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Biomedical subjects

A Trzebski

Publications and source records attributed to A Trzebski.

At least 55 records · Page 3Linked to original sources
PubMed1984

Effects of carotid chemoreceptor excitation on medullary expiratory neurons in cats.

A previous report (Lipski et al., 1977, J. Physiol. (London) 269, 797-810) demonstrated an inhibition of the medullary dorsal inspiratory neurons when a phasic chemoreceptor stimulus was applied during expiration. The present study tested the response of expiratory neurons which might mediate this inhibition. Recordings were made in cats anaesthetized with chloralose-urethane from the C5 phrenic rootlet and mainly from the rostral (Bötzinger) and caudal (nucleus retroambigualis, NRA) groups of medullary expiratory neurons. Carotid chemoreceptors were excited by close arterial injections of CO2-equilibrated saline. The stimuli were applied automatically with a preset delay within the respiratory cycle. The stimuli applied in inspiration excited both the phrenic activity and ventral inspiratory neurons within less than 0.5 sec. The stimuli applied in expiration excited 17 out of 25 NRA units, none of which projected to the contralateral dorsal (NTS) respiratory group. Four out of 9 units within be responsible for the expiratory inhibition of NTS inspiratory cells produced by chemoreceptor stimulation, while the caudal expiratory neurons are involved in the mediation of the chemoreceptor-induced effects upon the spinal neurons.

Animals↗
PubMed1984

Pressor effect of CO2 in the rat: different thresholds of the central cardiovascular and respiratory responses to CO2.

Rats were anesthetized with urethane and the vagi, aortic and carotid sinus nerves were sectioned bilaterally. Hypocapnia was induced by artificial hyperventilation with 100% O2. Administration of 5% CO2 in O2, without alteration of the respiratory rate or tidal volume, induced significant increases in mean systemic arterial pressure ( mSAP ) in rats with intact central nervous system (CNS) and after midcollicular section (36 +/- 4 and 34 +/- 2 mm Hg, respectively; mean +/- S.E.). Smaller but significant increases in mSAP (17 +/- 3 mm Hg) were induced by inhalation of 5% CO2 after section of the spinal cord at the C4 level. Ganglionic blockade with hexamethonium completely abolished the pressor response to CO2. In hypocapnic (paCO2 15.5 +/- 0.7 mm Hg) apneic rats with intact CNS, after denervation of the peripheral chemoreceptors, inhalation of 1.5% CO2 in O2 increased paCO2 to 22.3 +/- 1.2 mm Hg and mSAP by 16 +/- 1 mm Hg, but the animals remained apneic for up to 45 min of continuous CO2 administration. Higher FICO2s induced further immediate increases in mSAP and, after delays of up to 6-7 min, also a resumption of central rhythmic respiratory activity (monitored by the intercostal muscles or phrenic nerve electrogram). The paCO2 threshold for this respiratory response was 25 +/- 1 mm Hg. When rhythmic respiratory activity resumed, a further slight increase in mSAP and the appearance of respiratory modulated oscillations of the SAP were observed in most animals. When, after a period of CO2 inhalation, 100% O2 was again administered to the animals mSAP fell immediately, reaching the control level within 20-30 s, while the respiratory activity, if present, disappeared only after 1.5-2 min. From these experiments we conclude that in the hypocapnic rat, after denervation of the peripheral chemoreceptors: (1) CO2 induces a neurogenic hypertensive response even in the absence of rhythmic respiratory activity; (2) the central chemosensitive sites appear to be located in the ponto-medullary region and in the spinal cord; and (3) the central mechanisms responsible for the pressor response have a lower CO2 threshold and a much shorter latency than those responsible for the initiation of the rhythmic respiratory activity.

Animals↗
PubMed1982

Increased sensitivity of the arterial chemoreceptor drive in young men with mild hypertension.

Ventilatory, airway occlusion pressure, arterial blood pressure and heart rate responses to isocapnic progressive hypoxia and to hypercapnia in high oxygen, both induced by a rebreathing method, were measured in 20 hypertensive male subjects aged 20 to 21 years with a diastolic blood pressure of 13.1 KPa +/- 0.34 SD (98 mmHg +/- 2.6 SD) and in 20 age-matched normotensive male subjects. Ventilatory, airway occlusion pressure and blood pressure response to hypoxia was significantly greater in the hypertensive subjects. Hypoxic ventilatory drive measured as the parameter A denoting the shape of the V1-O2 curve was 28.8 +/- 2.7 SEM (range 7.0 to 44.2) in the normotensive group and 116.1 +/- 10.5 SEM (range: 71.6 to 234.77) in the hypertensive group, the difference being highly significant (P less than 0.001). The magnitude of respiratory sinus arrhythmia (RSA) recorded during progressive hypoxia and plotted against either PA. O2 or VI values was significantly greater in the hypertensive group. The difference in ventilatory and circulatory responses to hyperoxic hypercapnia between the two groups of subjects was not significant. There was a significant correlation between the responses to hypoxia and hypercapnia in the normotensive subjects (r = 0.56, t = 2.861, P less than 0.01) but no correlation in the hypertensive subjects (r = 0.07). It is concluded that dissociation of the responsiveness of the peripheral and central chemosensitivity, the former being significantly increased and predominant, occurs in early, mild hypertension.

Adult↗
PubMed1981

Is the central inspiratory activity responsible for pCO2-dependent drive of the sympathetic discharge?

Out of 27 cats anesthetized with chloralose-urethane mixture, paralyzed, vagotomized and artificially ventilated, phrenic nerve response to systemic hypercapnia (7-8 vol.% CO2/O2 mixture) was accompanied by an increase in blood pressure and sympathetic discharge in 19 cats. Out of these 19 cats, 12 were totally debuffered and in the remaining 7 cats one carotid sinus nerve was left intact. Single unit activity in the sympathetic cervical nerve and spontaneous mass activity in the cervical, splanchnic, renal sympathetic and phrenic nerves were recorded. Evoked response in the phrenic nerve was produced by electrical stimulation of the descending bulbospinal inspiratory pathways in the midplane area of the medulla or in the ventrolateral cervical spinal cord. Starting from the control mean end-tidal CO2 concentration of 4.7 vol.% (+/- 1.0 S.D.) a progressing hypocapnia was induced by hyperventilation up to the end-tidal CO2 concentration of 1.3-3.2 vol.% (mean 2.4 vol.% +/- 0.5 S.D.) significantly below paCO2 apneic threshold. In chemo- and baroreceptor denervated cats with a pressor and excitatory sympathetic response to hypercapnia, a hypocapnia resulted in a fall of the arterial blood pressure (mean 16.9 mm Hg +/- 7.5 S.D., 2.2 kpa +/- S.D.). With the increasing paCO2 over the period of hypocapnic apnea a pressor and excitatory sympathetic response preceded, in all experiments, the onset of the phrenic nerve rhythmic activity. The difference between paCO2 threshold for the pressor and sympathetic response (35.7 mm Hg +/- 3.6 S.D., 4.7 kpa +/- 0.5 S.D.) and paCO2 threshold for the reappearance of the phrenic nerve rhythmic activity (43.6 mm Hg +/- 2.6 S.D., 5.8 kpa +/- 0.3 S.D.) was highly significant. If apneic hypocapnia was combined with the continuous stimulation of the afferent fibers of the superior laryngeal nerve the CO2 threshold for phrenic rhythmic activity was significantly increased whereas CO2 threshold for the pressor and sympathetic excitatory response remained unchanged. CO2 administration during hypocapnia apnea caused a progressing reduction of the magnitude of the evoked phrenic nerve response. From these findings it is concluded that the central excitatory effect of CO2 on the sympathetic activity may be accomplished in the absence of the rhythmic respiratory activity and independently of the subthreshold tonic inspiratory activity. Pressor and sympathetic excitatory response to CO2 observed during hypocapnic apnea is presumably caused by a neuronal pool different from that responsible for the central inspiratory activity. It is suggested that this CO2 sensitive neuronal mechanism might be involved in the central generation of sympathetic tone.

Animals↗
PubMed1981

The effect of activation of carotid body chemoreceptors on baroreceptor inhibition of sympathetic activity.

The effect of combined stimulation of peripheral chemo- and baroreceptors upon sympathetic discharge was studied in cats anesthetized with chloralose and urethan, immobilized with tricuran, and artificially ventilated. The right carotid sinus was arterially isolated, the left sinus nerve and both vago-sympathetic trunks were cut. A rise of pressure in isolated carotid sinus from 100 to 200 mm Hg produced an inhibition of sympathetic activity recorded simultaneously from the inferior cardiac and the renal nerves. For a combined chemo- and baroreceptor stimulation, the carotid sinus was perfused at a constant pressure of 100 mm Hg with venous blood bubbled with CO2.Twenty seconds after the onset of the perfusion the carotid sinus pressure was raised up to 200 mm Hg. A combination of the chemoreceptor stimulation and of the rise of sinus pressure produced only a small inhibition of sympathetic activity in both nerves compared to the effect observed without concomitant chemoreceptor activation. It was demonstrated that chemically induced stimulation of the carotid body chemoreceptors strongly influences the magnitude of the sympathetic inhibition produced by activation of the baroreceptor reflex.

Animals↗
PubMed1980

Carotid baroreceptor reflex in man, its modulation over the respiratory cycle.

Carotid baroreceptors were stimulated in 40 healthy volunteers by a rapid increase of the carotid transmural pressure due to subatmospheric pressure applied to a tight neck chamber (neck suction). Heart rate, arterial blood pressure and respiratory response were recorded. Reflex vagal inhibition of the sinus node preceded a blood pressure fall. Cardiac response adapted in a few seconds during prolonged baroreceptor stimulation, whereas reflex hypotension was maintained over the whole stimulation period applied up to 30 s. Augmented inspiratory movements were observed during neck suction. Short-lasting baroreceptor stimuli produced much less cardiac inhibition if applied during the early inspiratory than during the expiratory phase. On the peak and on the plateau of the voluntarily sustained deep inspirations, a spontaneous sinus bradycardia and a facilitation of the baroreceptor-cardiac reflex appeared. Voluntarily delayed expiration following deep and sustained inspiration coincided with cardioacceleration and baroreflex inbibition. Thus voluntarily Imposed, breathing patterns may reverse both respiratory sinus arrhythmia and cyclical modulation of the baroreflex responsiveness over the respiratory cycle.

Adult↗
PubMed1979

Excitability changes of dorsal inspiratory neurons during lung inflations as studied by measurement of antidromic invasion latencies.

(1) Glass microelectrodes were used to record extracellularly the activity of single dorsal (in the region of nucleus tractus solitarius (NTS)) inspiratory neurons in either chloralose- or pentobarbitone-anaesthetized, paralyzed cats. (2) In the lateral and ventral part of NTS, 89 cells were localized which responded antidromically to stimulation applied to the contralateral spinal cord (C3). Seventy were not excited by lung inflation and were classified as Ralpha, while 19 excited by that stimulus were classified as Rbeta. Usually Rbeta neurons fired both during each pump-induced lung inflation and during the central inspiratory excitation (CIE). (3) A technique similar to Merrill's recording small variations in the antidromic latency measured to the SD spike was used to ascertain excitability of Ralpha and Rbeta cells during the CIE time and during lung inflation in expiration. The technique was extended by averaging antidromic latency patterns within many respiratory cycles. (4) In the majority of Ralpha cells the averaging revealed a shortening of the antidromic latency during lung inflation in expiration, which indicated a subthreshold depolarization. Lengthening of the antidromic latency by this stimulus was never observed. These results are in disagreement with the concept of a direct inhibitory input from Rbeta to Ralpha neurons. (5) It is concluded that the dorsal Ralpha and Rbeta neurons differ less in their properties than was previously assumed on the basis of classical extracellular techniques. The inhibitory influence of pulmonary stretch receptor input on inspiratory discharge of Ralpha cells seems to be exerted through an indirect action on the source of the CIE.

Afferent Pathways↗