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Influence of parasympathetic pathways on early post--infarction arrhythmias.

The close relation between heart rhythm disorders that follow acute myocardial infarction (MI) and autonomic nervous system activity has come into focus recently. In order to evaluate the influence of the parasympathetic outflow on the incidence and characteristics of the early arrhythmias that follow myocardial infarction, the authors developed an experimental model of MI in rabbits by acute occlusion of the left ventricular artery. They have found that after the acute experimental MI an early stage of rhythm disorders is developed in 60% of the animals. In a second group of animals submitted to vagotomy prior to coronary occlusion none of rabbits exhibited arrhythmias. A third experimental series was performed in animals pretreated with atropine before and during the coronary occlusion; in this group the incidence of arrhythmias was the same as in control animals. The haemodynamic data obtained from the animals pretreated with atropine were similar to those obtained in control animals. The influence of vagal afferent and efferent pathways and their role in the genesis of the early arrhythmias is discussed.

Animals↗

[Current concepts of the neuromorphology and neurochemistry of the striatal cholinergic system and its role in regulating movement].

The recent neuromorphological and neurochemical data are reviewed concerning the organization of the striatal cholinergic system. A conclusion is made that the nigrostriatal dopamine and intrastriatal acetylcholine have the opposite effects on the main efferent outputs of striatum, including the expression of peptides which determines their involvement. The crucial role was proposed of the striatal cholinergic system in switching on and regulation of the so called indirect efferent pathway which controls the main striatal targets: the medial part of globus pallidus and reticular part of substantia nigra. On the basis of experimental and clinical data, we have suggested an important role of the activation of the striatal cholinergic system in the muscle tone control and the control of the main component of postural adjustment (unloading the working limb), in the inhibition of phasic components of a movement, and in the inhibition of unwanted movements during a behavioural task realization. The conclusion was experimentally supported about the possibility of changes in the motor behaviour, using the adequate pharmacological influence on the striatal cholinergic system. At the same time, the long-term fixed imbalance in the function of striatal efferent systems leads to a pathology of motor activity. The increase in the striatal cholinergic activity and/or decrease in the nigrostriatal dopaminergic effects may be the cause of Parkinson's disease.

Animals↗

Orbicularis oculi and orbicularis oris reflexes in blepharospasm and torticollis spasmodica during spasm-free intervals.

To investigate possible abnormalities of the blink reflex pathways, we analyzed the latencies and amplitudes of the blink reflex responses in the orbicularis oculi (Ooculi) muscle, following supraorbital nerve stimulation, in 19 patients with blepharospasm, 16 patients with torticollis spasmodica and 22 control subjects. Furthermore, in order to examine the suprasegmental control of the responses, the reflex responses were also evoked in the orbicularis oris (Ooris) muscle after stimulation of the ipsilateral supraorbital nerve. The responses were recorded only when subjects had no contractions of the eyelid muscles, either involuntarily, voluntarily or spontaneously; this could be controlled by a sound signal. The metrics of the reflex responses in the Ooculi and Ooris muscles in patient groups were comparable to those in controls. Our data indicate that the afferent and efferent pathways of the reflex arc and the suprasegmental control of the reflex are intact in patients with blepharospasm and torticollis spasmodica, at least during spasm-free intervals. Alterations of responses may occur during spasms due to either segmental or suprasegmental changes.

Adult↗

Depression of the reflex tachycardia from the left atrial receptors by acidaemia.

1. The effects are described of an acidaemia, produced either by the inhalation of carbon dioxide or by an intravenous infusion of hydrochloric acid, on the reflex increase in heart rate which results from stimulation of the left atrial receptors in the anaesthetized dog.2. The results show that during acidaemia the reflex increase in heart rate from stimulation of the left atrial receptors is reduced. The extent of the reduction is related to the degree of the acidaemia.3. It is suggested that it is necessary to monitor and correct changes in the pH of arterial blood in experiments which involve reflex changes in heart rate, especially if the efferent pathway involves the sympathetic nerves.4. It is also suggested that the occurrence of such an acidaemia in anaesthetized surgically traumatized animals may be a factor contributing to the variability in results from investigations involving reflex changes in heart rate in response to stimulation of the left side of the heart.

Acidosis↗

Selective vagal postganglionic innervation of the sinoatrial and atrioventricular nodes in the non-human primate.

The distribution of parasympathetic postganglionic nerves to the atrioventricular (AVN) and sinoatrial nodal (SAN) regions was investigated in the non-human primate heart. Eight male monkeys (Macaca fascicularis) weighing 5.5-7.0 kg. were anesthetized (alpha-chloralose, 50 mg/kg and urethane, 500 mg/kg) and instrumented to measure arterial pressure, electrocardiogram, atrial and ventricular electrograms. The cervical vagi were electrically stimulated (20 Hz, 4 V, 2 ms) before and after selective denervation (D) of the AVN and/or SAN. Vagal stimulation was repeated during atrial pacing to assess parasympathetic modulation of AVN conduction. Ablation of parasympathetic pathways to the AVN, accomplished by the disruption of the epicardial fat and surface muscle layer at the junction of the inferior vena cava and inferior left atrium eliminated (P less than 0.01) the dromotropic effects of vagal stimulation without affecting the heart rate response (right vagus, before D, paced: atrial rate 218.0 +/- 6.3, ventricular rate 67.1 +/- 23.7; after D: atrial rate 210.3 +/- 6.4, ventricular rate 210.3 +/- 6.4 beats/min, means +/- S.D.). In sharp contrast, surgical dissection of the fat pad overlying the right pulmonary vein-superior vena cava junction significantly (P greater than 0.01) attenuated negative chronotropic effects of vagal stimulation (left vagus, before D the R-R interval increased by 832.7 +/- 146.4 ms, 209.5% increase; after D 37.4 +/- 18.0 ms, 8.8% increase). These data demonstrate discrete vagal efferent pathways innervate both the SAN and AVN regions of the non-human primate heart.

Animals↗

The effects of L-DOPA on regional cerebral glucose utilization in rats with unilateral lesions of the substantia nigra.

Using [14C]2-deoxyglucose autoradiography, we have studied the effects of systemically administered L-DOPA (10, 25 and 50 mg/kg s.c.) on regional cerebral glucose utilization (RCGU) in rats with unilateral substantia nigra lesions. In comparison with lesioned rats treated with saline, the lesioned-DOPA treated rats demonstrated contralateral turning and RCGU changes in both ipsilateral and contralateral brain regions. L-DOPA treatment markedly increased RCGU in the ipsilateral entopeduncular nucleus (EP) and substantia nigra pars reticulata (SNr), cell groups that receive direct striatal input and function as major outflow pathways of corpus striatal activity. In contrast, L-DOPA did not alter RCGU in the globus pallidus (GP), supporting the thesis that dopamine (DA) has different effects on striatal outflow to the GP compared with outflow to both the EP and SNr. Moderate RCGU increases were observed in the ipsilateral subthalamic nucleus (STN), lateral midbrain reticular formation (LMRF), and deep layers of the superior colliculus (DLSC), all regions which receive direct projections from the GP, EP or SNr. L-DOPA decreased RCGU in the ipsilateral lateral habenular nucleus (LHN) and increased RCGU in the contralateral LHN, changes that we suggest are mediated via altered neuronal activity in the striatum and EP. The results suggest that systemically administered L-DOPA, after conversion to DA in the brain, interacts with supersensitive DA receptors in the DA-depleted striatum to selectively activate efferent pathways. Furthermore, the data suggest that the LMRF and DLSC are functionally activated during L-DOPA induced turning and support the hypothesis that nigroreticular and nigrocollicular projections are of physiologic significance in the expression of striatal activity.

Animals↗

Paradoxical anticonvulsant activity of the excitatory amino acid N-methyl-D-aspartate in the rat caudate-putamen.

We used limbic seizures induced in rats by systemic injection of the cholinergic agonist pilocarpine (380 mg/kg; i.p.) to study the neuronal pathways within the basal ganglia that modulate seizure threshold. N-Methyl-D-aspartate (N-Me-D-Asp) is an excitatory amino acid derivative that is a powerful convulsant agent when injected into the cerebral cortex, amygdala, or hippocampus in rats. Bilateral microinjections of N-Me-D-Asp into the caudate-putamen, however, protected against limbic seizures induced by pilocarpine (injected systemically), with an ED50 of 0.7 nmol (range 0.5-1.0 nmol). Lesioning the caudate-putamen (by bilateral microinjection of the excitotoxin ibotenate) converted subconvulsant doses of pilocarpine into convulsant ones. The anticonvulsant action of N-Me-D-Asp in the caudate-putamen was reversed by blocking gamma-aminobutyrate-mediated inhibition in the substantia nigra pars reticulata or in the entopeduncular nucleus. The results suggest that the caudate-putamen and its gamma-aminobutyrate-dependent efferent pathways modulate the threshold for seizures in the limbic forebrain.

Animals↗

Visual pathways for postural control and negative phototaxis in lamprey.

The functional roles of the major visuo-motor pathways were studied in lamprey. Responses to eye illumination were video-recorded in intact and chronically lesioned animals. Postural deficits during spontaneous swimming were analyzed to elucidate the roles of the lesioned structures for steering and postural control. Eye illumination in intact lampreys evoked the dorsal light response, that is, a roll tilt toward the light, and negative phototaxis, that is a lateral turn away from light, and locomotion. Complete tectum-ablation enhanced both responses. During swimming, a tendency for roll tilts and episodes of vertical upward swimming were seen. The neuronal circuitries for dorsal light response and negative phototaxis are thus essentially extratectal. Responses to eye illumination were abolished by contralateral pretectum-ablation but normal after the corresponding lesion on the ipsilateral side. Contralateral pretectum thus plays an important role for dorsal light response and negative phototaxis. To determine the roles of pretectal efferent pathways for the responses, animals with a midmesencephalic hemisection were tested. Noncrossed pretecto-reticular fibers from the ipsilateral pretectum and crossed fibers from the contralateral side were transected. Eye illumination on the lesioned side evoked negative phototaxis but no dorsal light response. Eye illumination on the intact side evoked an enhanced dorsal light response, whereas negative phototaxis was replaced with straight locomotion or positive phototaxis. The crossed pretecto-reticular projection is thus most important for the dorsal light response, whereas the noncrossed projection presumably plays the major role for negative phototaxis. Transection of the ventral rhombencephalic commissure enhanced dorsal light response; negative phototaxis was retained with smaller turning angles than normal. Spontaneous locomotion showed episodes of backward swimming and deficient roll control (tilting tendency). Transections of different spinal pathways were performed immediately caudal to the brain stem. All spinal lesions left dorsal light response in attached state unaffected; this response presumably is mediated by the brain stem. Spinal hemisection impaired all ipsiversive yaw turns; the animals spontaneously rolled to the intact side. Bilateral transection of the lateral columns impaired all yaw turns, whereas roll control and dorsal light response were normal. After transection of the medial spinal cord, yaw turns still could be performed whereas dorsal light response was suppressed or abolished, and a roll tilting tendency during spontaneous locomotion was seen. We conclude that the contralateral optic nerve projection to the pretectal region is necessary and sufficient for negative phototaxis and dorsal light response. The crossed descending pretectal projection is most important for dorsal light response, whereas the noncrossed one is most important for negative phototaxis. In the most rostral spinal cord, fibers for lateral yaw turns travel mainly in the lateral columns, whereas fibers for roll turns travel mainly in the medial spinal cord.

Animals↗

Transtympanic pilocarpine in tinnitus.

In 48 patients who had neurosensory hypoacusia and whose main complaint was tinnitus, a 1% pilocarpine solution or a 2% carbachol Isopto solution was placed in the tympanic cavity by means of a No. 26 pencil-tipped lumbar puncture needle through the front quadrant of the eardrum. Patients were chosen without regard for age, gender, or topographical damage of the acoustic pathway. Evaluation of the drug's effect was performed audiometrically by masking with the minimum intensity of the pure sound or narrow band that most closely resembled the patients' own noises. The results of this medical therapy were positive and ranged from complete annulment to attenuation of the tinnitus, which was confirmed by audiometric masking 30 minutes after the intratympanic injection. These positive results reached 50% and would have been higher if the several cases submitted by accident insurance companies and cases of presbyacusia were discarded. The unsatisfactory element of the study was the short-term effect of the therapy, which usually lasted no more than 12-72 hours. Tinnitus reappeared in all patients at its original intensity. The best results involved the use of carbachol as compared with pilocarpine. The decision to replace pilocarpine with carbachol was based on the idea that the inhibitory cholinergic efferent pathways are damaged before the afferent pathways. The use of pilocarpine depends on efficient cholinergic functioning, as its activity is as an indirect agonist (i.e., to annul the cholinesterase enzyme).

Adult↗

Neurotransmission in the human labyrinth.

Different neuroactive substances have been found in the efferent pathways of both the olivocochlear and vestibular systems. In the present study, the distribution and role of three neurotransmitters, choline acetyltransferase (ChAT), gamma aminobutyric acid (GABA), and enkephalin were investigated in the human labyrinth of 4 normal-hearing individuals. Immunohistochemical studies in human inner ear research, however, face a problem of procuring well-preserved specimens with maintained neurotransmitter antigenicity and morphology. Methods and findings are reported and discussed.

Choline O-Acetyltransferase↗

Cholinergic and peptidergic projections from the medial septum and the nucleus of the diagonal band of Broca to dorsal hippocampus, cingulate cortex and olfactory bulb: a combined wheatgerm agglutinin-apohorseradish peroxidase-gold immunohistochemical study.

We have examined the distribution pattern and the density of various neuropeptide, neurotransmitter and enzyme containing neurons in the rat medial septum and the nucleus of the diagonal band of Broca to assess their possible involvement in the septohippocampal, septocortical and septobulbar pathways. Immunohistochemical methods were combined with the retrograde transport of a protein-gold complex injected in the hippocampus, the cingulate cortex or the olfactory bulb. Cholinergic neurons were the most numerous. Galanin-positive neurons were about two or three times less numerous than cholinergic cells. Both these cell types had a similar location though the choline acetyl transferase-like immunoreactive cells extended more caudally in the horizontal limb of the nucleus of the diagonal band of Broca. Immunoreactive cells for other neuroactive substances were few (calcitonin gene-related peptide, luteinizing hormone releasing hormone. [Met]enkephalin-arg-gly-leu) or occasional (dynorphin B, vasoactive intestinal polypeptide, somatostatin, neurotensin, cholecystokinin, neuropeptide Y and substance P). No immunoreactive cells for bombesin, alpha atrial natriuretic factor, corticotropin releasing factor, 5-hydroxytryptamine, melanocyte stimulating hormone, oxytocin, prolactin, tyrosine hydroxylase or arg-vasopressin were present. Choline acetyltransferase- and galanin-like immunoreactive cells densely participate to septal efferents. Cholinergic neurons constituted the bulk of septal efferent neurons. Galanin-positive cells were 22% of septohippocampal, 8% of septocortical, and 9% of septobulbar neurons. Galanin containing septohippocampal neurons were found in the medial septum and the nucleus of the diagonal band of Broca; galanin-positive septobulbar and septocortical cells were limited to the nucleus of the diagonal band of Broca. Occasional double-labellings were noticed with some peptides other than galanin. Luteinizing hormone-releasing hormone, calcitonin gene-related peptide and enkephalin were the most often observed; some other projecting cells stained for vasoactive intestinal polypeptide or dynorphin B. Luteinizing hormone-releasing hormone, calcitonin gene-related peptide and enkephalin were observed in septohippocampal neurons; luteinizing hormone-releasing hormone and vasoactive intestinal peptide were observed in septocortical neurons and calcitonin gene-related peptide, luteinizing hormone-releasing hormone and dynorphin B were observed in septo-bulbar cells. These results show that, in addition to acetylcholine, galanin is a major cellular neuroactive substance in septal projections to the hippocampus, the cingulate cortex and the olfactory bulb. The presence of septal projecting neurons immunoreactive for other peptides shows that a variety of distinct peptides may also participate, but in a smaller number, to septal efferent pathways.

Animals↗

Role of integrin CD103 in promoting destruction of renal allografts by CD8 T cells.

Infiltration of CD8(+)TCRalphabeta(+) T-effector populations (CD8 effectors) into graft epithelial compartments has long been recognized as a key lesion in progression of clinical renal allograft rejection. While the afferent phase of allograft immunity is increasingly well-defined, the efferent pathways by which donor-reactive CD8-effector populations access and ultimately destroy the graft renal tubules (rejection per se) have received remarkably little attention. This is an important gap in our knowledge of transplantation immunology, because epithelial compartments comprise the functional elements of most commonly transplanted organs including not only kidney, but also liver, lung, pancreas, and intestine. Furthermore, there is increasing evidence that attack of graft epithelial elements by CD8-effector populations not only causes short-term graft dysfunction but is also a major contributor to development of chronic allograft nephropathy and late graft loss, which now represent the salient clinical problems. Recent studies of the T-cell integrin, alpha(E)beta(7) (CD103), have provided insight into the mechanisms that promote interaction of CD8 effectors with graft epithelial compartments. The purpose of this communication is to review the known properties of the CD103 molecule and its postulated role in the efferent phase of renal allograft rejection.

Antigens, CD↗

Feeding induced by injections of muscimol into the substantia nigra of rats: unaffected by haloperidol but abolished by large lesions of the superior colliculus.

Intense activation of central dopamine systems has been associated with oral stereotyped behaviour, whereas less intense stimulation of these systems can increase feeding in non-deprived animals. There are several lines of evidence which suggest that the gamma-aminobutyric acid-containing striatonigral and nigrotectal projections are essential pathways mediating dopamine-related oral stereotypy. The present series of experiments was conducted to examine whether the same output route also mediates dopamine-related feeding. In the first experiment it was shown that bilateral injections of a sub-stereotypic dose of muscimol (0.05 nM) into the substantia nigra increased feeding of non-deprived rats. In Experiment II the feeding response was further characterised by demonstrating that food intake was initially suppressed for 30 min after which it was potentiated for 90 min. In Experiment III it was shown that a single dose of haloperidol (0.4 mg/kg), which was adequate to suppress overall food intake, was ineffective in preventing the increase in feeding produced by intranigral muscimol (0.05 nM). In contrast, it was demonstrated in Experiment IV that large lesions of the superior colliculus completely abolished the muscimol-induced increase in feeding. These results suggest that the striatonigral and nigrotectal projections may be important efferent pathways for both the oral stereotypy and the feeding responses linked with central dopamine transmission.

Animals↗

Axonal projections from respiratory centres towards the rostral ventrolateral medulla in the rat.

1. Efferent pathways from brainstem respiratory centres towards bulbospinal tyrosine hydroxylase immunoreactive neurons were identified in the rat using a combination of electrophysiology, retrograde and anterograde tract-tracing, and immunohistochemistry. 2. Varicose axons originating from respiratory centres were found in close apposition to bulbospinal tyrosine hydroxylase immunoreactive neurons in the ventrolateral medulla. 3. These findings support the idea that respiratory rhythms in sympathetic nerves may be due to a synaptic connection between brainstem respiratory neurons and bulbospinal tyrosine hydroxylase immunoreactive neurons of the C1 cell group.

Animals↗

Transmitter systems involved in neural plasticity underlying increased anxiety and defense--implications for understanding anxiety following traumatic stress.

Lasting changes in anxiety-like behavior (ALB) may be produced in several ways. These include partial limbic kindling, injection of the beta-carboline FG-7142, and brief, non-injurious, exposure of rodents to cats (predator stress). Both seizures and FG-7142 induce long-term potentiation (LTP) in efferent pathways of the amygdala known to participate in feline defensive behavior. By comparing the behavioral and physiological effects of partial kindling and injection of FG-7142, NMDA-dependent LTP in the right amygdalo-periacqueductal gray (PAG) pathway emerges as being critical to maintained increases in feline ALB. A similar dependence on NMDA-mediated processes is described for lasting increases in rodent ALB following predator stress. The lasting aftereffects of predator stress on a variety of measures parallel many of the symptoms of post-traumatic stress disorder (PTSD). Support is provided for the idea that behavioral changes following FG-7142 and predator stress may model anxiety associated with PTSD. Moreover, it is suggested that both models share mechanisms in common involving the PAG. These mechanisms likely involve initiation of LTP by NMDA receptors, and prolongation of LTP by CCKB receptors. To the extent that response to the stressors reviewed here mimics the symptoms of PTSD, the data implicate NMDA-mediated processes in the creation of what van der Kolk has called permanent emotional memories in PTSD. Their representation may be in the form of NMDA-dependent LTP of transmission within the amygdala and between the amygdala and its efferents. CCK may play a pivotal role in prolonging limbic LTP and anxiety following traumatic stress. Since block of CCKB receptors before and after the stressor prevents lasting increases in ALB, pharmacological intervention to block CCK receptors shortly after a traumatic stressor might be efficacious in mitigating the permanence of these emotional memories.

Aggression↗

The effects of cerebellar stimulation on the motor cortical excitability in neurological disorders: a review.

The cerebellum regulates execution of skilled movements through neural connections with the primary motor cortex. A main projection from the cerebellum to the primary motor cortex is a disynaptic excitatory pathway relayed at the ventral thalamus. This dentatothalamocortical pathway receives inhibitory inputs from Purkinje cells of the cerebellar cortex. These pathways (cerebellothalamocortical pathways) have been characterized extensively using cellular approaches in animals. Advances in non-invasive transcranial activation of neural structures using electrical and magnetic stimulation have allowed us to investigate these neural connections in humans. This review summarizes various studies of the cerebellothalamocortical pathway in humans using current transcranial electrical and magnetic stimulation techniques. We studied effects on motor cortical excitability elicited by electrical or magnetic stimulation over the cerebellum by recording surface electromyographic (EMG) responses from the first dorsal interosseous (FDI) muscle. Magnetic stimuli were given with a round or figure eight coil (test stimulation) for primary motor cortical activation. For cerebellar stimulation, we gave high-voltage electrical stimuli or magnetic stimuli through a cone-shaped coil ipsilateral to the surface EMG recording (conditioning stimulation). We examined effects of interstimulus intervals (ISIs) with randomized condition-test paradigm, using a test stimulus given preceded by a conditioning stimulus by ISIs of several milliseconds. We demonstrated significant gain of EMG responses at an ISI of 3 ms (facilitatory effect) and reduced responses starting at 5 ms, which lasted 3-7 ms (inhibitory effect). We applied this method to patients with ataxia and showed that the inhibitory effect was only absent in patients with a lesion at cerebellar efferent pathways or dentatothalamocortical pathway. These results imply that this method activates the unilateral cerebellar structures. We confirmed facilitatory and inhibitory natures of cerebellothalamocortical pathways in humans. We can differentiate ataxia attributable to somewhere in the cerebello-thalamo-cortical pathways from that caused by other pathways.

Animals↗

Alterations of sensori-motor functions of the digestive tract in the pathophysiology of irritable bowel syndrome.

Pathophysiology of irritable bowel syndrome (IBS) is based upon multiple factors that have been organised in a comprehensive model centred around the brain-gut axis. The brain-gut axis encompasses nerve pathways linking the enteric and the central nervous systems and contains a large proportion of afferent fibres. Functionally and anatomically, visceral nerves are divided in to two categories: the parasympathetic pathways distributing to the upper gut through the vagi and to the hindgut, through the pelvic and pudendal nerves, and the sympathetic pathways, arising form the spinal cord and distributing to the midgut via the paravertebral ganglia. Several abnormalities of gut sensori-motor function have been described in patients with IBS. Abnormal motility patterns have been described at the intestinal and colonic levels. Changes in colonic motility are mainly related to bowel disturbances linked to IBS but do not correlate with pain. More recently, visceral hypersensitivity has been recognised as a main characteristic of patients with IBS. It is defined by an exaggerated perception of luminal distension of various segments of the gut and related to peripheral changes in the processing of visceral sensations as well as modulation of perception by centrally acting factors including mood and stress. Viscero-visceral reflexes link the two edges of the brain-gut axis and may account for the origin of symptoms in some pathological conditions. Recent advances in the understanding of the role of myenteric plexus allowed recognition of several neurotransmitters involved at the level of both the afferent and efferent pathways. Targeting the receptors of these neurotransmitters is a promising way for development of new treatments for IBS.

Animals↗

Spontaneous baroreflex modulation of heart rate and heart rate variability during orthostatic stress in tetraplegics and healthy subjects.

OBJECTIVE: This study was addressed to investigate the contribution of vagal and sympathetic mechanisms to the genesis of low-frequency (LF) oscillations of RR-interval. DESIGN: To this aim, we utilized the pathophysiological model of tetraplegics, who have intact vagal afferent and efferent pathways of the baroreceptor reflex arc but interrupted medullary-spinal sympathetic pathways. METHODS: We studied nine complete, traumatic, tetraplegics (C4-C7, TET) and 10 normally healthy subjects (NR) at rest and during physiological baroreceptors unloading induced by 70 degrees head-up tilt. Autoregressive power spectral analysis was used to investigate RR-interval and systolic arterial pressure (SAP) variabilities. Baroreflex modulation of sinus node was assessed by the spontaneous baroreflex sequences method. RESULTS: Both at-rest and during-tilt LF and high frequency (HF) components were detected in RR-interval of NR, whereas in TET only the HF component was observed in both conditions (with one exception). Baroreflex sensitivity (BRS) did not significantly differ between TET and NR at rest, and underwent a significant and similar decrease during tilt in both groups, being accompanied in NR by a significant increase in LF relative power. Spectral analysis of SAP provided results similar to RR-interval. Tilt also slowed the centre frequency of the LF components of RR-interval and SAP. CONCLUSIONS: During unperturbed physiological conditions, a change in efferent vagal activity to the heart from baroreflex stimulation by spontaneous arterial pressure changes, is unlikely to contribute on its own to the genesis of LF heart period oscillations in humans who lack the ability to modulate sympathetic nerve traffic to the heart. However, the possibility that a baroreflex modulation of LF oscillations require an intact sympathetic control should be carefully considered.

Adult↗