ТRANSPLANTATION OF AUTOLOGOUS CELLS IN COMPLEX OF TREATMENT OF COMPLICATED ARTERIAL FORM IN THE THORACIC OUTLET SYNDROME.

Impact of the autologous cells transplantation in complex of treatment of complicated arterial form of thoracic outlet syndrome was estimated. In accordance to the proce' dure proposed 18 patients were operated on, in 16 patients a standard decompressive and reconstructive operative interventions were performed. The proposed procedure application have promoted improvement of the patients' treatment results due to opti' mization of microcirculation and angiogenesis.

The relationship between aortic baroreceptor activity and arterial pressure is not monotonic.

Previous reports indicate that when aortic pressure (AP) falls below the threshold (P (th)) for baroreceptor sensitivity, activity in the aortic depressor nerve (ADN) may increase. To quantify and explain this anomalous behaviour, we analysed curves describing the relationship of baroreceptor fibre activity in rabbit left ADN to AP. Data were obtained in anaesthetised New Zealand White rabbits. Occlusion and release of cuffs around the inferior vena cava and descending aorta generated AP ramps (25-140 mmHg). Response curves were obtained for 173 fibres in 26 animals. Thirty percent of curves had a nadir (J-shaped curve), and in 40% activity was always present. In fibres showing activity below P (th), firing was predominantly diastolic, switching to systolic firing at P (th). The unusual behaviour of a substantial fraction of aortic baroreceptors below P (th) accounts for the J-shaped response curve of the whole ADN. We suggest that fibres that fire during diastole at pressures below P (th) may have sensory endings close to the origin of the left subclavian artery. As a consequence of this anatomical location, low pressures can impose strain on these receptors, which is then relieved by the systolic pulse.

Measurement of subclavicular pressure on the subclavian artery and brachial plexus in the costoclavicular space during provocative positioning for thoracic outlet syndrome.

BACKGROUND: Thoracic outlet syndrome is thought to be caused by compression of the brachial plexus or subclavian artery in the interscalene, costoclavicular, or subcoracoid space. Some provocative tests are widely used for diagnosing thoracic outlet syndrome. However, whether provocative positions actually compress the neurovascular bundle in these spaces remains unclear. The purpose of this study was to investigate the possibility of neurovascular bundle compression in the costoclavicular space by measuring the pressure applied to the brachial plexus and subclavian artery in provocative positions. METHODS: Bilateral shoulders of eight fresh-frozen transthoracic human cadavers with no obvious anatomical abnormalities were used in this study. There were three female and five male cadavers with a mean age of 81.7 years (range 72-90 years). The pressure on the brachial plexus and subclavian artery between the clavicle and first rib were measured using a 0.13-mm thin pressure sensor in each of four provocative positions (depressed position, alternative Eden position, throwing position, Wright position). RESULTS: Nerve contact pressure was increased in seven shoulders in the Wright position (2.87 +/- 3.13 N/cm(2); range 0.81-9.76 N/cm(2)). The frequency of nerve compression in the Wright position was significantly higher when compared to that in the other three limb positions (P = 0.018). Artery contact pressure was increased in three shoulders in the Wright position (mean 0.59 +/- 0.13 N/cm(2); range 0.45-0.7 N/cm(2)). As was the case with nerve compression, the frequency of compression tended to be higher for the Wright position, but no significant difference was seen. CONCLUSIONS: In four of eight specimens with no obvious anatomical abnormalities, the brachial plexus was compressed in the costoclavicular space in the Wright position. The Wright position thus may be a useful position for inducing nerve compression in the costoclavicular space.

The ansa subclavia: a review of the literature.

The ansa subclavia, subclavian loop, Vieussens' ansa or Vieussens' loop is a nerve cord that connects the middle cervical and inferior cervical sympathetic ganglia, forming a loop around the subclavian artery. The structure of the ansa subclavia is evolutionarily conserved from rats, guinea pigs, the porcine species and dogs to humans. A common application in physiological studies is to electrically stimulate the ansa subclavia in animal models as a robust protocol to modulate stimulatory cardiac sympathetic input. Despite a large number of physiological studies utilizing the ansa subclavia, only very brief descriptions have been devoted to it in standard anatomy texts. An extensive search found only one report in the English language literature concerning the anatomy of the ansa subclavia. The aim of this report, therefore, was to provide a comprehensive review of the clinical anatomy of the ansa subclavia and to discuss its potential physiological functions.

Cranial sensory neuron development in the absence of brain-derived neurotrophic factor in BDNF/Bax double null mice.

To investigate the role of brain-derived neurotrophic factor (BDNF) in differentiation of cranial sensory neurons in vivo, we analyzed development of nodose (NG), petrosal (PG), and vestibular (VG) ganglion cells in genetically engineered mice carrying null mutations in the genes encoding BDNF and the proapoptotic Bcl-2 homolog Bax. In bax(-/-) mutants, ganglion cell numbers were increased significantly compared to wild-type animals, indicating that naturally occurring cell death in these ganglia is regulated by Bax signaling. Analysis of bdnf(-/-)bax(-/-) mutants revealed that, although the Bax null mutation completely rescued cell loss in the absence of BDNF, it did not rescue the lethality of the BDNF null phenotype. Moreover, despite rescue of BDNF-dependent neurons by the bax null mutation, sensory target innervation was abnormal in double null mutants. Vagal sensory innervation to baroreceptor regions of the cardiac outflow tract was completely absent, and the density of vestibular sensory innervation to the cristae organs was markedly decreased, compared to wild-type controls. Moreover, vestibular afferents failed to selectively innervate their hair cell targets within the cristae organs in the double mutants. These innervation failures occurred despite successful navigation of sensory fibers to the peripheral field, demonstrating that BDNF is required locally for afferent ingrowth into target tissues. In addition, the bax null mutation failed to rescue expression of the dopaminergic phenotype in a subset of NG and PG neurons. These data demonstrate that BDNF signaling is required not only to support survival of cranial sensory neurons, but also to regulate local growth of afferent fibers into target tissues and, in some cells, transmitter phenotypic expression is required.

Sonographic mapping of the normal brachial plexus.

BACKGROUND AND PURPOSE: Mapping of the brachial plexus with MR imaging has been reported and may have potential clinical applications (eg, precise localization of traumatic or tumoral nerve lesions, selective anesthesia of the brachial plexus). We sought to demonstrate that mapping of the brachial plexus may be performed by means of sonography. METHODS: Twelve healthy adult volunteers (seven women and five men; age range, 24-38 years; mean, 31 years) underwent bilateral sonographic examination for the assessment of the nerve structures of the brachial plexus from the extraforaminal part to the axillary part. Four formolated cadavers (two male and two female; age range, 66-84 years; mean, 77.5 years) were frozen and sawed into 3-mm-thick contiguous sections in the same plane as that used for the sonographic exploration. RESULTS: A satisfactory sonographic examination was performed in 10 of 12 volunteers, leading to a good association with anatomic sections. Two volunteers were excluded from the study because a clear depiction of the brachial plexus was difficult owing to a short neck and low echogenicity at examination. The association between sonographic images and anatomic sections allowed us to map the brachial plexus. The subclavian and deep cervical arteries were useful landmarks for this mapping. The eighth cervical nerve root and the first thoracic nerve root were the most difficult part of the brachial plexus to depict because of their deep location. CONCLUSION: The brachial plexus can be mapped with sonography. However, this technique requires a good grounding in anatomy and may be impossible in short-necked individuals.

Vagal modulation of ventricular tachyarrhythmias induced by left ansae subclaviae stimulation in rabbits.

Previous evidence has shown that vagal nerve activity modulates ventricular arrhythmias in patients and in animal models. However, the effects of direct vagus nerve stimulation on ventricular tachyarrhythmias brought by direct sympathetic nerve stimulation have not been elucidated. In the present study, the effects of electrical stimulation of the left cervical vagus nerve on ventricular tachycardia (VT) which was induced by electrical stimulation of the left ansae subclaviae (LAS) in rabbits were assessed. Monophasic action potentials (MAPs) of the left ventricular endocardium were recorded simultaneously with surface ECG. In 27 rabbits tested, the stimulation of LAS induced VT in 19 rabbits. Polymorphic VT (PVT) was induced in 14 rabbits (PVT group), whereas monomorphic VT (MVT) was induced in 5 rabbits (MVT group). Vagus nerve stimulation during the sympathetically-induced PVT led to a restoration of sinus rhythm in 10 of 14 rabbits, while that during the sympathetically-induced MVT did not restore sinus rhythm in any of the 5 rabbits. Vagus nerve stimulation during the stimulation of LAS, which was of subthreshold intensity for the induction in VT, did not result in an induction of PVT in any of the 14 rabbits in the PVT group, while it induced slow MVT in 3 of 5 rabbits in the MVT group. These results indicate that vagus nerve stimulation preferentially exerts protective antiarrhythmic effects against PVT induced by sympathetic neural stimulation in this model, while it occasionally induces slow MVT under conditions in which sympathetic nerve activity in potentially elevated.

Inhibition of cardiac vagal effects by neurally released and exogenous neuropeptide Y.

Neuropeptide Y (NPY) attenuates vagal effects on cardiac cycle length, presumably by inhibiting the release of acetylcholine from vagal nerve endings. We sought to determine if NPY inhibited the vagal effects on atrioventricular (AV) interval and atrial contraction in a manner similar to its inhibition of the vagal effects on cycle length. In 19 anesthetized dogs we measured the vagal effects on cycle length, AV interval, and atrial contraction before and after 3-minute trains of sympathetic stimulation or before and after exogenous NPY (20 micrograms/kg i.v.). Three minutes after 10-Hz sympathetic stimulation, the vagal effects on cycle length and AV interval were attenuated by 52 +/- 9% and 63 +/- 8%, respectively. Phentolamine significantly augmented this attenuation, but propranolol had no appreciable effect. In the control group of animals or in the group that received phentolamine, the vagal effects on atrial contraction measured before and after sympathetic stimulation were not significantly different. In these two groups, however, the basal atrial contraction was reduced substantially after the cessation of sympathetic stimulation. Propranolol prevented this reduction in atrial contraction. After propranolol, the vagal effects on atrial contraction 3 minutes after sympathetic stimulation were attenuated by 31 +/- 6%. Exogenous NPY had no direct effect on cycle length, AV interval, or atrial contraction, but exogenous NPY did persistently inhibit the vagal effects on each of these cardiac processes. Three minutes after NPY was given, the vagal effects on cycle length, AV interval, and atrial contraction were inhibited by 62 +/- 7%, 69 +/- 5%, and 68 +/- 5%, respectively. We conclude that NPY attenuates the vagal effects on the atrial myocardium and on the sinus and AV nodes. In the absence of beta-blockade, the inhibitory effect of neurally released NPY on the vagally induced decreases in atrial contraction may be masked by the reduction in the atrial contraction that occurs after sympathetic stimulation.

[Anatomical organization, organogenesis and innervation of the arteries of the hand]. / Notions d'organisation anatomique, organogenèse et innervation des artères de la main.

The authors sum up the anatomical aspects of the arteries of the hand. They emphasise the fact that, by the side of the classical description; there is a lot of variations. These can be explained by organogenesis, showing that hand arteries pass over several stages, before reaching the terminal one. Generally, it seems that the classical diagram correspond to the majority of cases, and that there is a main flow for hand's arteries: this are the superficial and deep arches, which give common and proper digital arteries. About the innervation, this structures are very richly innervated, but this sympathetic innervation is not so precisely delimited in its topography, and for that reason, its seems to be difficult to give an clear diagram of its origin and distribution. That can explain surgical treatment's failure in vasomotor syndromes of upper limbs.

The nerve loops crossing below the subclavian artery and their anatomical variations.

60 dissections analysed the variability of three types of nerve loops crossing beneath the subclavian artery : Vieussens' annulus, the anastomotic ansa between the lower laryngeal nerve and the cervical sympathetic, and the anastomotic ansa between the phrenic nerve and the stellate ganglion. The classic disposition of these loops, situated below the artery and present simultaneously, was found in only 10% of the cases. Though Vieussens' annulus was present in most of the dissections, the anastomotic ansa between the cervical sympathetic and both the lower laryngeal nerve and the phrenic nerve corresponds more rarely to the conventional pattern.

Development of reflexogenic zone innervation of the human cardiovascular system.

The development of the innervation of the human branchial aortic arches and the heart has been investigated. The early growth of nerve fibres to the 1st, 2nd, 3rd, 4th and 6th aortic arches has been established. Evidence of the transformation of the 1st and 2nd aortic arches and the 4th right one into highly sensitive zones is presented. The order in which nerve connections of the arch regions which develop into reflexogenic zones in a definitive organism are formed is demonstrated. The cranial nerve fibres grow first, and are followed by the sympathetic trunk fibers. Investigations carried out on the extensive material corroborate Koch's hypothesis (1931) that all aortic arches of the embryo develop into reflexogenic zones.

Cardiac responses to stimulation of thoracic afferents in the primate and canine.

Excitatory cardiovascular responses to electrically stimulated upper thoracic sympathetic afferent nerves were observed in halothane-anesthetized mongrel dogs and monkeys. The central end of the transected ventral limb of the left ansa subclavia was stimulated before and after several types of denervation. Significant increases in right and left ventricular maximum systolic pressures, systolic and diastolic systemic blood pressures, and aortic flow were observed. The carotid sinuses were denervated bilaterally and stimulation of the ansa was repeated. The cardiovascular responses to stimulation of the ventral ansa after carotid sinus denervation were greater in magnitude than those observed prior to denervation. This carotid sinus modulation of cardiovascular responses was observed in dogs and monkeys. Cardiovascular responses to stimulation of the ventral ansa after bilateral vagotomy were significantly less than the responses observed after carotid sinus denervation prior to vagotomy. However, the responses after vagotomy were statistically identical to responses obtained while stimulating the ventral ansa when the carotid sinuses and vagi remained intact.

[The reactivity of the sinocarotid, aortic, and subclavian baroreceptors during artificial circulation in the rabbit]. / Etude de la réactivité des barocepteurs sinocarotidiens, aortiques et subclaviaires au cours de circulations artificielles chez le lapin

During artificial circulation (cardiopulmonary bypass) in rabbits, it appears that there is no alteration in the reactivity of the baroceptors, although the transfer function of the receptors is reset at a higher level in some rabbits with low pressure.

Light, fluorescence and electron microscopic studies of rabbit subclavian glomera.

The subclavian glomera (aortic bodies) of young New Zealand white rabbits were studied with the light, fluorescence, and electron microscopes. Two cell types were identified: type I, granule-containing (chief) cells, and type II, agranular (sustentacular) cells. The type I cells possessed large nuclei, the normal complement of cytoplasmic organelles and numerous electron-opaque cytoplasmic granules. The type II cells were agranular with attenuated cytoplasmic processes which partially or completely ensheathed the type I cells. The glomera were well vascularized. Capillary endothelial cells contained numerous pinocytotic vesicles, but few fenestrae. Two profiles of nerve terminals were observed. One, apposing the type I cells, contained numerous electron-lucent vesicles, several dense-cored vesicles, mitochondria and possessed membrane specializations resembling those usually observed in synaptic zones. The other profile contained abundant mitochondria and a few electron-lucent and dense-cored vesicles. Structural specializations were not observed on the apposed membranes of these terminals or adjacent to type II cells. Fluorescence histochemistry revealed an intense yellow-green fluorescence in the glomera, which indicated the presence of biogenic amines, possibly primary catecholamines or an indolamine. The electron-opaque granules observed in the type I cells were believed to be the storage sites for these amines. The subclavian glomera were found to be morphologically similar to the carotid body which is a known chemoreceptor.

An electron microscopic study on the effects of reserpine on the subclavian glomera of the rabbit.

Young male and female New Zealand white rabbits were given a daily subcutaneous injection of reserpine (Serpasil, Ciba; 3 mg/kg) for two days and were sacrificed 24 hours after the last injection. The subclavian glomera (aortic bodies) were processed for electron microscopy to determine the effects of this biogenic amine depleting agent on the electron-opaque cytoplasmic granules of the parenchymal type I cells. Observations of glutaraldehyde-osmium tetroxide fixed glomera from reserpinized animals showed a slight decrease in granule density of the type I cells. Glomera fixed in glutaraldehyde and incubated in potassium dichromate (pH 4.1) demonstrated a reduction in granule opacity following reserpine treatment. Control glomera incubated in potassium dichromate displayed electron-opaque granules. These results indicate that reserpine does deplete the amines without granule disappearance or changes in granule population. The positive reaction of the control tissue granules to potassium dichromate incubation suggests that the predominant biogenic amines in the electron-opaque granules are unsubstituted monoamines. Persistence of the opaque granules following reserpinization and glutaraldehyde-osmium tetroxide double fixation, may be due to amine-binding protein within the granules. The mode of granule depletion could not be ascertained with certainty.

Respiratory fluctuations in pupil size.

Regular fluctuations in pupil size of the cat were measured and the properties, nervous pathways, and origin of these oscillations were investigated. The rhythm of pupil movements under control conditions appeared to be either locked to the central respiratory cycle or to the artificial ventilatory cycle. These movements were only seen in lightly anesthetized or tranquilized cats, but not in alert or deeply anesthetized cats (ether, halothane or pentobarbital). The fluctuations proved to be independent of sympathetic innervation but related to variations in parasympathetic outflow. At least two sources for pupil oscillations appeared to be involved: central respiratory activity and respiratory blood pressure fluctuations that modulated pupil width via sinoaortic baroreceptors. Lung movements per se, as a third possible factor, did not modulate pupil width, whereas electrical stimulation of the afferent lung vagi did; therefore the role of this mechanical factor is not clear. A review of the pertinent literature shows that in the organism there are many phenomena exhibiting respiratory oscillations. It seems likely that these oscillations have the same origin as the respiratory pupil fluctuations.