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1

Hypoxic ventilatory profile in the anesthetized rat

100%

Marczak M. , Kolesnikova E. E. , Pokorski M.

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nr 3

89-94

EN

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.

2

Ultrastructural degradation of the carotid body in the aged rat: is there a role for atherosclerosis in the main carotid arteries?

100%

Dymecka A. , Walski M. , Pokorski M.

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nr 4

85-90

EN

In this study we examined the potential role of atherosclerosis in the main arteries supplying blood to the carotid body in the organ’s morphological degradation with age. We addressed this issue by comparing the ultrastructural picture of carotid bodies and of fragments of the carotid artery bifurcation in two age-extreme groups of rats: young - 3 months old and senescent - 24 months old. Tissues were excised under surgical anesthesia, fixed in aldehydes, and processed for transmission electron microscopy. We found that the old carotid body parenchyma exhibited profound degenerative changes. Chemoreceptor cells were at various stages of atrophy, ranging from swollen mitochondria and fewer secretory vesicles to dark dehydrated cells. In contrast, the senescent carotid artery bifurcation was little different from that in young rats. Particularly, endothelial cells were in perfect condition. There were some changes in deeper arterial wall layers such as breaks in the continuity of elastic bands or a subtly different phenotype of smooth muscle cells. No foam cells or calcium build-ups were found in the arterial walls. Such changes correspond to the process of arterial wall stiffening in old age rather than to the outright atherosclerosis. Lack of atherosclerosis in the common carotid arteries, which could hamper blood flow, argues against its playing a role in the morphological age-changes in the carotid bodies.

3

The aging corotid body

84%

Pokorski M. , Walski M. , Dymecka A. , Marczak M.

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nr 3

107-113

EN

The respiratory system is subject to the aging process, which could limit its responsiveness to hyperventilatory stimuli. Attenuation of the ventilatory response to hypoxia in old age is, as yet, an unresolved issue. Such attenuation may be germane for the pathogenesis of respiratory disorders developing more often in elderly subjects. The aim of this study was to determine the potential adverse effects of age on the morphology and function of carotid bodies. Morphology was studied at the level of electron microscopy on carotid bodies dissected from adult young (3 months) and old (>2 years) rats and function by comparing the hypoxic ventilatory response in populations of young (mean age 24 years) and old (mean age 71 years) female subjects. The human protocol consisted of a progressive hypoxia test, based on a rebreathing technique in a closed system. The hypoxic ventilatory response was evaluated from the slopes of minute ventilation on arterial oxygen saturation. The results of the morphological study showed degenerative changes developing with age in the ultrastructure of carotid bodies. On the other side, respiratory responses to hypoxia in old women were well preserved and were no less than those in young women. Therefore, a discrepancy appeared between the morphological and functional aspects. These findings suggest development of compensatory mechanisms in brain respiratory areas which maintain primary defensive reflexes, such as the hyperventilation of hypoxia.

4

84%

Kolesnikova E. E. , Safronowa O. S. , Serebrovskaya T. V.

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nr 1

20-24

EN

Aging is associated with changes in breathing regulation, particularly, in respiratory sensitivity to hypoxic stimuli. One theory of aging holds that reactive oxygen species play a key role in this process. These species have also been implicated in the carotid body O2 sensing. In the present study we investigated hypoxic ventilatory responses (HVR) and antioxidant enzymes activity in healthy young and elderly people under a 14-day adaptation to intermittent hypoxic training (IHT). The elderly demonstrated decreased HVR and blood catalase (CAT) activity on a background of strong negative correlation between the levels of end-tidal CO2 tension and superoxide dismutase (SOD) activity. The adaptation to IHT resulted in increased HVR and SOD activity in both groups, and decreased CAT activity in young persons compared with its augmentation in the elderly. Increased SOD activity testifies to an overproduction of reactive oxygen species during IHT. We hypothesize that reactive oxygen species might potentiate a periodical augmentation of cytosolic Ca2+ in the carotid body. This, in turn, might determine an increase in tyrosine hydroxylase gene expression and promote neurotransmitter synthesis/release, resulting in enhanced HVR.

5

A common oxygen sensor regulates the sensory discharge and glomus cell HIF-1alpha in the rat carotid body

84%

Lahiri S. , Antosiewicz J. , Pokorski M.

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tom 58

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nr 5

6

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

84%

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

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nr 3

EN

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.

7

Influence of the stimulation of carotid body chemoreceptors on the gastric mucosal blood flow in artificially ventilated and spontaneously breathing rats

84%

Sinski M. , Kowalczyk P. , Stolarczyk A. , Sawionek L. , Przybylski J.

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nr 3

EN

The cardiovascular effects of the stimulation of arterial chemoreceptors are different in spontaneously breathing and artificially ventilated animals. Respiratory failure and long term sojourn at high altitude coincide frequently with the occurrence of gastric ulceration. In both these situations a profound stimulation of arterial chemoreceptors is present. The purpose of the paper was to investigate the reflex effect of stimulation carotid chemoreceptors on gastric mucosal blood flow in the rat. Arterial chemoreceptors were stimulated by two methods (I) substitution gas mixture of 10% oxygen in nitrogen for room air and (II) direct injection of acid saline ( 0.05 ml, pH=6.8) into the distal part of left common carotid artery. In artificially ventilated rats stimulation of arterial chemoreceptors caused significant increase in gastric mucosal vascular resistance, accompanied by marked decline in blood flow. This effect was mediated by adrenergic mechanism. On the contrary to artificially ventilated rats, decline of gastric mucosal vascular resistance with concomitant increase in blood flow was found in spontaneously breathing animals. This effect was not abolished either by phentolamine or atropine. As vasodilatatory effect of arterial chemoreceptors stimulation was abolished by bilateral vagotomy, we postulate that non adrenergic and non cholinergic vagal fibers mediate observed vascular changes in gastric mucosa in spontaneously breathing rats. We hypothesize that in artificially ventilated patients with respiratory failure stimulation of arterial chemoreceptors by hypoxemia and or acidosis may contribute to the development of gastric mucosal lesions.

8

NADPH-diaphorase in the cat carotid body

84%

Walski M. , Pokorski M.

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nr 1

9

Protein kinase C in the carotid body

67%

Pokorski M. , Faff L.

Acta Neurobiologiae Experimentalis

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1999

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tom 59

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nr 2