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1

Aktywność mechanoreceptorów płucnych, motoneuronów nerwu błędnego i neuronów przeponowych w skurczu dróg oddechowych

100%
Szereda-Przestaszewska M.
Acta Physiologica Polonica
|
1968
|
tom 19
|
nr 4
2

Badania nad neurolegulacją światła dróg oddechowych

100%
Szereda-Przestaszewska M.
Acta Physiologica Polonica
|
1968
|
tom 19
|
nr 2
3

Laryngeal effects of serotonin in rabbits

100%
Szereda-Przestaszewska M.
Acta Neurobiologiae Experimentalis
|
1979
|
tom 39
|
nr 4
4

The effect on the larynx on the breathing pattern in anaesthetized rabbits

63%
Glogowska M., Szereda-Przestaszewska M.
Acta Physiologica Polonica
|
1981
|
tom 32
|
nr 4
5

Respiratory effects of serotonin challenge to laryngeal artery in cats

63%
Wypych B., Szereda-Przestaszewska M.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
6
Content available remote

The potential role of the nodose ganglion adenosine A1 receptor in regulation of breathing in anaesthetized rats

63%
Kaczynska K., Szereda-Przestaszewska M.
Journal of Physiology and Pharmacology
|
2008
|
tom 59
|
nr 4
759-770
The respiratory effects of stimulation of adenosine A1 receptors were studied in spontaneously breathing rats that were either (1) neurally intact and subsequently bilaterally vagotomized in the neck, or (2) neurally intact and subjected to supranodosal vagotomy or (3) midcervically vagotomized before and after pharmacological blockade of A1 receptors. Before neural interventions an intravenous bolus of the A1 receptor agonist N6-cyclopentyladenosine (CPA, 5 µg kg-1) decreased breathing rate, tidal volume, mean arterial blood pressure (MAP) and heart rate. After section of the midcervical vagi, CPA still decreased respiratory rate and tidal volume. Supranodose vagotomy abolished the fall in respiratory rate but did not affect the depression of tidal volume. Blockade of A1 receptors with intravenous doses of DPCPX (100 µg kg-1) eliminated all respiratory effects of CPA challenge. In all the neural states, CPA caused significant falls in mean arterial blood pressure and heart rate. DPCPX pre-treatment prevented these cardiovascular effects. The present data suggest that: (1) CPA-evoked activation of A1 receptors decreases breathing rate and tidal volume and this occurs central to the cervical vagi; (2) supranodosal vagotomy prevents the decrease in breathing rate, which is presumably due to stimulation of nodosal A1 receptor; and (3) depression of tidal volume and the hypotensive response result from the excitation of central nervous A1 expressing neurones.
7

Distinct cardio-respiratory response patterns elicited by neuropeptide Y and neuropeptide Y 13-36

63%
Kaczynska K., Szereda-Przestaszewska M.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
Neuropeptide Y (NPY) and its receptors have been involved in many physiological functions such as: regulation of cardiovascular system, anxiety, circadian rhythm, pain processing, inflammation, and among others, regulation of breathing. Microinjections of NPY to the dorsal medulla oblongata evoked respiratory and cardiovascular depression (Barraco et al., Brain Res. Bull., 1990; Dunbar et al., Am. J. Physiol., 1992). There is also evidence that respiratory failure or severe dyspnoea in humans was related to a high content of NPY in the infundibular nucleus (Corder et al., Neuroendocrinol., 1990). The objective of this study was to determine and compare the effects of systemic administration of neuropeptide Y and neuropeptide Y 13-36 (NPY 13-36) on the pattern of breathing and cardiovascular function and to evaluate the contribution of vagal input and the role of NPYY1 and/or Y2 receptors in these responses. Anaesthetized, spontaneously breathing rats were used. Tidal volume was measured at tracheostomy. The timing components of the breathing pattern, arterial blood pressure and heart rate were recorded. Intravenous injection of 100µg/kg-1 of NPY before and after midcervical vagotomy induced immediate slowing down of the respiratory rate and decreased tidal volume. Depressed ventilation was accompanied by a significant hypertension and bradycardia. Blockade of NPYY1 receptors with an intravenous dose of 5 mg/kg of BMS 193885, significantly reduced post-NPY cardio-respiratory effects. NPY 13-36, an agonist of NPYY2 receptors, at a dose of 10 mg/ kg provoked completely different respiratory response consisting of increased tidal volume, short-lived acceleration of the respiratory rhythm resulting in hyperventilation. Increased blood pressure but no effect on heart rate were observed. Section of the lung vagi abrogated the increase in respiratory rate thus reducing an enhanced ventilation. The rise in blood pressure was diminished. This study shows that intravenous injection of neuropeptide Y by acting on NPYY1 receptors outside of the lung vagi depresses ventilation by decreasing tidal volume and respiratory rate. Hypertension and bradycardia occur also besides this pathway and might result from the activation of peripheral vascular or heart Y1 receptors. Yet, NPY 13-36 acting through NPYY2 receptors stimulates ventilation augmenting the tidal component of the breathing pattern independent of the vagal pathway. This latter mediates the respiratory timing and hypertensive responses to NPY 13-36.
8

Ventilatory response to intracarotid serotonin challenge in cats

63%
Kopczynska B., Szereda-Przestaszewska M.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
9
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Content available

Apnoeic responses to pulmonary and systemic challenge of capsaicin in cats

63%
Kopczynska B., Szereda-Przestaszewska M.
Journal of Physiology and Pharmacology
|
1998
|
tom 49
|
nr 1
10
Content available remote

Apnoeic responses to intracarotid nicotine challenge in anaesthetized cats

63%
Szereda-Przestaszewska M., Kopczynska B.
Journal of Physiology and Pharmacology
|
2003
|
tom 54
|
nr 2
To determine the effects of an intraarterial administration of nicotine on the occurrence of apnoea and the activity of rib cage respiratory muscles, we studied 31 anaesthetized, spontaneously breathing cats. Phrenic activity was used as an index of neural inspiratory drive. Activity of parasternal intercostal (PIM) and triangularis sterni (TS) muscles was recorded. Nicotine in a dose of 65 µg/kg was injected into the left common carotid artery prior to and after midcervical vagotomy, preceded by section of the superior laryngeal nerves (SLNs). In eight additional cats, initially neurotomized as mentioned, nicotine was injected after bilateral disruption of the carotid sinus nerves (CSNs). Nicotine induced prompt expiratory apnoea of mean duration of 5.4±0.3 s in 19 non-vagotomized and of 5.92±0.51 s (mean±S.E.M.) in 13 vagotomized cats. The occurrence and duration of the temporary arrest of breathing were reduced by midcervical vagotomy but not by subsequent CSNs neurotomy, which abolished post-apnoeic acceleration of breathing.In post-nicotine breathing of increased tidal volume and respiratory rate, peak activity of the parasternal intercostal muscles increased from baseline of 3.2±1.2 to 9.5±2.0 arbitrary units (p<0.001). The peak height of the phrenic nerve elevated from 7.9±0.9 to 14.5±1.7 arbitrary units (p<0.001). That of the triangularis sterni showed no change.The response of the respiratory effectors elicited by nicotine was independent of the vagal integrity and may be attributed to activation of nicotine receptors within the brainstem respiratory neurones.
11
Content available remote

Involvement of vagal opioid receptors in respiratory effects of morphine in an anaesthetized rats

63%
Kaczynska K., Szereda-Przestaszewska M.
Journal of Physiology and Pharmacology
|
2005
|
tom 56
|
nr 2
Respiratory effects of morphine injection to the femoral vein were investigated in urethane and chloralose anaesthetized and spontaneously breathing rats, prior to and after midcervical vagotomy. Bolus injection of morphine HCl at a dose of 2 mg/kg of body weight induced depression of ventilation in all rats, due to the significant decrease in tidal volume and to the decline in respiratory rate both pre- and post-vagotomy. Expiratory apnoea of mean duration of 10.0±3.4 s was present in the vagally intact rats only. Bilateral midcervical section of the vagus nerve precluded the occurrence of apnoea. Prolongation of the expiratory time (TE morphine / TE control), which amounted to10.7±2.2-fold in the intact state, was apparently reduced to 1.5±0.3-fold after division of the vagi. Morphine significantly decreased mean arterial pressure (MAP) at 30 s after the challenge, the effect persisted for not less than 1 minute and was absent in vagotomized rats. The respiratory changes evoked by morphine reverted to the control level after intravenous injection of naloxone at a dose of 1 mg/kg. Results of this study indicate that opioid receptors on vagal afferents are responsible for the occurrence of apnoea and hypotension evoked by morphine.
12

Respiratory effects of capsaicin occur beyond the lung vagi in anaesthetized rats

63%
Kaczynska K., Szereda-Przestaszewska M.
Acta Neurobiologiae Experimentalis
|
2000
|
tom 60
|
nr 2
The effects of an intravenous capsaicin challenge on the respiratory pattern and ventilation were studied in 15 urethane/chloralose-anaesthetized, spontanously breathing rats. Bolus injection of capsaicin at a dose of 5 |Lig/kg into the right femoral vein evoked respiratory arrest in all animals (both prior to and after bilateral midcervical vagotomy), which effect was abolished by ruthenium red pretreatment. Breathing that followed the apnoea was of enlarged tidal volume and initially increased respiratory rate, which resulted in an augmented ventilation. The capsaicin-induced respiratory changes were independent of vagal integrity and may depend on stimulation of vanilloid receptors within the nodose ganglia.
13

Superior laryngeal nerve section abolishes capsaicin evoked chemoreflex in anaesthetized rats

63%
Kaczynska K., Szereda-Przestaszewska M.
Acta Neurobiologiae Experimentalis
|
2002
|
tom 62
|
nr 1
14

Respiratory effects of serotonin challenge to pulmonary and laryngeal circulation in anaesthetized cats

63%
Szereda-Przestaszewska M., Wypych B.
Acta Neurobiologiae Experimentalis
|
1996
|
tom 56
|
nr 4
15

Action of serotonin on the laryngeal airway in anaesthetized cats

63%
Szereda-Przestaszewska M., Kopczynska B.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 3
16
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Laryngeal constriction produced by capsaicin in the cat

63%
Szereda-Przestaszewska M., Wypych B.
Journal of Physiology and Pharmacology
|
1996
|
tom 47
|
nr 2
17

my-opioid receptors’ share in cardiorespiratory response to systemic injection of the analgesic chimeric peptide in anaesthetized rats

51%
Wojciechowski P., Szereda-Przestaszewska M., Lipkowski A. W.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
18

Non-vagal apnea evoked by intra-common carotid artery injection of N-methyl-D-aspartic acid (NMDA) in anesthetized rats

51%
Kaczynska K., Szereda-Przestaszewska M., Chrapusta S. J.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 3
19

Neurotensin NTS1 receptors mediate the cardio-respiratory effects of [Ile 9]PK20, a novel chimeric peptide

51%
Kaczynska K., Szereda-Przestaszewska M., Kleczkowska P., Lipkowski A. W.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Opioids with their large potency in pain relieve have certain undesirable effects like tolerance, dependence and respiratory depression. This is the reason for permanent efforts to create new analgesic compounds devoid of the adverse side effects. PK20 is a novel hybrid of opioidneurotensin peptides synthetized from the C-terminal hexapeptide of neurotensin and endomorphine-2 pharmacophore. This chimeric compound shows clear central and peripheral antinociceptive activity in experimental animals, however nothing is known about the influence of PK20 on respiratory and cardiovascular parameters. The present study was designed to determine the cardiorespiratory effects exerted by an intravenous injection of [Ile9]PK20, analog of PK20 with substitution of tert-leucine by isoleucine9. We also attempted to evaluate whether the effects of the hybrid are mediated by the peripheral neural pathway like vagus nerve. Finally, the contribution of NTS1 neurotensin and opioid receptors in the [Ile9]PK20 cardiorespiratory pattern was tested. Anaesthetized, spontaneously breathing rats were used. Tidal volume was measured at tracheostomy. The timing components of the breathing pattern, arterial blood pressure and heart rate were recorded. Intravenous injection of [Ile9]PK20 at a dose of 100 μg/kg in the intact rats provoked an increase in tidal volume preceded by a prompt shortlived decrease. Immediately after the end of injection brief acceleration of the respiratory rhythm, was ensued by the slowing down of breathing. Changes in respiration were concomitant with a bi-phasic response of the blood pressure: immediate increase was followed by prolonged hypotension. Bilateral midcervical vagotomy eliminated both: tidal volume and respiratory rate responses. Blockade of NTS1 receptors with an intravenous dose of 500 μg/kg of SR 142948, significantly lessened post-[Ile9]PK20 cardiorespiratory effects. Naloxone hydrochloride – antagonist of opioid receptors – failed to block [Ile9]PK20-evoked responses. This study depicts that [Ile9]PK20 acting through neurotensin NTS1 receptors augments the tidal component of the breathing pattern through the vagal pathway. This latter mediates also the respiratory timing response to the drug. Blood pressure effects evoked by an intravenous injection of [Ile9]PK20 occur besides the vagal pathway and might result from activation of the central and peripheral vascular NTS1 receptors. In summary the respiratory effects appeared not to be profound. However, considerable and extended hypotension evoked by [Ile9]PK20 sets the main disadvantage of an analgesic compound.
20
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Diverging respiratory effects of serotonin and nicotine in vagotomised cats prior to and after section of carotid sinus nerves

51%
Szereda-Przestaszewska M., Kopczynska B., Kaczynska K., Chrapusta S. J.
Journal of Physiology and Pharmacology
|
2001
|
tom 52
|
nr 1
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