertrophy. Additional experiments determined whether increased lung polyamine contents could be ascribed to elevated activity of ornithine decarboxylase (ODC), the rate-limiting enzyme in conversion of ornithine to putrescine. Lung ODC activity did not differ from controls at 40 h posthypoxia and was reduced below control levels from 4–14 days of exposure. Putrescine transport kinetics were assessed in isolated, salt solution-perfused lungs. Apparent Km for putrescine uptake was increased from 10.4 microM in control lungs to 16.9 microM in lungs from rats maintained for 7 days in an hypoxic environment. Maximal velocity (Vmax) of lung putrescine transport was increased from 1.67 nmol.g-1.min-1 in controls to 2.65 in hypoxic lungs. Putrescine efflux also was altered by hypoxic exposure; T1/2 for loss of diamine from a slowly effluxing pool was increased from 60.6 min in controls to 91.5 min in hypoxic lungs.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Passive And Active Intermittent Hypoxic Exposure Pre-acclimatization Does Not Alter Heart Rate Variability At Altitude.

2017 ◽  
Vol 49 (5S) ◽  
pp. 247-248
Author(s):  
Elisabeth M. Board ◽  
Theocharis Ispoglou ◽  
Amanda Seims ◽  
Max Garrard ◽  
Ingle Lee
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Hypoxic Exposure

ANP binding sites in rat lung are decreased after hypoxic exposure

Neuropeptides ◽  
1993 ◽  
Vol 24 (4) ◽  
pp. 193
Author(s):  
D.R. Springall ◽  
M.M. Mannan ◽  
A. Moradoghli-Haftvani ◽  
J.M. Polak
Keyword(s):  
Binding Sites ◽  
Hypoxic Exposure ◽  
Rat Lung

Paradoxical Bradycardia during Exercise and Hypoxic Exposure

CHEST Journal ◽  
1992 ◽  
Vol 102 (6) ◽  
pp. 1893-1895 ◽  
Author(s):  
Shyuichi Kobayashi ◽  
Kazuhiro Yoshida ◽  
Masaharu Nishimura ◽  
Kenji Miyamoto ◽  
Yoshikazu Kawakami
Keyword(s):  
Hypoxic Exposure

Physiological and hypoxic O2 tensions rapidly regulate NO production by stimulated macrophages

2008 ◽  
Vol 294 (4) ◽  
pp. C1079-C1087 ◽  
Author(s):  
Mary A. Robinson ◽  
James E. Baumgardner ◽  
Virginia P. Good ◽  
Cynthia M. Otto
Keyword(s):  
Protein Concentration ◽  
Cultured Cells ◽  
Raw 264.7 Cells ◽  
Hypoxic Exposure ◽  
Convection Cell ◽  
No Production ◽  
Inos Protein ◽  
Substrate Limitation ◽  
No Consumption

Nitric oxide (NO) production by inducible NO synthase (iNOS) is dependent on O2 availability. The duration and degree of hypoxia that limit NO production are poorly defined in cultured cells. To investigate short-term O2-mediated regulation of NO production, we used a novel forced convection cell culture system to rapidly (response time of 1.6 s) and accurately (±1 Torr) deliver specific O2 tensions (from <1 to 157 Torr) directly to a monolayer of LPS- and IFNγ-stimulated RAW 264.7 cells while simultaneously measuring NO production via an electrochemical probe. Decreased O2 availability rapidly (≤30 s) and reversibly decreased NO production with an apparent KmO2 of 22 (SD 6) Torr (31 μM) and a Vmax of 4.9 (SD 0.4) nmol·min−1·10−6 cells. To explore potential mechanisms of decreased NO production during hypoxia, we investigated O2-dependent changes in iNOS protein concentration, iNOS dimerization, and cellular NO consumption. iNOS protein concentration was not affected ( P = 0.895). iNOS dimerization appeared to be biphasic [6 Torr ( P = 0.008) and 157 Torr ( P = 0.258) >36 Torr], but it did not predict NO production. NO consumption was minimal at high O2 and NO tensions and negligible at low O2 and NO tensions. These results are consistent with O2 substrate limitation as a regulatory mechanism during brief hypoxic exposure. The rapid and reversible effects of physiological and pathophysiological O2 tensions suggest that O2 tension has the potential to regulate NO production in vivo.

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