Wyniki wyszukiwania

1

Oxygen breathing and ventilation

100%

Marczak M., Pokorski M.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 1,1

We investigated the ventilatory response to normobaric poikilocapnic hyperoxia in healthy subjects. The study was carried out in 26 subjects of the mean age 26 ±0.9 (SE) years, who breathed pure oxygen through a two-way valVE for 10 min. The subjects were in the sitting position with a mouthpiece and nose clip attached. Ventilatory flow was recorded using a pneumotachograph and minute ventilation was calculated from the tidal and frequency components. The SaO2 and alveolar CO2 tension were continuously monitored. Ten of the same subjects constituted a control group in which room air was substituted for oxygen and the tests repeated in the same way at another occasion. We found that oxygen breathing caused a transient 8.4% decline in ventilation, whose nadir was 1 min after the introduction of oxygen. Thereafter, ventilation increased significantly aboVE the baseline value and showed a further rising tendency toward the end of the test. We conclude that acute oxygen treatment is unlikely to haVE a major inhibitory effect on the carotid body-dependent ventilatory driVE in normal subjects. The determinants of the hyperoxic ventilatory stimulation remain to be established in further studies.

2

Hyperoxia blunts renal sympathetic nerve activity response to acute intermittent hypercapnia in rats

75%

Madirazza K., Pecotic R., Pavlinac Dodig I., Valic M., Dogas Z.

Journal of Physiology and Pharmacology

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2019

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tom 70

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nr 5

3

Metabolic changes in rat brain synaptosomes after exposure to normobaric hyperoxia in vitro

75%

Gordon-Majszak W. L., Rafalowska U., Lazarewicz J. W.

Bulletin of the Polish Academy of Sciences. Biological Sciences

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1987

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tom 35

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nr 4-6

4

Prenatal exposure to hyperoxia modifies the thromboxane prostanoid receptor-mediated response to H2O2 in the ductus arteriosus of the chicken embryo

75%

van der Sterren S., Kessels L., Perez-Vizcaino F., Cogolludo A. L., Villamor E.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 2

5

Inhibition of hypoxia-induced tolerance to subsequent hyperoxic injury in lung cells by phosphatidyl inositol 3-kinase inhibitors: LY294002 and wortmannin

75%

Ahmad S., Ahmad A., Gerasmivoskaya E., Stenmark K. R., White C. W.

Cellular and Molecular Biology Letters

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2003

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tom 08

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nr 2A

6

Superoxide dismutase mimetic modulates hyperoxic augmentation of the diaphragmatic response to poikilocapnic hypoxia in non-vagotomized rats

63%

Budzinska K., Ilasz R.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

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nr 6

163-172

7

Female headstart in resistance to hyperoxia-induced oxidative stress in mice

63%

Saric A., Sobocanec S., Safranko Z. M., Popovic-Hadzija M., Aralica G., Korolija M., Kusic B., Balog T.

Acta Biochimica Polonica

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2014

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tom 61

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nr 4

8

Hypoglossal and phrenic nerve responses to changes in oxygen tension during picrotoxin-induced seizures in the rat

63%

Budzinska K.

Journal of Physiology and Pharmacology. Supplement

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2004

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tom 55

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nr 3

31-39

The aim of this study was to examine the response of phrenic and hypoglossal motor outputs to hyperoxia and 11% hypoxia during picrotoxin-induced seizures. Adult rats were anesthetized with a mixture of urethane with alpha-chloralose. The animals were bilaterally vagotomized, paralyzed, and artificially ventilated. Picrotoxin was administered intravenously in a cumulative dose until seizures occurred. The response to changes in oxygen tension was studied after the convulsive dose of picrotoxin and compared with the baseline level. The results show that the picrotoxin-induced seizures evoked a complex respiratory response that consisted of an augmentation of phrenic and hypoglossal nerve activities and irregular disturbances in phasic respiratory discharges. The excitation of the hypoglossal activity appeared earlier and showed a more irregular pattern than that of the phrenic activity. Hyperoxia elicited a similar decrease in neural respiratory outputs during the control and seizure conditions, suggesting the unaltered peripheral chemoreceptor mechanism. In the pre-seizure condition, hypoxia caused an initial excitation of the phrenic and hypoglossal outputs followed by some decline of the effect. During seizures, the striking effect of hypoxia was a decrease of the respiratory rate. A biphasic response to hypoxia was maintained in the hypoglossal activity due to stimulation of the hypoglossal amplitude. In contrast, in the phrenic activity the excitatory phase of hypoxia was absent and depression ensued. The mechanism underlying the facilitation of hypoxic respiratory depression during seizures is discussed.

9

Hyperoxia intensifies postischemic lipid peroxidation in gerbil brain synaptosomes

63%

Gordon-Majszak W. L., Lazarewicz J. W.

Bulletin of the Polish Academy of Sciences. Biological Sciences

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1990

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tom 38

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nr 1-12

10

Exposure to sixty minutes of hyperoxia upregulates myocardial humanins in patients with coronary artery disease - a pilot study

63%

Karu I., Tahepold P., Ruusalepp A., Reimann E., Koks S., Starkopf J.

Journal of Physiology and Pharmacology

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2015

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tom 66

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nr 6

11

Moderate exercise training reduces arterial chemoreceptor reflex drive in mild hypertension

63%

Izdebska E., Izdebski J., Cybulska I., Makowiecka-Ciesla M., Trzebski A.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 11

93-102

The aim of our study was to check the responsiveness the chemoreceptor reflex in 28 young mildly hypertensive men (HTS), aged 18-32 years and 25 normotensive male subjects (NTS) aged 19-32 years, before and after 3-months dynamic exercise training. We tested the hypothesis that dynamic training reduces arterial chemoreceptor drive in mild hypertension. Circulatory response to 3-min hyperoxic inactivation of arterial chemoreceptors induced by 70% oxygen breathing was measured before and after training. Arterial blood pressure (BP) was recorded continuously by Finapres method, stroke volume and arm blood flow were registered by impedance reography, heart rate by ECG. Both groups were submitted to moderate 3-months dynamic exercise training. Before training the hyperoxic breathing caused in HTS a significant decrease in systolic BP by 6±1mmHg p<0.01, in diastolic BP by 2±0.6mmHg p<0.01, and in total peripheral vascular resistance (TPR) by 0.24±0.04 TPRU (p<0.01). After training hyperoxia augmented systolic BP by 2.64±1.9mmHg (NS), diastolic BP by 2±1mmHg p<0.05, and TPR by 0.043±0.05 TPRU (ANOVA). In NTS before training brief hyperoxia produced insignificant change in BP and TPR. In NTS after training hyperoxia increased systolic BP by 4.2 mm Hg±1.23 p<0.01 and diastolic BP by 3.1±0.6mmHg p<0.01 respectively and TPR by 0.053±0.02 TPRU. Our results confirm earlier finding on the enhanced arterial chemoreceptor reflex drive in mild human hypertension. We conclude that normalizing arterial blood pressure in subjects with mild hypertension which occurred after 3-months dynamical exercise training is due to attenuation of the sympathoexcitatory chemoreceptor reflex drive by exercise training. The mechanism of this effect requires further study.

12

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The effects of increased inspired oxygen with and without dopamine on lung and diaphragm hydrogen peroxide and apoptosis following hemorrhagic shock

63%

Mach W. J., Thimmesch A. R., Slusser J. G., Clancy R. L., Pierce J. D.

Journal of Pre-Clinical and Clinical Research

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2010

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tom 04

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nr 1

13

Neurotransmitter mechanisms in the enhancement of the hypoxic ventilatory response by antecedent hyperoxia in the anesthetized rat

63%

Pokorski M., Kolesnikova E., Marczak M., Budzinska K.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 3

A brief period of antecedent oxygen breathing enhances the ventilatory response to hypoxia. The mechanisms of this phenomenon are uncertain and have been variably linked to the central glutamatergic or nitrergic pathways. In the present study we put a question of how blockade of either neurotransmitter pathway would compare with the concurrent blockade of them both in terms of the enhancement of posthyperoxic hypoxic ventilation. The study was performed on the anesthetized, vagotomized, spontaneously breathing rats divided into the following experimental groups: control NaCl-treated, glutamate blocker 2-amino-5-phosphonopentanoic acid (AP5)-treated, nitric oxide synthase blocker 7-nitroindazol (7NI)-treated, and AP5+7NI-treated. The protocol consisted of measuring the ventilatory response to 12% O2, a steady-state poikilocapnic hypoxia, undertaken in three consecutive conditions in each animal: the initial control, 25 min after injection of a given chemical agent, and then after a 15-min period of oxygen breathing. Respiration was evaluated from the diaphragmatic EMG signal. We found that the posthyperoxic hypoxic ventilatory enhancement was but partially dampened by either AP5 or 7NI. Concurrent administration of the two blockers further diminished, but did not abolish, the hypoxic ventilatory enhancement. We conclude that although the glutamate-NO system accounts for an appreciable part of the posthyperoxic hypoxic ventilatory enhancement, other, as yet unclear, mechanisms contribute as well. These mechanisms may be worth exploring given the substantial enhancing effect the antecedent oxygen has on hypoxic hyperventilation.

14

Transient O2-dependent effects of CO2 on ventilation in the anesthetized mouse

63%

Pokorski M., Izumizaki M., Homma I.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 3

In this study we sought to determine the effects of background hyperoxia on the ventilatory response to hypercapnia. We addressed this issue by examining the temporal profile of the first minute transients of minute ventilation, and its frequency and tidal components, in response to 5% and 10% CO2 each co-applied with the natural (balanced with air) and hyperoxic (balanced with O2) levels of oxygen. The study was performed on the urethane-anesthetized, tracheostomized, spontaneously breathing mouse, placed in a flow-through body plethysmograph. We identified an early suppressant effect of CO2-in-O2 on breathing frequency. The frequency declined to 88.5 ±1.4% and 87.8 ±1.9% relative to the pre-test, baseline level for 5% and 10% CO2, respectively. There was a compensatory rise in tidal volume and no major change in the overall ventilation. In contrast, CO2-in-Air resulted in ventilatory stimulation caused in equal measure by frequency and tidal components. Thus, the inhibitory effect on breathing frequency of the CO2-in-O2 resulted from the O2 content in the mixture and had the temporal characteristics consistent with carotid body function. In conclusion, transient O2-dependent effects can bear on the nascent hypercapnic ventilatory response. The complexity of the O2-CO2 interaction regarding the breathing pattern components should be taken into account while designing the optimal conditions for a hypercapnic test.

15

Poly(ADP-ribose) polymerase activity in the cat carotid body in hypoxia and hyperoxia

63%

Strosznajder R. P., Jesko H., Pokorski M.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 3

Reactive oxygen species (ROS) induce DNA damage with the ensuing activation of the chromosomal repair enzyme poly(ADP-ribose) polymerase (PARP). ROS also interact with the function of carotid body chemoreceptor cells. The possibility arises that PARP is part of the carotid chemosensing process. This study seeks to determine the presence of PARP and its changes in response to contrasting chemical stimuli, hypoxia and hyperoxia, both capable of generating ROS, in cat carotid bodies. The organs were dissected from anesthetized cats exposed in vivo to acute normoxic (PaO290 mmHg), hypoxic (PaO225 mmHg), and hyperoxic (PaO2> 400 mmHg) conditions. Carotid body homogenate was the source of PARP and [adenine 14C] NAD was the substrate in the assay. Specimens of the superior cervical ganglion and brainstem were used as reference tissues. We found that PARP activity amounted to 27 pmol/mg protein/min in the normoxic carotid body. The activity level more than doubled in both hypoxic and hyperoxic carotid bodies. Changes of PARP in the reference tissues were qualitatively similar. We conclude that PARP is present in the carotid body but the augmentation of the enzyme activity in both hypoxia and hyperoxia reflects DNA damage, induced likely by ROS and being universal for neural tissues, rather than a specific involvement of PARP in the chemosensing process.

16

Cellfood improves respiratory metabolism of endothelial cells and inhibits hypoxia-induced reactive oxygen species (ROS) generation

51%

Ferrero E., Fulgenzi A., Belloni D., Foglieni C., Ferrero M. E.

Journal of Physiology and Pharmacology

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2011

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tom 62

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nr 3

Endothelial mitochondria, the major site of ATP generation, modulate the intracellular dynamics of reactive oxygen species (ROS), which, in turn, control endothelial function. Adequate oxygen (O2) supply is required by endothelial cells (EC). Both hypoxia and hyperoxia may favor the overproduction of ROS leading to oxidative stress, mitochondrial damage and endothelial dysfunction. We investigated the capability and mechanisms of CellfoodTM (CF), an antioxidant compound, to modulate O2 availability and mitochondrial respiratory metabolism and to regulate ROS generated by hypoxia in EC in vitro. Human umbilical vein endothelial cells (HUVEC) and ECV-304 were evaluated for the O2 consumption using a Clark's electrode. The O2 consumption rate rose, during the first minutes after CF addition and was associated with increase in mitochondrial oxidative capacity and good cell viability. Similar behaviours were observed when EC were exposed to CF for up to 8 days. The O2 consumption increased and was accompanied by both intracellular rise of ATP and maintainment of LDH concentration. Hypoxia-induced ROS generation was significantly inhibited by CF, through the up-regulated expression of MnSOD, an anti-oxidant responsible for mitochondrial function preservation. The EC hypoxic response is mediated by the hypoxia master regulator HIF-1alpha whose activation was attenuated by CF, in concomitance with MnSOD up-regulation. Our results suggest a role for CF in improoving respiratory metabolism and in activating anti-oxidant mechanisms in EC, thus preserving endothelial function.

17

Hemodynamic responses to brief hyperoxia in healthy and in mild hypertensive human subjects in rest and during dynamic exercise

51%

Izdebska E., Izdebski J., Trzebski A.

Journal of Physiology and Pharmacology

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1996

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tom 47

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nr 2

18

Catalase and superoxide dismutase activity in Rana esculenta organs

32%

Czarniewska E., Adamski Z., Mackowiak J., Ziemnicki K.

Biological Bulletin of Poznań

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1995

|

tom 32

Ograniczanie wyników

Oxygen breathing and ventilation

Hyperoxia blunts renal sympathetic nerve activity response to acute intermittent hypercapnia in rats

Metabolic changes in rat brain synaptosomes after exposure to normobaric hyperoxia in vitro

Prenatal exposure to hyperoxia modifies the thromboxane prostanoid receptor-mediated response to H2O2 in the ductus arteriosus of the chicken embryo

Inhibition of hypoxia-induced tolerance to subsequent hyperoxic injury in lung cells by phosphatidyl inositol 3-kinase inhibitors: LY294002 and wortmannin

Superoxide dismutase mimetic modulates hyperoxic augmentation of the diaphragmatic response to poikilocapnic hypoxia in non-vagotomized rats

Female headstart in resistance to hyperoxia-induced oxidative stress in mice

Hypoglossal and phrenic nerve responses to changes in oxygen tension during picrotoxin-induced seizures in the rat

Hyperoxia intensifies postischemic lipid peroxidation in gerbil brain synaptosomes

Exposure to sixty minutes of hyperoxia upregulates myocardial humanins in patients with coronary artery disease - a pilot study

Moderate exercise training reduces arterial chemoreceptor reflex drive in mild hypertension

The effects of increased inspired oxygen with and without dopamine on lung and diaphragm hydrogen peroxide and apoptosis following hemorrhagic shock

Neurotransmitter mechanisms in the enhancement of the hypoxic ventilatory response by antecedent hyperoxia in the anesthetized rat

Transient O2-dependent effects of CO2 on ventilation in the anesthetized mouse

Poly(ADP-ribose) polymerase activity in the cat carotid body in hypoxia and hyperoxia

Cellfood improves respiratory metabolism of endothelial cells and inhibits hypoxia-induced reactive oxygen species (ROS) generation

Hemodynamic responses to brief hyperoxia in healthy and in mild hypertensive human subjects in rest and during dynamic exercise

Catalase and superoxide dismutase activity in Rana esculenta organs