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PubMedDate not supplied

Abnormal respiratory drive in vibroacoustic disease.

INTRODUCTION: Central nervous system disorders in workers exposed to low frequency noise (LFN, < 500 Hz, including infrasound) were first observed 25 years ago among aircraft technicians. Concurrently, respiratory pathology was identified in these workers, and later reproduced in LFN-exposed animal models. Today vibroacoustic disease (VAD) is defined as the systemic pathology caused by excessive exposure to LFN. The respiratory tract continues to be under heavy scrutiny in both LFN-exposed humans and animal models and has been confirmed as a major target for LFN-induced damage. Given that both the respiratory and central nervous systems were compromised in these workers, it became pertinent to investigate the status of the neurological control of breathing in VAD patients. METHODS: The P- 0.1 value, a measure of the suction pressure developed at the mouth 0.1 seconds after the start of inspiration, depends on the respiratory centres and the autonomic nervous system pathway of the neural control of respiratory function. By rebreathing CO2, (6% in air) normal individuals present an average seven-fold increase in P0.1 (CO2) as compared to basal P- 0.1. Twenty-two male VAD patients (ave. age 50.5 +/- 8.5 years, range: 36-66 years) underwent the P0.1(CO2) index respiratory drive tests, as well as standard pulmonary function tests. Seven individuals (ave. age 42.4 +/-14 years, range: 25- 61 years) with reduced LFN exposure served as controls. RESULTS: Pulmonary function tests were normal in both VAD patients and controls. The P0.1 (CO2) in- dex was below average value in VAD patients (average: 22.9%) while it presented normal values in the control group (average > 60%). DISCUSSION: In the involuntary response to increased PCO2 levels, central chemoreceptors are responsible for 70% of the ventilatory stimulus. In VAD patients, this dysfunction may originate in the brainstem. This is corroborated by the fact that VAD patients register abnormal values for auditory brainstem evoked potentials, and disclose lesions with magnetic resonance imaging. The neurological control of breathing is compromised in VAD patients. The P0.1 (CO2) index may be a useful clinical indicator for VAD diagnosis and follow-up.

Adult↗
PubMedDate not supplied

Contrastive effects of prostaglandin F2 alpha on normal cardiac rhythm and ouabain-induced cardiac arrhythmias in cats: possible neural basis.

The effects of prostaglandin F2 alpha (PGF2 alpha) on normal cardiac rhythm and ouabain-induced cardiac arrhythmias were investigated in chloralose-anaesthetized cats. PGF2 alpha (1-16 micrograms/kg i.v. bolus) produced ventricular arrhythmias and few incidences of AV conduction disturbances in normal cats. Changes in heart rate and blood pressure caused by PGF2 alpha in normal cats were complex, namely a decrease, an increase, or an initial decrease followed by an increase. Bilateral vagotomy antagonized the ventricular arrhythmias, AV conduction disturbances and hemodynamic changes produced by 16 micrograms/kg i.v. PGF2 alpha. On the other hand, atropine (2 mg/kg i.v.) pretreatment blocked the AV conduction disturbances and the reduction in heart rate and blood pressure, but not the ventricular arrhythmias or the increase in heart rate and blood pressure caused by 16 micrograms/kg i.v. PGF2 alpha. The ventricular arrhythmogenic effect of PGF2 alpha was prevented by propranolol (1 mg/kg i.v.). Intervention with cardiotoxic doses of ouabain augmented the PGF2 alpha-induced AV conduction disturbances, sinus bradycardia and hypotension, and attenuated the ventricular arrhythmias. Subsequent bilateral vagotomy prevented the ouabain-potentiated PGF2 alpha-induced AV block and sinus bradycardia, attenuated the hypotension and further reduced the ventricular arrhythmias. PGF2 alpha (2-16 micrograms/kg i.v.), contrary to its arrhythmogenic effect in normal cats, mainly suppressed ouabain-induced ventricular and supraventricular arrhythmias in ouabain-intoxicated cats, but aggravated the same in few cats. PGF2 alpha (16 micrograms/kg), prior to ouabain administration, produced ventricular arrhythmias in a group of 8 cats and later, in the same group of animals, when tested on ouabain-induced arrhythmias, it mainly antagonized them. These results suggest that PGF2 alpha evokes an arrhythmogenic effect on cardiac rhythm of normal hearts and mainly an antiarrhythmic effect on ouabain-induced arrhythmias largely through the mediation of two functionally opposing excitatory and inhibitory autonomic neural reflex pathways, respectively. The afferents of these pathways are of vagal origin. The efferent pathways of the inhibitory and excitatory reflexes involve in part increased vagal activity and increased sympathetic activity to the heart, respectively. Alteration by ouabain of the arrhythmogenic nature of PGF2 alpha on normal heart to its antiarrhythmic effect on the arrhythmic heart may be due to its selective potentiating effect on the inhibitory reflex pathway.

Anesthesia↗
PubMed1989

Induction of tumorigenicity and lack of in vitro growth requirement for 12-O-tetradecanoylphorbol-13-acetate by transfection of murine melanocytes with v-Ha-ras.

A nontumorigenic line of murine melanocytes, Mel-ab, has been transfected with the v-Ha-ras gene under transcriptional control of the Moloney murine leukemia virus long terminal repeat. Transfectants produced rapidly growing undifferentiated melanomas in recipient mice. The inhibition of melanin production in transformed cells, observable both in vitro and in vivo, suggests that ras may affect melanocyte cytodifferentiation. Mel-ab cells require the continual presence of 12-O-tetradecanoylphorbol-13-acetate, or other activators of protein kinase C, for in vitro growth. Transfectants expressing v-Ha-ras no longer manifested this requirement and were actually growth inhibited by the addition of protein kinase C activators. These results are consistent with the notion that ras acts via the protein kinase C pathway in conferring autonomous growth on Mel-ab cells.

Animals↗
PubMed1984

Pain-depressing agents and the spinal nociceptive system.

The spinal nociceptive system is the target of various pain depressing agents. It is capable to function without control from the brain. It is activated by tissue damage which, by excitation of nociceptive afferents, evokes activity in axons ascending to the brain (sensory nociceptive response) and in spinal reflex pathways (motor and autonomic responses). The prototype of an analgesic agent, morphine, suppresses nociceptive responses by binding to opiate receptors; it imitates the effect of the transmitter(s) released from endorphinergic neurones. Pentobarbital and diazepam reduce nociceptive (and non-nociceptive) responses by acting on the GABA receptor complex; both drugs facilitate the effect of the transmitter GABA which mediates presynaptic inhibition in the spinal cord. Pentobarbital may produce its effects by an additional action on postsynaptic neurone membranes. Clonidine depresses nociceptive responses, probably by imitating the action of the inhibitory transmitter, noradrenaline. Substance P acts as a "synaptic modulator"; it may facilitate or inhibit nociceptive responses. Ceruletide and cholecystokinin octapeptide depress nociceptive motor responses but do not affect the nociceptive sensory response. This indicates that motor and sensory responses of the spinal nociceptive system are not rigidly linked together. With the help of appropriate drugs, it is possible to manipulate them separately.

Analgesics↗
PubMed1983

[Activity of the neurons of the abdominal-aortic plexus in the guinea pig during preservation of its connections with the large intestine].

With intracellular recording, peripheral inputs from the mechanoreceptor C--afferents of the colon which signal the motor status of its isolated oral and aboral segments were shown to converge on neurons of the abdominal aortic plexus of the guinea pig. A proportion (19.8%) of synapthcally activated neurons of this plexus send axons to the periphery within mesenteric nerves, thus forming the efferent link of an extracentral intestio--intestinal reflex.

Action Potentials↗
PubMedDate not supplied

Visceral reflex responses following right intra-atrial injection of phenyldiguanide in rats.

1. Intra-atrial injection (right atrium) of pdg in nembutal anaesthetised rats produced bradycardia, hypotension and apnoea followed by hyperpnoea. In very lightly anaesthetised rats, injection of pdg close to the aortic valves produced similar responses and those responses disappeared on maintaining the animals in well-anaesthetised condition. 2. Administration of pdg either into the cerebral circulation or into cerebral ventricles did not produce bradycardia and apnoea. 3. The afferent pathway for these autonomic responses runs in vagus nerve, as shown by experiments before and after bilateral vagotomy. 4. The electrical activity of both expiratory and inspiratory muscles was inhibited during end-expiratory apnoea phase following injection of pdg into the right atrium. 5. Glycine, administered centrally or intravenously, exhibited blockade of pdg induced autonomic responses for more than forty minutes.

Animals↗
PubMed1995

Fabry's disease: report of a case.

Fabry's disease is a rare hereditary disorder of glycosphingolipid metabolism. Its clinical features have not been adequately described in Taiwan. This paper reports on a 32-year-old man who had painful acroparesthesia, disseminated skin angiokeratomas, whorled corneal opacity, mitral valve prolapse and renal insufficiency. There was also involvement of the central motor pathways and the autonomic nervous system. A sural nerve biopsy showed loss of small myelinated and unmyelinated fibers. A reduced serum activity of alpha-galactosidase A and a large amount of urinary globotriaosylceramide confirmed the diagnosis of Fabry's disease.

Adult↗
PubMed1977

[Clinical picture of cranio-cerebral trauma combined with trauma to the cervical region of the spine].

On the basis of 60 observations the peculiarites of clinical manifestations of skull-brain injuries combined with trauma of the cervical vertebrae are described. It is demonstrated that in such cases the syndrome of the cerebral lesion often plays the leading part, masking the symptoms of the spinal cord injury. The disorders in circulation in the vertebral-basilar system due to the compression of the vertebral artery canal by the dislodged fragments, its thrombosis, and irritation of the periarterial sympathetic plexus are of importance in the genesis of the developing syndrome in the rombencephalic portion of the brain. In the mechanism of vestibular disorders a certain place belongs, apart from the direct traumatization of the rombencephalic portion and circulation disorders in the vertebral-basilar system, to injuries of the vestibulospinal pathways. The autonomous-visceral pathology observed in cases of cervical injuries can be attributed to the direct effect of the trauma upon the segmental innervation appratus of the heart, diaphragm, thorax.

Adolescent↗
PubMed2004

Electrophysiological evaluation of peripheral and autonomic involvement in leprosy.

OBJECTIVE: Motor and sensory nerve conductions, F responses, sympathetic skin responses and R-R interval variations (RRIV) were studied to determine the type of peripheral neuropathy among patients with leprosy. METHODS: Twenty-nine consecutive patients with leprosy (25 male, 4 female) hospitalized in the "Istanbul Leprosy Hospital" between January - December, 1999 were included in this study. Ten patients had borderline lepromatous leprosy, and 19 had lepromatous leprosy. None of the patients studied had the tuberculoid form. The mean age was 55 +/- 12 years. The control group consisted of 30 (26 male, 4 female) healthy volunteers (mean age: 58.1 +/- 7.8 years). All subjects included in the study underwent neurological examination and electrophysiological evaluation. Standard procedures were performed for evaluating sensory and motor conduction studies. Motor studies were carried out on both left and right median, ulnar, tibial and common peroneal nerves while median, ulnar, sural and superficial peroneal nerves were examined for sensory studies. Sympathetic skin response recordings on both hands and RRIV recordings on precordial region were done in order to evaluate the autonomic involvement. RESULTS: The lower extremity was found to be more severely affected than the upper, and sensory impairment predominated over motor. Of 58 upper limbs examined, no sympathetic skin responses was recorded in 46 (79.3%). Compared with the controls, the RRIVs of the leprosy patients were found to be reduced during both resting and deep forced hyperventilation. CONCLUSION: Our results indicate that leprosy causes a predominantly axonal polyneuropathy that is more severe in the lower extremities. Sensory nerve damage is accompanied by autonomic involvement.

Adult↗
PubMed1989

[Effect of pharmacologic blockade of the autonomic nervous system on electrophysiologic properties of the accessory pathway and atrioventricular node in patients with Wolff-Parkinson-White syndrome].

In 17 patients aged 21-61 (mean 32) with WPW syndrome the transoseophageal stimulation was performed before and after intravenous administration of propranolol (0.1 mg/kg b.w.) and atropine (0.02 mg/kg b.w.). Pharmacological blockade of the autonomic nervous system resulted in statistically significant increase of heart rate (from 81 to 111/min), shortening of a-v nodal and atrial refraction (from 298 to 272 ms) as well as in shortening of stimuli cycle length revealing Wenckebach's point (from 324 to 291 ms). The Kent bundle refraction did not at the average change (333 and 324 ms), while in individuals great differences were observed. Generally, pharmacological blockade of the autonomic nervous system improves a-v nodal conduction, but in patients with WPW syndrome does not significantly effect on the accessory pathway.

Adult↗
PubMed2005

Elevated serum cytokines correlated with altered behavior, serum cortisol rhythm, and dampened 24-hour rest-activity patterns in patients with metastatic colorectal cancer.

PURPOSE: Incapacitating symptom burden in cancer patients contributes to poor quality of life (QOL) and can influence treatment outcomes because of poor tolerance to therapy. In this study, the role of circulating cytokines in the production symptoms in cancer patients is evaluated. EXPERIMENTAL DESIGN: Eighty patients with metastatic colorectal cancer with either normal (group I, n = 40) or dampened (group II, n = 40) 24-hour rest/activity patterns measured by actigraphy were identified. Actigraphy patterns were correlated with QOL indices, serum cortisol obtained at 8:00 a.m. and 4:00 p.m. and with serum levels of transforming growth factor-alpha, tumor necrosis factor-alpha, and interleukin 6 (IL-6) obtained at 8:00 a.m. and analyzed in duplicate by ELISA. Cytokine levels and survival were also correlated. RESULTS: Group II patients had significantly higher pre treatment levels of all three cytokines, displayed significantly poorer emotional and social functioning, had higher fatigue, more appetite loss, and poorer performance status compared with group I patients. Transforming growth factor-alpha (TGF-alpha) and IL-6 were significantly increased in the patients with WHO performance status >1 and in those with appetite loss. Fatigue was significantly associated with elevated TGF-alpha only. IL-6 was increased in those patients with extensive liver involvement and multiple organ replacement, and it was significantly correlated with dampened cortisol rhythm. In a multivariate analysis, IL-6 was correlated with poor treatment outcome. CONCLUSIONS: Significant correlations were found between serum levels of TGF-alpha and IL-6, circadian patterns in wrist activity and serum cortisol and tumor-related symptoms in patients with metastatic colorectal cancer. These data support the hypothesis that some cancer patient's symptoms of fatigue, poor QOL, and treatment outcome are related to tumor or host generated cytokines and could reflect cytokine effects on the circadian timing system. This interplay between cytokine signaling pathways, the hypothalamic-pituitary-adrenal axis, the autonomic nervous system, and efferent pathways of the suprachiasmatic nucleus that control circadian physiology, opens the way to new rational interventions for symptom management in cancer patients.

Activities of Daily Living↗
PubMed1983

Distribution of catecholamine-containing cell bodies and blood vessels in the rat nucleus tractus solitarius.

Glyoxylic acid-induced monoamine fluorescence (GIF) was used to map the distribution of catecholamine-containing cell bodies and terminals in the rat nucleus tractus solitarius (NTS) and dorsal medulla. In addition, the relative vascularity of the NTS was quantified by examination of tissue perfused with Pontamine sky blue. The GIF-reactive cell bodies within the NTS complex were caudal to the rostral pole of the area postrema and are therefore considered to be the A2 cell body group as defined by Dahlström and Fuxe. The A2 cell body group was composed of 900 (890 +/- 43, n = 3) small to medium sized neurons (15-25 micron diameter) located on the dorsal and lateral edges of the dorsal motor nucleus of the vagus. GIF terminal density was found to be most dense in the medial portion of the NTS as compared to the lateral or midline portions of the NTS, dorsal motor nucleus of the vagus, or hypoglossal nucleus. Quantitative blood vessel analysis revealed that the NTS is significantly less vascularized than the surrounding nucleus gracilius, central gray, or dorsal motor nucleus of the vagus. A full serial section analysis of NTS, stained either for GIF cell bodies, terminals or blood vessels, has been obtained; this detailed presentation of catecholamine-containing profiles and blood vessels in the dorsal medulla may facilitate future studies aimed at examining central control of autonomic function.

Afferent Pathways↗
PubMed1987

The rat medial frontal cortex projects directly to autonomic regions of the brainstem.

Pressure injections of the anterograde tracer wheat germ agglutinin conjugated with horseradish peroxidase (WGA-HRP) into the infralimbic (IL) and prelimbic (PL) regions of the medial frontal cortex of the rat produced anterograde, terminal-like labeling in the lateral dorsal tegmental nucleus (LDTg) of the dorsal pons and the ventral, ventrolateral, intermediate, medial and commissural subnuclei of the nucleus of the solitary nucleus (NTS) in the dorsomedial medulla. Injections involving IL resulted in heavier labeling than the labeling seen after PL injections only. The LDTg has been described as the pontine micturition center, involved in the micturition reflex. The possible role that the projections to the LDTg may play in fluid homeostasis is discussed. The labeled NTS subnuclei receive visceral afferent inputs from the heart, baroreceptors, lungs and gut. The direct cortical projections to these areas may be involved in mediating the bradycardia, depressor responses, and changes in respiratory and gastric activity which are seen after electrical stimulation of the rat medial frontal cortex. The present data support the concept that the infralimbic and prelimbic cortices function as a "visceral motor" cortex, involved in control of a variety of autonomic functions.

Afferent Pathways↗
PubMed1981

The central nervous system and its operation in cardiovascular control.

In the intact organism environmental disturbances affecting the circulation often result in simultaneous changes of several groups of peripheral afferents. These elicit characteristic patterns of autonomic activity with distinctive patterns of vagal activity, of regional sympathetic neural activity and of adrenal catecholamine secretion. During simultaneous changes in several groups of afferents the autonomic responses are often non-linear, with the response to one input markedly influenced by the level of the others. When these non-linear interactions involve the central arterial baroreflex pathways the properties of the body's blood pressure system can become greatly altered. With certain combinations of afferents these interactions make it possible for the organism to better withstand large perturbations than it could do through the normal properties of the arterial baroreceptor reflex. The different neuron groups contributing to the CNS autonomic pathways release many different transmitters including noradrenaline or serotonin and changes in reflex properties result from alterations in transmitter release in one or other of the pathways of the particular network. The peripheral arterial baroreceptors become rapidly reset during sustained alterations in blood pressure. Their 'memory' for any given absolute blood pressure is only a few minutes duration. Hence sustained changes in autonomic activity depend on the properties of the CNS either through signals arising from other groups of peripheral receptors, from central 'command' or owing to changes in transmitter release in a given pathway.

Animals↗
PubMed1981

Organization of the sympathetic innervation supplying the hairless skin of the cat's paw.

The sympathetic outflow supplying the hairless skin of the cat's hind paw has been analyzed in brain-intact and chronic low spinal animals. For this purpose the activity of postganglionic axons in fascicles of the medial plantar nerve which innervate the central pad and the respective responses of the target organs (transient skin potentials, skin temperature) have been recorded. (1) Blood vessels and sweat glands in the hairless skin of the cat's hind paw are under efferent control of vasoconstrictor neurons, sudomotor neurons, and possibly vasodilatator neurons. (2) Vasoconstrictor neurons are largely under inhibitory control of various afferent input systems from the body surface and from the internal milieu, and sudomotor neurons under excitatory control in brain-intact as well as in chronic spinal cats. (3) The basic neuronal network or "machinery" for the this reciprocal organization is probably located in the spinal cord. (4) Effects of anesthetics on the sudomotor reflexes indicate that this spinal neuronal organization is controlled in a complex manner by descending spinal systems from the brain stem. (5) The existence of vasodilatator neurons, a third efferent control system supplying the hairless skin, which can only be activated by spinal cord warming in brain-intact as well as in chronic spinal cats is not very well established. Neurons with this property are rare and it is unclear whether they course through the sympathetic trunk or dorsal roots or through both. The axons of these neurons are unmyelinated. (6) The organization of the neuronal control of vessels and sweat glands in the hairless skin may be a paradigmatic model for studying the respective neuronal organization in the spinal cord and its descending control.

Afferent Pathways↗