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PubMed2005

Thyroliberin blocks the potassium A-current in neurons in the respiratory center of adult rats in vitro.

Thyroliberin is a neuropeptide with marked respiratory activity. The neuronal mechanisms underlying this activity were addressed in experiments on transverse slices of brainstem from adult rats in conditions of membrane potential clamping to study effect effects of thyroliberin (10 nM) on the potassium A-current in neurons of two areas of the respiratory center--the ventrolateral areas of the solitary tract nucleus and the pre-Betzinger complex. The A-current, seen in all study neurons in the respiratory center, was partially and reversibly blocked by thyroliberin. A significant reduction in the amplitude of the current was accompanied by an increase in the inactivation constant. The effect of thyroliberin on the amplitude of the A-current was analogous to that of 5 mM 4-aminopyridine. These results show that the stimulatory effects of thyroliberin at the level of respiratory center neurons is at least partly explained by its ability to block the potassium A-current.

Animals↗
PubMed2005

Nitric oxide in the A5 region modulates reaction of the respiratory center and blood pressure to hypoxia in rats.

Hypoxia was followed by more pronounced activation of the respiratory center and pronounced hypotensive response after unilateral injection of nitric oxide synthase blocker L-NAME into the A5 region. Microinjection of exogenous nitric oxide donor sodium nitroprusside into the A5 region abolished the effect of L-NAME on hypoxia-induced changes in activity of the respiratory center and blood pressure. Bilateral transection of the vagal and sinocarotid nerves suppressed the response of the respiratory center to hypoxia. However, the hypotensive response to hypoxia in these rats did not differ from that in intact animals. Under conditions of peripheral chemoreceptor deafferentation, the hypotensive response to hypoxia did not differ before and after blockade of nitric oxide synthase in the A5 region. The regulation of respiratory center activity and blood pressure during hypoxia was modulated by A5 neurons with the involvement of nitric oxide.

Animals↗
PubMed1982

[Compensatory reactions of the respiratory center and their manifestations at the periphery of animals with respiratory tract and lung injuries].

The microelectrode and stereotaxic techniques were used in experimental injuries to the respiratory tract and lungs to demonstrate that the respiratory center (RC) was in a state of enhanced excitation whatever the focus of injury. It was found that the efferent flow of impulses from the RC was not uniformly manifested by electrical activity of the respiratory muscles. In tracheitis, the respiration was effected by the inspiratory and expiratory muscles but remained of the diaphragmal type. Considerable reserve possibilities of the RC compensation were discovered in response to additional adequate stimulants. In unilateral pneumonia, the electrical activity of the diaphragm and that of different groups of the expiratory muscles were found to be enhanced, whereas the respiration became of the diaphragmal-abdominal type. The compensatory reactions of the RC were unchanged. In grave bilateral injuries to the lungs, the main factors having a stimulant action on the RC were additional resistance to the respiration and developing hypoxemia. At the same time there was a decrease in the electrical activity of the respiratory muscles. There is every reason to believe that the decline in the electrical activity of the respiratory muscles serves an important protective reaction of the body in grave lung injuries.

Abdominal Muscles↗
PubMed1975

Occlusion pressure as a measure of respiratory center output in conscious man.

The output of the "respiratory centers" has been estimated by measuring ventilation, inspiratory muscle power, EMG of the diaphragm, and by various other means, each of which has serious disadvantages. The static pressure generated by the inspiratory muscles at FRC against an obstructed airway is here suggested as a useful alternative. Ten conscious, normal, sitting human subjects were subjected to CO2 rebreathing (Read, 1967) and their airways were occluded at end-expiration at intervals without the subjects being aware in advance. The inspiratory pressure waves so generated were found to be distorted by conscious or unconscious responses to the occlusion which had a minimum latency of 0.15 sec. The pressure generated at 0.1 sec after the onset of inspiration (P0.1) was nevertheless easy to measure and was reproducible in each subject. The CO2 response obtained by plotting P0.1 against PCO2, was curvilinear, the P0.1 increasing more rapidly at high PCO2. The P0.1 is independent of pulmonary mechanics. Since it measures the rate of rise of inspiratory activity and not the peak activity it is also independent of mechanisms that alter the respiratory pattern by affecting inspiratory duration, in particular the vagal volume-related inspiratory-inhibitory reflex. It is concluded that measurements of P0.1 represent a useful index of the output of the respiratory centers.

Airway Obstruction↗
PubMed1983

Effects of aminophylline on respiratory center and reflex activity in premature infants with apnea.

Fourteen preterm infants with apnea (body weight, 1052 +/- 44 g; gestational age, 30.2 +/- 0.5 wks; and postnatal age, 9.9 +/- 1.5 days) were studied in an effort to evaluate the effects of aminophylline on respiratory center output and respiratory reflex activity in the preterm infant with idiopathic apnea. This was done by using the airway occlusion technique. The infants were studied before and 48 h after aminophylline was begun as a treatment for apnea. Occlusion pressure, which reflects respiratory center output, was measured at 100 msec after occlusion started (P100) and at its maximum (Pmo). P100 increased from 2.4 +/- 0.2 to 3.1 +/- 0.2 cmH2O (P less than 0.005), and Pmo from 6.1 +/- 0.7 to 8.8 +/- 1.0 cmH2O (P less than 0.001) after aminophylline therapy was started. The % prolongation of inspiratory time during the occluded breaths, when compared to the unoccluded breaths increased from 26.2 +/- 10.6 to 55.8 +/- 12.5% (P less than 0.01). This reflects a significant increase in the strength of the Hering Breuer reflex. Effective elastance, a measure of respiratory load compensation, was significantly higher during aminophylline treatment. It increased from 1.09 +/- 0.14 to 1.33 +/- 0.14 cmH2O/ml (P less than 0.02).

Aminophylline↗
PubMed1990

[The effect of the somatic afferentation on the activity of the respiratory center].

Contraction of the muscles of flexing and stretching hind-limbs changed the indexes of external respiration and activity of the medulla neurons. The neurons of the respiratory center differed in direction and intensity of their responses and ability of convergence of afferent signals from both muscles. The ways of afferents from flexing and stretching muscles into the respiratory center were studied with the method of evoked potentials. They represented both simple and complex functional links, with the participation of medullary somatic nuclei. The data obtained revealed the role of the respiratory center different structures and neurons in the participation of the muscle afferents in the respiration control.

Afferent Pathways↗
PubMed1979

[The rate of isometric inspiratory pressure change as a measure for the CO2 sensitivity of the respiratory center in patients with obstructive lung disease].

In healthy persons with and without loaded breathing, in asthmatics, and in patients with chronic obstructive lung disease (COLD) the rate of isometric inspiratory pressure development ([dp/dt]max) has been measured in order to assess the clinical significance of (dp/dt)max as an index of the motor output of the respiratory center in response to increased levels of carbon dioxide. During unloaded breathing normal subjects showed an excellent correlation between the ventilatory and the (dp/dt)max responses to CO2. Normal persons breathing through an external expiratory flow resistance, the asthmatics, and the patients with COLD had not only a blunted ventilatory response, but also a reduced (dp/dt)max response. The parallel changes observed in both variables indicate that under conditions of mechanical loading the (dp/dt)max does not exclusively reflect the motor output of the respiratory center, but is influenced by other factors such as the work of breathing and the mechanical efficiency of the respiratory pump. Accordingly, measurements of (dp/dt)max are of little help in deciding whether the development of CO2 retention in patients with obstructive airway disease is primarily due to increased mechanical load or to decreased sensitivity of the respiratory center.

Adult↗
PubMed1991

High pressure reduces pH sensitivity of respiratory center in isolated rat brainstem.

We examined the effect of high pressure (10.1 MPa) on the sensitivity of the respiratory center to alterations in pH (range 5.8-7.6) which were obtained by varying either PCO2 or [HCO3-] in superfused Krebs solution. Isolated rat brainstem-spinal cord preparations were placed in a pressure chamber and respiratory-related motor neuron activity was recorded from severed ventral roots C1 and C5. At atmospheric pressure, respiratory burst frequency in both C1 and C5 varied inversely with pH. Only the time integral of a single C5 response was sensitive to acidification. High helium pressure reduced by 60% the sensitivity of the respiratory frequency to alteration in pH, while the time integral of both C1 and C5 responses became independent of PCO2, causing the relative respiratory drive between the two roots to change. These modifications in the chemoresponse of the respiratory center may contribute to the respiratory difficulties encountered under high pressure conditions.

Animals↗
PubMed2004

Effects of thyroliberin on membrane potential and the pattern of spontaneous activity of neurons in the respiratory center in in vitro studies in rats.

Patch-clamp experiments on transverse brainstem slices from rats were performed to study the effects of thyroliberin (10(-8) M) on the membrane potential and spontaneous activity of neurons in two areas of the respiratory center: the ventrolateral area of the solitary tract nucleus and the pre-Botzinger complex. Thyroliberin induced membrane depolarization of neurons in the respiratory center and increased their spike activity. The pattern of activity of neurons in the pre-Botzinger complex showed decreases in the time intervals between the beginnings of bursts in response to thyroliberin. In some cases, thyroliberin led to the appearance of spike activity in initially "silent" neurons; "silent" neurons in the solitary tract nucleus became tonically active, while those in the pre-Botzinger complex showed burst activity. These results provide evidence for the existence of an indirect regulatory influence for thyroliberin on respiratory center neurons, operating at the membrane level.

Animals↗
PubMed2006

The effects of leucine-enkephalin on the membrane potential and activity of rat respiratory center neurons in vitro.

Studies of transverse slices of Wistar rat brainstem using a patch clamp technique addressed the effects of the opioid peptide leucine-enkephalin (10 nM-1 microM) on the membrane potential and pattern of spontaneous activity of neurons in two parts of the respiratory center: the ventrolateral area of the solitary tract nucleus and the pre-Bötzinger complex. Leucine-enkephalin induced membrane hyperpolarization of respiratory center neurons and decreased the level of spike activity in spontaneously active cells. In pre-Bötzinger complex neurons showing a burst pattern of activity, leucine-enkephalin decreased the burst frequency, and two cells showed a transition from burst activity to tonic activity. These results provide evidence that the mechanism of the central respiratory activity of leucine-enkephalin results from its direct action on the membranes of respiratory center neurons.

Action Potentials↗
PubMed2002

Functional reconnections established by central respiratory neurons regenerating axons into a nerve graft bridging the respiratory centers to the cervical spinal cord.

The present work investigated, in adult rats, the long-term functional properties and terminal reconnections of central respiratory neurons regenerating axons within a peripheral nerve autograft bridging two separated central structures. A nerve graft was first inserted into the left medulla oblongata, in which the respiratory centers are located. Three months later, a C3 left hemisection was performed, and the distal tip of the graft was implanted into the C4 left spinal cord at the level of the phrenic nucleus, a natural central inspiratory target. Six to eight months after medullary implantation, the animals (n = 12) were electrophysiologically investigated to test 1) the phrenic target reinnervation by analyzing the phrenic responses elicited by bridge electrical stimulation and 2) the bridge innervation by unitary recordings of the spontaneous activity of regenerated axons within the nerve bridge. In the control group (n = 6), the medullary site of implantation corresponded to the dorsolateral medulla, a region known to be an unsuitable site for inducing respiratory axonal regrowth after nerve grafting. Stimulation of the nerve bridge never elicited phrenic nerve response, and no respiratory units were found within the nerve bridge. In the experimental group (n = 6), the proximal tip of the nerve bridge was implanted within the ventrolateral medulla at the level of the respiratory centers. Electrical stimulation of the nerve bridge induced phrenic nerve responses that reflected a postsynaptic activation of the phrenic target. Subsequent unitary recordings from teased fibers within the bridge revealed the presence of regenerated inspiratory fibers exhibiting discharge patterns typical of medullary inspiratory neurons, which normally make synaptic contacts with the inspiratory phrenic target. These results indicate that, when provided with an appropriate denervated target, central respiratory neurons with regenerated axons along a nerve bridge can remain functional for a long period and can make precise and specific functional reconnections with central homotypic target neurons.

Animals↗
PubMed1981

[Activity of the respiratory center as a paired formation during stimulation of the anterior gyrus cinguli in rats].

A total of 65 acute experiments on rats anesthetized with urethane were made to study bioelectrical activity of the external intercostal muscles on the right and left sides of the chest and neuronal activity of both halves of the respiratory center during electrical stimulation (4--15 v, 60 Hz) of the right or left anterior gyrus cinguli. The data obtained showed varied asymmetrical and asynchronous changes in the electromyogram of the respiratory muscles and disclosed some features of the effect of the left and right anterior gyrus cinguli on the electromyogram of the respiratory muscles and diverse reactions of respiratory center neurons to unilateral stimulation of the gyrus cinguli. The presence of functional asymmetry of the right and left anterior gyrus cinguli and their effect on the respiratory center are suggested.

Animals↗
PubMedDate not supplied

[Effect of a hyperbaric nitrogen-oxygen atmosphere on respiratory center activity].

In anesthesized cats inspiratory activity of the respiratory center at first increased and then decreased with increases in total pressure of the nitrogen-oxygen atmosphere to 7, 11, and 21 atm (at normal PO2). The effort made by respiratory muscles increased gradually. These changes were augmented by hypercapnia. Possible role of nitrogen anesthesia and compensatory reactions to the increased breathing resistance in the department of the above changes is discussed.

Animals↗
PubMedDate not supplied

[The respiratory center in normal subjects at 2,240 meters above sea level. The ventilatory and occlusion pressure (P 0.1) responses upon CO2 stimulation].

Altitude hypoxia imposes acute changes and long term adjustments in the ventilation of human beings. Most of the present knowledge of the respiratory center behavior at high altitude derives from the studies of ventilatory response to both hypoxia and hypercapnea. Other indexes of respiratory center output such as the occlusion pressure (P 0.1) response to a variety of stimuli are at present being evaluated. We could not find, however, studies on the P 0.1 responses to CO2 at high altitude. In this study we analyze the ventilatory and P 0.1 responses to CO2 in a group of 32 normal subjects, all of them natives and residents of Mexico city (altitude of 2,240 meters) and we compared them with those reported at sea level. The slope of both, the ventilatory and P 0.1 responses to CO2 was found to be similar to that reported at sea level; 4.52 +/- 1.29 L. min. mmHg and 0.07 +/- 0.01 cm H2O/mmHg respectively. The crossing over of such responses, however, is shifted to the left of the reported at sea level. This means higher levels of both ventilation and P 0.1, for the same level of end-tidal PCO2, at high altitude. This finding might be explained in the basis of the so-called "acclimatization to hypocapnea".

Acclimatization↗
PubMed1995

Studies of the respiratory center using isolated brainstem-spinal cord preparations.

It has been ten years since a brainstem-spinal cord preparation isolated from a newborn rat was introduced for study of the mammalian respiratory center. Here, I briefly summarize first, these studies, which include the tissue condition of in vitro preparations, respiratory reflexes, pharmacology, rhythm generation, respiratory chemoreception, phrenic motoneurons, regulation from pons, and development of a respiratory center. In the latter half of this paper, I focus on the neural mechanisms of respiratory rhythm generation. A current hypothesis for the central pattern generator of respiration proposed by the author's group is that the respiratory rhythm generator, composed of pre-inspiratory neurons in the rostral ventrolateral medulla, produces the primary rhythm of respiration and triggers an inspiratory pattern generator composed of inspiratory neurons in the rostral and the caudal ventrolateral medulla.

Animals↗