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1
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Reflex respiratory responses to progressive hyperoxic hypercapnia and normocapnic hypoxia in normocapnic and hypercapnic obstructive sleep apnea patients

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Tafil-Klawe M., Klawe J. J., Sikorski W., Drzewiecka B.
Journal of Physiology and Pharmacology. Supplement
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2004
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tom 55
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nr 3
135-138
Ventilatory responses to progressive hypercapnia were analyzed in the normocapnic and hypercapnic obstructive sleep apnea patients (OSA). The rebreathing hypercapnic and hypoxic tests were performed using the computerized equipment (Lungtest, MES), according to Read's method. The ventilatory response to hypoxia was impaired in all OSA patients. Concerning the hypercapnic ventilatory response, there were no differences between the OSA patients with normal end-tidal PCO2 and controls. Nine moderately hypercapnic OSA patients showed a right shift with a normal slope of the regression curve describing the relationship between the end-tidal PCO2 and minute ventilation. In contrast, three severely hypercapnic OSA patients showed a right shift with a decreased slope of this regression curve. We conclude that awake OSA patients who developed hypercapnic ventilatory insufficiency showed an impaired hypercapnic defense reaction.
2
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Hypoxic ventilatory profile in the anesthetized rat

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Marczak M., Kolesnikova E. E., Pokorski M.
Journal of Physiology and Pharmacology. Supplement
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2004
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tom 55
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nr 3
89-94
In the present study we investigated whether hypocapnia that accompanies hypoxic hyperventilation might affect the biphasic, stimulatory/depressant, ventilatory response to hypoxia. The experiments were carried out in anesthetized, vagotomized, spontaneously breathing, and poikilocapnic rats. The animals were subjected to acute steady-state hypoxia consisting of 12% O2 in N2 in inspiratory mixture. Ventilation and its frequency and volume components were assessed from the integrated electromyographic activity of the diaphragm. We found that despite the development of significant hypocapnia, the hypoxic ventilatory response consisted of rapid stimulation followed by a gradual decline. The frequency component contributed more to the ventilatory increase than that of volume. The results indicate that the hypoxic ventilatory profile in the anesthetized poikilocapnic rat resembles that known to be present during isocapnia. We conclude that hypocapnia neither hampers the hypoxic ventilatory reactivity nor alters the biphasic hypoxic ventilatory profile. These observations may aid planning experimental rat model studies.
3
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Ventilatory augmentation by acute intermittent hypoxia in the rabbit

100%
Sokolowska B., Pokorski M.
Journal of Physiology and Pharmacology. Supplement
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2006
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tom 57
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nr 4
341-347
This study seeks to determine the effects on respiratory function of acute intermittent hypoxia. The experiments were performed on anesthetized, spontaneously breathing rabbits. The experimental protocol consisted of 5 one-minute episodes of hypoxia (14% O2 in N2) interspersed with three-minute normoxic recovery periods. Ventilatory variables, minute ventilation (MV) and its tidal and frequency components, were derived from the continuously recorded airflow signal. We found that MV progressively increased with each next hypoxic-normoxic cycle; the increases were driven by both ventilatory components. Ventilatory augmentation concerned both the stimulus (hypoxic) and recovery (normoxic) periods, but it was significantly greater in the former. The augmented ventilation was sustained for up to 30 min after the last hypoxic run, which suggests the appearance of ventilatory long-term facilitation. The results demonstrate that acute intermittent hypoxia consisting of a few hypoxic-normoxic cycles is capable of inducing appreciable ventilatory changes. Such changes reflect plasticity of the respiratory motor output developing on a short-term basis during ongoing cycles of hypoxia, which, in the present study, correlated with the number of hypoxic cycle. Ventilatory augmentation in response to acute cyclic hypoxic episodes may give insights into the mechanisms of respiratory improvement by intermittent hypoxic training, increasingly used in both sports physiology and medicinal approaches.
4
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NMDA glutamate receptor antagonism and the ventilatory response to hypoxia in the anesthetized rat

84%
Tarakanov I., Dymecka A., Pokorski M.
Journal of Physiology and Pharmacology. Supplement
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2004
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tom 55
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nr 3
139-147
This study seeks to discern the influence of the NMDA glutamate-mediated pathway in the early stimulatory and late depressant phases of the hypoxic ventilatory response. We addressed this issue by recording ventilation before and after intravenous administration of the NMDA receptor antagonist MK-801 during acute, steady-state hypoxic challenges in the anesthetized, spontaneously breathing rats. Minute ventilation and its volume and frequency components were calculated and compared at the peak and nadir of the hypoxic response. We found that NMDA receptor antagonism appreciably affected both ventilatory phases of hypoxia. The early stimulation of ventilation was attenuated and the late depression was accentuated. The latter consisted of abolishment of the characteristic sustenance of hypoxic ventilation above the baseline level in the depressant phase, so that ventilation declined down to the baseline after NMDA receptor blockade. The inability to uphold ventilation in the depressant phase suggests that the NMDA glutamate-mediated pathway is operative in shaping the late hypoxic ventilatory response. The role of the glutamatergic pathway may thus be extended beyond the hitherto recognized early ventilatory stimulation of hypoxia.
5

Hypoxic ventilatory response in the rats with 6-hydroxydopamine lesion of the medial forebrain bundle and peripheral dopamine receptor blockade

84%
Andrzejewski K., Budzinska K.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
The rat model of Parkinson’s disease (PD) based on experimental impairment of nigrostriatal dopaminergic system by 6-hydroxydopamine (6-OHDA) has been elaborated to study mechanisms of respiratory disturbances associated with PD. Following striatal injection of 6-OHDA breathing with hypoxic mixture augments the hyperventilatory response to hypoxia suggesting an attenuation of the depressant effect of dopamine on ventilation. In the present study we ask whether injection of 6-OHDA into the medial forebrain bundle (MFB), that evokes more severe motor symptoms, elicits changes in the hypoxic ventilatory response and whether changes in ventilatory response to hypoxia following the unilateral dopaminergic denervation are transmitted by peripheral dopamine D2 receptors. The experiments were performed on adult rats. Ventilatory parameters: tidal volume, minute ventilation, and frequency of breathing were measured with the use of body plethysmograph method before and two weeks following unilateral, double injection of 6-OHDA into the MFB. Changes in the body weight and behavioral cylinder test were evaluated at the same time points and compared with the results obtained in sham operated rats. Effects of peripheral dopamine D2 receptor antagonist, domperidone (1 mg/ kg i.p.) on ventilation during rest breathing and during 3 minutes exposure to hypoxia (8% O2)were studied before and after 6-OHDA injection. Two weeks after 6-OHDA treatment the cylinder test showed limb use asymmetry. Body weight increased less than in animals without 6-OHDA injection. Following the MFB lesion the hyperventilatory response to hypoxia was augmented mainly by an increment of tidal volume. Before the MFB lesion the pretreament with domperidone enhanced resting ventilation and hypoxic hyperventilatory response. After 6-OHDA injection domperidone no longer altered both normoxic breathing and the hyperventilatory hypoxic response. The study shows that an impairment of dopaminergic system by MFB lesion causes comparable changes in breathing and ventilatory response to hypoxia as lesions in the other locations of the nigrostriatal pathways. In 6-OHDA model of Parkinson’s disease changes in the hypoxic ventilatory response seem to be related to a reduction of peripheral D2 dopaminergic neurotransmission involved in the control of breathing.
6
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Neurotransmitter mechanisms in the enhancement of the hypoxic ventilatory response by antecedent hyperoxia in the anesthetized rat

84%
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.
7
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Alterations in the hypoxic ventilatory response with advancing age in awake rats

67%
Pokorski M., Antosiewicz J.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 2
This study seeks to determine the influence of aging on hypoxic ventilatory responsiveness. We addressed the issue by comparing the hypoxic ventilatory responses in three age-groups of conscious rats: 3, 12, and 24 months old animals. Ventilation was recorded in a whole body rodent plethysmograph. Minute ventilation (E), respiratory rate, and tidal volume were considered for analysis. The rats were subjected to two levels of acute hypoxia: 14 and 11% O2 in N2. Hypoxic exposures were separated by a 15 min recovery interval in air. The part of the study between the 12 and 24 months age interval was longitudinal in that the same animals were studied twice, whereas the youngest animals belonged to a separate breed. All data were normalized to body mass. All hypoxic responses were biphasic with the stimulatory peak at 0.5 min after onset of hypoxia. The results demonstrate that there were no appreciable differences in magnitude of the peak hypoxic E responses between 3 and 12 months old rats. The hypoxic E responses and also the hypoxic ventilatory gain were, however, enhanced in the senescent rats. In these rats, the increment in peak E from 14 to 11% hypoxia amounted to 364.1±95.8 ml.min-1.kg-1, which was more than double compared with 12 and 3 months old rats (P<0.02). We conclude that ventilatory responsiveness is not curtailed in senescent rats. The respiratory system is able to compensate for any age-related handicaps in the respiratory system to maintain a stimulatory response to ventilatory stress.
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