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Biomedical subjects

A Trzebski

Publications and source records attributed to A Trzebski.

At least 19 recordsLinked to original sources
PubMed1998

Postexercise decrease in arterial blood pressure, total peripheral resistance and in circulatory responses to brief hyperoxia in subjects with mild essential hypertension.

The objective of our study was: (1) to compare the influence of moderate exercise on circulatory after-response in mildly hypertensive (n = 8) and normotensive male subjects (n = 9); (2) to examine the circulatory response to 3-min hyperoxic inactivation of arterial chemoreceptors at rest and during postexercise period in both groups. Hypertensive men (HTS) with a systolic blood pressure (SBP) 148 +/- 5 mm Hg, diastolic blood pressure (DBP) 92.4 +/- 4 mm Hg; and normotensive men (NTS), with a SBP 126 +/- 3 mm Hg, DBP 75.6 +/- 1.3 mm Hg, were submitted to 20-min of moderate exercise on a cycloergometer (up to the level of 55% of each subject's resting heart rate reserve). Finger arterial BP was recorded continuously with Finapres, impedance reography was used for recording stroke volume, cardiac output and arm blood flow. In HTS a significant decrease in SBP by 14.5 +/- 3.4 mm Hg, DBP by 8.9 +/- 1.9 mm Hg, total peripheral resistance (TPR) by 0.45 +/- 0.05 TPR u. (33.7 +/- 2.7%), and in arm vascular resistance (AVR) by 11.0 +/- 2.7 PRU u. (35.6 +/- 7%), was observed over a 60-min postexercise period. NTS exhibited insignificant changes in SBP, DBP, AVR except a significant decrease in TPR limited only to 20-min postexercise period. Hyperoxia decreased SBP, DBP and TPR in HTS. This effect was significantly attenuated during the postexercise period. Long-lasting antihypertensive effect of a single dynamic exercise in HTS suggests that moderate exercise may be applied as an effective physiological procedure to reduce elevated arterial BP in mild hypertension. We suggest also that the attenuation of the sympathoexcitatory arterial chemoreceptor reflex may contribute to a postexercise decrease in arterial BP and in TPR in mildly hypertensive subjects.

Adult↗
PubMed1996

Systemic hypoxia facilitates somato-cardiac sympathetic A- and C-reflexes in anesthetized rats.

In rats anesthetized with urethane, electrical stimuli applied to tibial nerve afferents produced a somato-sympathetic A-reflex of 41 +/- 2 (mean +/- SEM)ms latency and C-reflex of 210 +/- 13 ms latency recorded in the left inferior cardiac sympathetic nerve. Hypoxia was induced by switching room air to nitrogen/oxygen gas mixture in the inspiratory line reducing end-tidal oxygen from about 18% FETO2 to 10% FETO2 and 6% FETO2 for 60s, respectively. During 6% FETO2 hypoxia, the amplitude of the somato-cardiac sympathetic A-reflex increased significantly to 138 +/- 13% of the control, and that of the C-reflex increased to 186 +/- 18% of the control. During 10% FETO2 hypoxia, the A-reflex increased insignificantly to 117 +/- 8%; the amplitude of the C-reflex was augmented significantly to 149 +/- 11% of the control. Peripheral carotid chemoreceptor denervation abolished the facilitatory effects of systemic hypoxia. It is concluded that carotid chemoreceptor stimulation enhances the responsiveness of somato-cardiac sympathetic excitatory reflexes originating in the hind limb receptors.

Animals↗
PubMed1996

Cardiovascular periodicities in healthy humans in the absence of breathing and under reduced chemical drive of respiration.

In 20 healthy human subjects (aged 20-24 years) power density spectra in 1-min time series were computed by modified MATLAB procedures from inter-beat heart intervals and systolic and diastolic finger blood pressure. High- (HF), mid- (MF) and low-frequency (LF) peaks (0.16-0.37 Hz, 0.08-0.12 Hz and 0.02-0.05 Hz, respectively) were distinguished in power density spectra (PDS). During 1-min voluntary apneas MF and LF power increased and in 18 out of 20 subjects HF peaks disappeared in PDS. Breath holding performed in hyperoxia or in hyperoxia accompanied by 1-min hyperventilation preceding apnea augmented power at MF and LF range and abolished marginal HF peaks present in the spectrum in two subjects. It is concluded that apneic PDS is characterized by augmented power of MF and LF rhythms, and represents endogenous free running cardiovascular periodicities released from feed-back mechanical, reflex and feed-forward central entrainment to respiratory rhythm.

Adult↗
PubMed1996

Sexual behavior in male rats after nitric oxide synthesis inhibition.

The influence of the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) on the copulatory behavior of sexually experienced male Wistar rats was investigated. L-NAME was injected i.p. 10 min before the onset of a session using a dose of 30 mg/kg (L-NAME 30 group), or 60 mg/kg (L-NAME 60 group). The copulatory sessions were terminated after the third ejaculation in the control group or after 1500 s in the L-NAME 30 and L-NAME 60 groups. L-NAME administration reduced the number of rats that achieved ejaculation by 43% and 86% in the L-NAME 30 and 60 groups, respectively. In both experimental groups only a few intromissions and an increased number of mountings were observed. An increase in the number of ultrasonic vocalizations in the 50 kHz band, a dose-dependent effect, was observed. The level of sexual motivation evaluated by mount latency was not influenced by inhibition of NO synthesis.

Animals↗
PubMed1996

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

Hemodynamic consequences of the withdrawal of arterial chemoreceptor drive (ACD) by brief systemic hyperoxia were studied in 16 mild hypertensive subjects (HT) and in 16 healthy subjects (NT) in horizontal position at resting metabolic rate. In another 9 mild HT and match NT measurements were made in resting sitting position and during steady-state mild physical exercise on cycloergometer, (30% of VO2 max.) Tidal volume, minute ventilation, end tidal CO2 and O2 concentration, K+, Na+, pO2, pCO2 values in blood were recorded. Impedance reography was used for recording stroke volume (SV) and arm blood flow (ABF). Cardiac output (CO), ABF and arterial blood pressure (ABF) values were used for calculation of the total peripheral resistance (TPR) and vascular resistance in the arm (AVR). To assess the neurogenic circulatory response to withdrawal of ACD in HT attenuated by opposite peripheral effects of high oxygen, the values of AVR, ABP, TPR and AVR changes during brief hyperoxia in NT, assumed to be of peripheral origin, were subtracted from respective values in HT, assumed to be of mixed neurogenic and peripheral origin. In HT hyperoxia applied in sitting position produced a brief decrease in systolic and diastolic ABP by 5.4 +/- 0.8% and 3.4 +/- 1.1% respectively, of TPR by 12.4 +/- 3% and of AVR by 4.7 +/- 4.6%. Decrease in AVR during hyperoxia was significantly greater in sitting than in horizontal position. In NT hyperoxia produced opposite effects in ABP, TPR and AVR, as compared to those in HT. In HT subjects during steady-state exercise the TPR decreased by 21 +/- 3.7% reaching a value no different from that in NT. We suggest, that in primary hypertension neurogenic sympathoexcitatory ACD is augmented and interacts with the peripheral mechanisms related to tissue oxygen supply.

Adult↗
PubMed1995

Inhibition of nitric oxide synthesis potentiates the responsiveness of carotid chemoreceptors to systemic hypoxia in the rat.

Carotid sinus nerve afferent activity was recorded in the peripheral end of the cut carotid sinus nerves in rats anesthetized with urethane, paralyzed and artificially ventilated with pure oxygen in order to abolish any resting chemoreceptor activity. Hypoxic stimuli were applied by switching pure oxygen to a nitrogen/oxygen gas mixture in the inspiratory line, reducing end-tidal oxygen concentrations to 10% FETO2, 8% FETO2 and 6% FETO2 respectively. Each stimulus was applied for 60 s and ventilation was switched again to pure oxygen. Increases in the carotid sinus nerve activities were due to chemo- and not to baroreceptor stimulation as arterial blood pressure decreased during hypoxia. After administration of nitric oxide synthase blocker L-NG-nitroarginine methyl ester, 30 mg/kg weight i.v., chemoreceptor excitatory response to all hypoxic stimuli increased significantly. Subsequent administration of L-arginine, 300 mg/kg weight i.v., restored chemoreceptor response to hypoxia to initial magnitude. It is concluded that NO is generated in the carotid body and attenuates chemoreceptor responsiveness in rats in vivo, as reported on isolated carotid bodies in cats in vitro.

Afferent Pathways↗
PubMed1995

Dual response of cerebrocortical blood flow and arterial blood pressure to transient CO2 stimulus after inhibition of nitric oxide synthesis in rats.

Inhibition of nitric oxide synthase (NOS) by Nitro-L-arginine-methyl-ester (L-NAME 15 mg and 70 mg/kg i.v.) in 16 male Wistar rats anaesthetized with urethane, paralysed and artificially ventilated, increased significantly local peripheral vascular resistance in the parietal cortex (CVR) along with augmentation of the mean arterial blood pressure (MAP) and no change of the local cerebrocortical blood flow (CBF) recorded with a Laser-Doppler-Flowmeter. In 11 rats L-NAME reversed a pressor effect of brief hypercapnia induced by 10% CO2/air mixture (PaCO2 84.1 +/- 5 mm Hg) into a depressor response, reduced CBF response proportionally to the reduction of MAP and did not influence CVR response to CO2. In 5 rats L-NAME did not abolish the central pressor effect of a CO2-stimulus and significantly augmented CO2-induced vasodilatatory response in the cortex (43.4 +/- 24% before L-NAME and 137.8 +/- 38.8% after L-NAME) by a larger reduction of CVR (-11 +/- 8% before L-NAME and -47.1 +/- 7.6% after L-NAME). It is concluded that NO does not mediate the vasodilatatory effect of brief hypercapnia in the cortex. NO appears critical for the central pressor effect of CO2. In those rats in which the central pressor effect of a CO2-stimulus was not abolished by an NOS blocker, an increased CBF and augmented decrease in CVR was observed during brief hypercapnia. Possible mechanisms of this dual responsiveness of cortical blood flow and arterial blood pressure to CO2, induced by inhibition of NOS, are discussed.

Amino Acid Oxidoreductases↗
PubMed1995

Modulation of human sympathetic periodicity by mild, brief hypoxia and hypercapnia.

We determined the influence of brief mild normocapnic hyperoxia, hypoxia, and hyperoxic hypercapnia on human muscle sympathetic nerve activity and R-R intervals, as quantified by both time- and frequency-domain analyses. We obtained measurements in nine healthy young adult men and women during uncontrolled and frequency (but not tidal volume) controlled breathing. Responses were evaluated with forward selection and backward elimination statistical models, with muscle sympathetic nerve activity as the dependent variable, and power spectral techniques. Hyperoxia and hypoxia did not alter arterial pressure; hypercapnia increased diastolic pressure modestly. Average R-R intervals tended to increase during hyperoxia, and decrease during hypoxia and hypercapnia. During uncontrolled breathing, changes of inspiratory gases exerted only minor effects on muscle sympathetic nerve activity; during controlled breathing, both hypoxia and hypercapnia tended to increase muscle sympathetic nerve activity. Statistical modeling suggested that chemoreceptor stimulation increased muscle sympathetic neural outflows, but that increases of sympathetic traffic were opposed by secondary increases of ventilation. Inspiratory gases modulated the frequency distribution of muscle sympathetic nerve activity strikingly: hypoxia increased sympathetic power at respiratory frequencies and hypercapnia increased sympathetic power at both respiratory and (primarily in one subject) cardiac frequencies. Our data suggest that mild brief hypoxia and hypercapnia increase human muscle sympathetic nerve activity, but that this tendency is opposed by chemoreflex-induced increases of ventilation. Our results suggest also that chemoreceptor activity exerts important influences on the frequency content, as well as the quantity of sympathetic neural outflow.

Adult↗
PubMed1995

Role of the endogenous nitric oxide in the vasodilatory tone and CO2 responsiveness of the rostral ventrolateral medulla microcirculation in the rat.

The study was designed to check the role of endogenous NO in maintaining the vasodilatory tone and in mediation of local cerebral blood flow (CBF) responses to CO2 in rostral ventrolateral medulla (RVLM) in the rat. The ventral surface of the medulla was exposed and CBF in the RVLM continuously recorded with a laser-Doppler flowmeter. Local vascular resistance (CVR) was estimated as the ratio of mean arterial pressure (MAP) to CBF. During 1 min exposure to 10% CO2 in oxygen PaCO2 rose from 39.9 +/- 2 mm Hg to 89.7 +/- 4.6 mm Hg and pH fell from 7.4 +/- 0.04 to 7.1 +/- 0.03. After intravenous administration of 15 mg/kg L-NAME (Nitro-L-arginine-methyl ester) MAP increased by 43 +/- 2.9 mm Hg (p < 0.001), local CBF increased by 33 +/- 6% (p < 0.001) and CVR increased by 17 +/- 6% (p < 0.01). L-NAME significantly reduced CBF flow response to 60 s hypercapnia from 47 +/- 9% (p < 0.001) before administration of L-NAME to 14 +/- 5% (p < 0.001). This effect was due to reversal by L-NAME of a pressor response to hypercapnia to a depressor response. The attenuation of CVR response to CO2 by L-NAME was too small to account alone for the significant reduction of local CBF responsiveness to hypercapnia. We conclude that endogenous NO plays a role in maintaining a local vasodilatory tone in RVLM, but it is less significant than in the cortical microcirculation. NO is not a major mediator in the increase in local CBF in RVLM during brief hypercapnia. Endogenous NO is critical for the neurogenic pressor response to brief hypercapnia.

Animals↗
PubMed1994

Homeodynamics versus homeostasis: periodicities superimposed on non-linear dynamic sympathetic tone generated in ventral medulla.

Homeodynamics based on theories of complexity and chaos and its impact on mechanisms generating sympathetic activity are presented. Activity in rats cervical, lumbar and renal sympathetic nerves was analyzed. In time domain glutamate stimulation of neurons within medullary periambigual area (PAA) disturbed temporal pattern of respiratory-sympathetic synchronization. Divalént calcium antagonists, Co2+ and Mg2+, blockers of synaptic transmission, uncoupled respiratory oscillator and sympathetic activity. PAA neurons act as an interphase between different subsets of respiratory neurons and bulbospinal sympathoexcitatory neurons in rostral ventrolateral medulla (RVLM). In frequency domain sympathetic activity analyzed by FFT algorithm and power density spectra (PDS) exhibited periodicities at the range from 0.4 Hz to 7.5 Hz. Blockers of synaptic transmission microinjected bilaterally into RVLM reduced total power exhibited in PDS to low level of magnitude generated in spinal cord and increased total, yet non-synchronized sympathetic activity and arterial blood pressure. A two component hybrid model of generation of sympathetic activity was proposed: a tone-generating system confined mainly to intrinsic activity of RVLM pacemaker neurons responsible for chaos-like discharges and a second component-neuronal circuits superimposed on tone-generating neurons and shaping the pattern of PDS. Contribution of spinal cord oscillatory mechanism to overall power of sympathetic periodicities was discussed.

Animals↗
PubMed1993

The excitatory response of the adrenal sympathetic nerve to severe hypoxia decreases in aged rats.

The age-related changes in the sensitivity of the adrenal sympathetic nerve to hypoxia were investigated in anesthetized young adult (3-4 months old) and aged rats (25-26 months old). Hypoxia with end-tidal O2 concentration (FETO2) at 6-2% caused excitation of adrenal nerve activity in the young adult and the aged rats. There was a significant decrease in the responses at 3 and 2% FETO2 in the aged rats compared to the young adult rats at either peripheral chemoreceptors-intact or -denervated condition. Reduced responsiveness of the central chemoreceptors to severe hypoxia is suggested as a possible factor in the age-related decreases.

Adrenal Medulla↗
PubMed1993

Role of the central and arterial chemoreceptors in the response of gastric tone and motility to hypoxia, hypercapnia and hypocapnia in rats.

The contribution of autonomic nerve activity to stomach tone and motility during central and arterial chemoreceptor excitation or inhibition was analyzed in urethane anesthetized, artificially ventilated rats. Systemic severe hypoxia at end-tidal O2 concentration (FETO2) 6% and systemic hypercapnia at end-tidal CO2 concentration (FETCO2) 6%, 8% and 10% applied for 1 min produced a significant depression in gastric tone and motility. Hypocapnia at 3% FETCO2 increased gastric tone and motility. Hypoxia co-activated both the sympathetic and the vagal efferent gastric nerve branches. Hypercapnia augmented only sympathetic gastric efferent nerve activity but not vagal efferent nerve activity. Hypocapnia slightly increased vagal nerve activity to the stomach. Bilateral denervation of the arterial chemoreceptors significantly attenuated the inhibitory gastric response to hypoxia. Similar attenuation of hypoxia-induced depression of gastric tone and motility was produced by bilateral gastric sympathectomy but not by vagotomy. In contrast, the inhibitory effect of severe hypercapnia and the facilitatory effect of hypocapnia upon gastric tone and motility were unaffected by arterial chemoreceptor denervation, by severance of gastric sympathetic branches or by gastric vagal denervation. Hyperoxia at 90% FETO2 had no effect on the gastric nerve activities, gastric tone or motility. It is concluded that in the rat hypoxia co-activates sympathetic and vagal efferent nerve activities to the stomach via an arterial chemoreceptor reflex, and that hypercapnia activates sympathetic gastric nerve activity via central chemoreceptors. Hypocapnia activates efferent vagal gastric nerve activity. All chemical stimuli except that of hyperoxia have a significant local effect on the gastric tone and motility.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Fast inhibitory postsynaptic potentials and responses to inhibitory amino acids of sympathetic preganglionic neurons in the adult cat.

Intracellular recordings were obtained from sympathetic preganglionic neurons (SPNs) of the intermediolateral nucleus (IML) in slices of upper thoracic spinal cord of the anesthetized cat. A total of 44 neurons was studied. Single shock stimulation of an area of white matter dorsolateral to the IML, close to the recording electrode (< 0.5 mm), evoked fast IPSPs with rise time of 3.8 ms and 1/2 decay time of 14.7 ms (n = 12). In 17 other cells only fast EPSPs were recorded but, after suppression of the EPSPs by the excitatory amino acid receptor antagonists CNQX (20 microM) and APV (100-250 microM), fast IPSPs were unmasked. The IPSP reversed polarity at -63 mV (-67 mV in the presence of CNQX and APV). The reversal potential shifted to a less negative value when the extracellular chloride concentration was reduced. The IPSP was reversibly abolished by the GABAA receptor antagonist bicuculline in 32% of the cells, by the glycine receptor antagonist strychnine in 47% of the cells and by the combination of the two in 21% of the cells. The IPSP was abolished by TTX (0.5 microM), had constant latency and showed no failures during high frequency stimulation. The IPSP presumably resulted from the excitation of inhibitory axons and/or inhibitory neuron somata with monosynaptic connections to the SPN. Glycine and GABA (1-3 mM) produced hyperpolarization associated with decreased membrane resistance. Sixty-nine percent of cells responded to both agonists, 19% to glycine only and 12% to GABA only. The GABAB agonist baclofen (5 microM) had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗
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↗