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Biomedical subjects

A Trzebski

Publications and source records attributed to A Trzebski.

At least 37 records · Page 2Linked to original sources
PubMed1992

Local cerebral blood flow responses in rats to hypercapnia and hypoxia in the rostral ventrolateral medulla and in the cortex.

The effects of hypercapnia and hypoxia on two local cerebral blood flows in the parietal cortex (PC-BF) and rostral ventrolateral medulla (RVLM-BF) were examined using laser Doppler flowmetry in anesthetized rats. Hypercapnia for 45 s duration at the end-tidal CO2 between 5% and 10%, induced by increasing inspiratory CO2, increased both cerebral blood flows and systemic blood pressure in a degree-dependent manner. The response of RVLM-BF was significantly stronger than that of PC-BF. Both cerebral blood flow responses to hypercapnia were not influenced by cutting peripheral chemoreceptor afferent nerves. Hypoxia for 45 s duration at the end-tidal O2 between 12% and 6%, induced by decreasing inspiratory O2, produced an increase of similar magnitude in both RVLM and PC local blood flows in a degree-dependent manner and a decrease in systemic blood pressure. The responses of both PC-BF and RVLM-BF to hypoxia were significantly diminished after cutting peripheral chemoreceptor afferent nerves. It is concluded that: (1) the RVLM-BF is much more sensitive to hypercapnia than the PC-BF; and (2) activation of peripheral arterial chemoreceptors possibly contributes to hypoxia-induced increase in the RVLM-BF and PC-BF.

Animals↗
PubMed1992

Role of the rostral ventrolateral medulla in the generation of synchronized sympathetic rhythmicities in the rat.

In artificially ventilated, paralyzed rats anesthetized with Nembutal or urethane, power density spectral analysis (PDS), using direct FFT algorithm, was used to quantify rhythmicities in the sympathetic cervical and lumbar nerves after bilateral microinjections into rostral ventrolateral medulla (RVLM) of CoCl2 and MgCl2--unspecific synaptic transmission blockers. Later overall sympathetic activity, phrenic nerve discharge, heart rate and arterial blood pressure were recorded. Block of synaptic transmission in RVLM was tested by elimination of sympathoinhibitory or sympathoexcitatory reflex responses to aortic nerve and vagal afferents stimulation respectively. In animals vagotomized with bilateral section of carotid sinus nerve the power in all frequency bands was very significantly reduced to a level not different from that which remained after spinal cord transsection. If carotid baroreceptors were intact, a small peak corresponding to cardiac frequency band persisted. Overall, non-synchronized sympathetic activity and arterial blood pressure increased. All effects were transient, lasted up to 15 min, and could be reproduced several times in one experiment. Respiratory rhythmic activity was unchanged yet respiratory-sympathetic synchronization was abolished. It is concluded that RVLM reticulospinal sympathoexcitatory neurons are responsible for non-synchronized tonic sympathetic activity but are not able to generate synchronized sympathetic rhythms. Synaptic input, presumably inhibitory, either from local neuronal circuits within ventral medulla and/or from other brain stem neuronal circuitries is needed to shape out the flexible pattern of sympathetic oscillations.

Animals↗
PubMed1991

Reflex responses in adrenal sympathetic nerves to stimulation of glucoreceptors and chemoreceptors in aging rats.

The age-related changes in the sensitivity of reflex responses of adrenal sympathetic nerve activity following stimulation of glucoreceptors and arterial chemoreceptors were investigated in young adult rats 4-5 months old and aged rats 24-26 months old. The sensitivity of the inhibitory reflex responses to stimulation of glucoreceptors and the sensitivity of excitatory reflex responses to systemic hypoxia with end-tidal O2 concentration at 8% and 6% were well maintained in the same ranges in aged rats as in young adult rats. The sensitivity of the excitatory reflex responses to mild systemic hypoxia with end-tidal O2 concentration at 10% increased slightly but significantly in aged rats compared with that in young adult rats.

Adrenal Glands↗
PubMed1990

Respiratory-related discharge pattern of sympathetic nerve activity in the spontaneously hypertensive rat.

1. Synchronization of spontaneous sympathetic discharge during the respiratory cycle was studied in the cervical and renal nerves of vagotomized, normotensive Wistar-Kyoto rats (WKYs) and age-matched spontaneously hypertensive rats (SHRs). Phrenic nerve discharge was used as an index of central inspiratory activity. 2. In normotensive Wistar-Kyoto rats depression of sympathetic activity appeared at the onset of inspiration reaching a minimum at mid-inspiration. Peak maximal sympathetic discharge corresponded to postinspiratory phase; a second increase sometimes appeared in late expiration. Variations of respiratory frequency over wide range of experimental conditions by hypoxia, hyperoxia, hyper- or hypocapnia and transection of carotid sinus nerves did not affect this pattern. 3. In SHRs the respiratory-phase-related timing of sympathetic discharge was variable. In normoxia, the maximal sympathetic activity occurred in late inspiration, preceded by short depression at early inspiration and followed by postinspiratory depression. A second increase in sympathetic activity was observed in mid-expiration. 4. The pattern of respiratory phase modulated sympathetic activity in SHRs was altered by hypoxic stimulation of the peripheral chemoreceptors. The early inspiratory depression of sympathetic activity was substantially prolonged and the maximal sympathetic discharge was shifted from inspiration to early expiration. This effect was abolished after carotid sinus nerves had been cut. 5. Hypercapnic stimulation of central chemoreceptors in SHRs with carotid sinus nerves cut did not influence the timing of the sympathetic activity in relation to the respiratory phase, though the magnitude of rhythmical sympathetic discharges was increased. 6. We discuss the possibility that altered synchronization between central respiratory drive and sympathetic neuronal system may contribute to the neurogenic mechanisms of arterial hypertension in SHRs.

Action Potentials↗
PubMed1990

Effects of stimulation of cervical sympathetic trunks with various frequencies on the local cortical cerebral blood flow measured by laser Doppler flowmetry in the rat.

The effects of electrical stimulation of cervical sympathetic trunks for 1-min duration at supramaximal intensity with various stimulus frequencies on local cortical cerebral blood flow were investigated in urethane-anesthetized rats. Electrical stimulation with low frequency (1-2 Hz) produced a significant increase in local cortical cerebral blood flow during the stimulation. The local cortical CBF reached 111% of the resting value during the stimulation at 10 Hz, and slightly decreased for about 30s after the end of stimulation. High-frequency stimulation (20-30 Hz) produced the short-term increase during the stimulation, which was followed by the dominant and long-lasting decrease, and the local cortical CBF reached 87% (at 30 Hz) of the resting value after the end of stimulation. The response of increase in flow was abolished by intravenous administration of beta adrenergic blocking agent (propranolol, 1.3 mg/kg i.v.), while the response of decrease in flow was abolished by alpha adrenergic blocking agent (phenoxybenzamine, 0.5 mg/kg i.v.).

Animals↗
PubMed1990

Opposite excitatory and inhibitory effects of central administration of glucagon and of insulin upon the sympathetic cervical and adrenal nerve activities in the rat.

The central effects of pancreatic glucagon and insulin given intracerebroventriculary (i.c.v.) upon sympathetic activity in the cervical trunk and adrenal nerve were examined in Wistar Kyoto rats. Glucagon i.c.v. administration led to an increase in sympathetic nerve activity in both nerves. Insulin injected into lateral ventricle caused opposite to glucagon inhibitory influence on sympathetic discharge in the cervical trunk and adrenal nerve. This two different central effects of glucagon and insulin on sympatho-adrenal system may contribute to glycemia homesthasis.

Adrenal Glands↗
PubMed1990

The effect of an alerting acoustic stimulus on the heart rate, sympathetic activity and aortic baroreceptor discharge in conscious rabbits before and after naloxone administration.

Blood pressure, heart rate, aortic nerve activity and cervical sympathetic discharge were recorded simultaneously in 10 rabbits. Chronic recordings were made with electrodes implanted to the uncut aortic and cervical sympathetic nerves. 1. The alerting acoustic stimulus produced a short lasting decrease in sympathetic activity with a transient bradycardia. 2. In 6 out of 8 rabbits i.v. administration of naloxone chloride (100 mg/kg) diminished or abolished early inhibitory effects evoked by acoustic stimulus. 3. The sympatho-inhibitory system involved in the startling response appears to be independent of the baroreceptor inhibitory reflex and has opposite responsiveness to naloxone. 4. A decrease in efferent sympathetic activity with no accompanying change in the aortic nerve activity suggests some central resetting of the baroreceptor-sympatho-inhibitory reflex. 5. We suggest that the observed autonomic effects following an alerting stimulus are typical for a fear-anxiety drive.

Acoustic Stimulation↗
PubMed1990

Respiratory modulation of the cutaneous somatosympathetic reflex in normotensive (WKY) and in spontaneously hypertensive rats (SHR): species and strain-dependent patterns.

In 6 normotensive Wistar-Kyoto (WKY) and 6 spontaneously hypertensive rats (SHRs) anesthetized with urethane and chloralose, paralyzed, artificially ventilated, vagotomized with carotid sinus nerves bilaterally cut, somatosympathetic reflex discharges were recorded in cervical and renal nerves by stimulating group II and III cutaneous afferents in the sural nerve. Only a long-circuited, late supraspinal component reflex discharge could be elicited. After averaging the responses evoked by random stimulation, the latency of the reflex discharge was significantly longer in the renal than in the cervical sympathetic nerve, equally in the WKY rat and in SHR. In WKY rats the peak of sympathetic discharge corresponded to early expiration, whereas in SHRs--to late inspiratory phase. The duration of the reflex discharge elicited in inspiration was greater in SHR than in WKY rats. In WKY rats stimuli applied during phrenic discharge produced a reflex response of longer latency and of reduced amplitude than those applied in expiration. In SHRs the latency of the reflex response in the sympathetic cervical nerve was shorter during inspiration than in expiratory phase. The timing of the sympathetic reflex responsiveness within respiratory cycle in SHR and in WKY rats corresponded to strain-dependent opposite respiratory synchronization pattern of the spontaneous sympathetic activity characterizing each strain. No respiratory modulation of the somatosympathetic reflex was observed in the renal nerve of SHR. It is concluded that both spontaneous and evoked sympathetic activity is synchronized differently in SHR and in WKY rats and this difference is both species- and strain-dependent.

Animals↗
PubMed1989

Centrally administered glucagon stimulates sympathetic nerve activity in rat.

The effect of pancreatic glucagon given intravenously, intracerebroventricularly and microinjected into the nucleus of the solitary tract on sympathetic activity in the cervical trunk and adrenal nerve was examined in rat. In each case glucagon caused a relatively long-lasting substantial increase in discharge of both nerves. This finding shows that glucagon can act centrally to stimulate sympathetic activity. The most probable site for the sympathoexcitatory effect of glucagon is the nucleus of the solitary tract.

Action Potentials↗
PubMed1989

Stimulation of the rostral ventrolateral medullary neurons increases cortical cerebral blood flow via activation of the intracerebral neural pathway.

In urethane-anesthetized, artificially ventilated rats, electrical or chemical (by L-glutamate) focal stimulations of the rostral ventrolateral medulla (RVLM) produced an increase in cortical cerebral blood flow (CBF). The RVLM-induced cortical vasodilative response was present in animals with spinal cords sectioned at levels of Th3-4 and with bilateral extracerebral cervical sympathetic trunks (CSTs) severed. The RVLM-induced cortical vasodilative response was totally eliminated by an alpha 2 adrenergic blocker, but not by blockers for muscarinic, nicotinic, alpha 1 and beta receptors. It was concluded that there is an intracerebral vasodilative neural pathway including an alpha 2 adrenergic receptor originating in the RVLM for regulation of cortical blood vessels.

Adrenergic Fibers↗
PubMed1989

Autonomic nerve and cardiovascular responses to changing blood oxygen and carbon dioxide levels in the rat.

Contribution of autonomic nervous system activity to the heart rate and blood pressure responses during chemoreceptor excitations by systemic hypoxia and hypercapnia and to hyperoxia and hypocapnia was analyzed in the urethane-anesthetized, artificially ventilated rats. Systemic hypoxia induced a co-activation of two antagonistic nerves: an increase in cardiac sympathetic and in cardiac vagal efferent nerve discharges. Increased heart rate was due to predominance of the cardiac sympathetic over the cardiac vagal activation. In spite of a marked reflex increase in the renal and cardiac sympathetic nerve activities, the local vasodilator effect of hypoxia prevented consistent changes in arterial blood pressure. Bilateral section of the carotid sinus nerves (CSN) mostly abolished autonomic nerve responses and produced a profound decreases in the blood pressure during hypoxia. Hyperoxia elicited a pressor response due to peripheral vasoconstriction with no significant change in the autonomic nerve activities except for a decrease in the cardiac sympathetic nerve discharges. Hypercapnia significantly increased blood pressure and renal nerve sympathetic activity. In contrast to hypoxia, hypercapnia excited cardiac sympathetic and inhibited cardiac vagal activity. This reciprocal effect did not elicit neurogenic cardioacceleration, because it was masked by the local inhibitory action of CO2 on the heart rate. The increase in sympathetic activities and in blood pressure during hypercapnia persisted after bilateral CSN section indicating that the responses were mediated by central rather than by peripheral chemoreceptors. Hypocapnia produced a significant increase in cardiac vagal discharges yet a cardioacceleratory response occurred due to the local effect upon heart rate. The present results indicate that in the rat, autonomic nervous responses differ depending on the type, i.e. hypoxic or hypercapnic, chemoreceptor stimuli. Reflex heart rate and blood pressure responses do not follow the autonomic nerve activities exactly. Circulatory responses are greatly modified by local peripheral effects of hypoxic, hyperoxic, hypocapnic or CO2 stimuli on the cardiovascular system. Species differences characterizing the autonomic nerve responsiveness to chemical stimuli in the rat are described.

Animals↗
PubMed1989

Sympatho-inhibitory baroreflex in conscious rabbits: simultaneous recordings of sympathetic and aortic nerve activity.

The purpose of this study was to evaluate simultaneously the activity of afferent and efferent neuronal pathways of the sympatho-inhibitory baroreceptor reflex in conscious rabbits. Bipolar electrodes were implanted around the intact aortic nerve and cervical sympathetic trunk. Baroreceptor activity and sympathetic discharges were continuously recorded along with mean blood pressure. The baroreceptor reflex response was evoked by changes in mean arterial pressure induced by i.v. administration of phenylephrine 10 micrograms/kg and sodium nitroprusside 10 micrograms/kg. The baroreflex was analysed as parallel changes of afferent and efferent activities per mmHg of mean blood pressure rise or fall. This method of investigation of baroreflex responsiveness permits analysis of afferent and efferent neural activities under different behavioural conditions in conscious animals.

Action Potentials↗
PubMed1989

Hypoxia and hypercapnia increase the sympathoadrenal medullary functions in anesthetized, artificially ventilated rats.

Graded hypoxia (FETO2 14-6%) and hypercapnia (FETCO2 6-10%), which were applied for 45s and 2 min, respectively, to urethane anesthetized and artificially ventilated rats produced an increase in adrenal sympathetic efferent nerve activity in parallel with increases in adrenaline and noradrenaline secretion measured in the adrenal venous effluent. Percentage increases in adrenaline and noradrenaline were almost equal. In rats whose carotid sinus nerves (CSN) were bilaterally cut, hypoxia did not produce any effect on adrenal sympathetic nerve activity or catecholamine secretion. In contrast, excitatory adrenal nerve and catecholamine secretory responses to hypercapnia remained unchanged in CSN denervated rats. After severing a splanchnic nerve whose branches innervated the adrenal gland, while maintaining the resting level of catecholamine secretion by low-frequency stimulation of the peripheral end of the splanchnic nerve, hypoxia did not produce any increase in catecholamine secretion. Hypercapnia (FETCO2 8 and 10%), however, induced catecholamine secretion from denervated adrenal medulla, although the magnitude of the response was significantly lower than that in animals with adrenal nerve intact. It is concluded that hypoxia stimulates the adrenal medulla via the carotid chemoreceptor reflex whereas hypercapnia acts mainly via mechanisms besides carotid chemoreceptors such as central chemoreceptors with some direct stimulatory effect on the adrenal medulla. The functional significance of these dual mechanisms of sympathoadrenal excitation during hypoxia and hypercapnia is discussed.

Adrenal Medulla↗
PubMed1987

Excitatory and inhibitory effects on respiration of L-glutamate microinjected superficially into the ventral aspects of the medulla oblongata in cat.

L-Glutamate (4-40 nmol) was microinjected at superficial depths beneath the ventral surface of the medulla oblongata in cats. Injections (100-300 microns beneath the surface) made rostromedial to the hypoglossal nerve, less than 1.5 mm lateral to the pyramidal tract, caused stimulation of phrenic nerve activity. Injections (100-500 microns beneath the surface) up to 1 mm further lateral caused a marked increase in arterial pressure and depression of phrenic nerve activity. These findings support the existence of two cell groups in the ventral medulla that are involved in regulation of respiration; when activated, one (medial group) causes facilitation and the other (lateral group) inhibition of respiration.

Animals↗
PubMed1987

Respiratory rhythmicity in a split medulla preparation of the cat.

Splitting the medulla in the cat resulted in the disappearance of inspiratory activity in the phrenic but not in the recurrent laryngeal nerves with minor changes in respiratory cycle duration. In one animal a complete desynchronization of respiratory rhythms was observed in the opposite recurrent laryngeal nerves. We conclude that each half of the cat's brain stem has its own respiratory phase-switching mechanism. Commissural connections are involved in the bilateral synchronization of activity and the mutual excitatory interactions between medullary respiratory neurons.

Action Potentials↗
PubMed1987

Carotid chemoreceptor discharge responses to hypoxia and hypercapnia in normotensive and spontaneously hypertensive rats.

The carotid chemoreceptor discharge responses to hypoxia and hypercapnia were quantitatively compared between normotensive (NTR) and spontaneously hypertensive rats (SHR). For this purpose we recorded afferent mass discharges from the carotid sinus nerve (CSN) at various levels of end-tidal O2 and CO2 concentrations (FetO2, FetCO2 (%)) in the urethane-anesthetized, vagotomized and artificially ventilated rats. The CSN chemoreceptor discharge was evaluated by subtracting the small activity remaining in acute hyperoxia (chemoreceptor inactivation), which was estimated as baroreceptor in origin, from the large total CSN activity. The CSN chemoreceptor discharges at various levels of FetO2 or FetCO2 were expressed as the percent of control activity measured in normoxic and normocapnic conditions (FetO2, 15-16%; FetCO2, 4.5-5.1%). There was an exponential increase in the CSN chemoreceptor discharge as FetO2 was decreased from hyperoxic to various hypoxic levels (maximally 6%) at a maintained FetCO2 (normocapnia). The relationship between the CSN chemoreceptor discharge and the hypoxic stimulus was quantitatively assessed by the regression analysis using an exponential function. Exponential increases in the CSN chemoreceptor discharge by hypoxia and the parameters in the exponential function reflecting the sensitivity to hypoxia were significantly higher in the SHR than in the NTR, which indicated a high carotid chemoreceptor discharge response to hypoxia in the SHR. The CSN chemoreceptor discharge was increased linearly by increasing the FetCO2 from the normocapnic level up to about 10% at a maintained FetO2 (normoxia). Increases in discharge produced by severe hypercapnia were, however, much smaller than that caused by hypoxia. The slope of the CO2 stimulus-CSN chemoreceptor discharge response line was almost the same in NTR and SHR. The results demonstrated that the responsiveness of rat carotid chemoreceptor to hypoxia is augmented in the SHR. The role of carotid chemoreceptor afferents in ventilatory reflex responses to hypoxia and their alterations in the SHR are discussed.

Animals↗