Short-term and long-term effects of nordic walking training on balance, functional mobility, muscle strength and aerobic endurance among Hungarian community-living older people: a feasibility study.

AIM: The aim of this study was to investigate the short-term and long-term effects of a moderate intensity nordic walking program, and the feasibility of this exercise form among Hungarian community-living older adults. METHODS: Forty one community-living older adults aged over 60 years (mean 67.5, SD 4.8 years) participated in a nordic walking program consisting of a 10-week supervised period and a 25-week unsupervised period. The age and gender matched control group did not receive any types of exercise programs. The balance, functional mobility, lower limb strength, and aerobic endurance were measured at baseline, after 10 weeks and after 25 weeks. RESULTS: The balance, the functional mobility and the aerobic endurance significantly improved in the nordic walking group (P=0.001; P=0.04; P<0.0001, respectively), whereas there were significant deteriorations in the control group. In terms of lower limb muscle strenght (including iliopsoas, quadriceps, gluteus muscles, and hamstring muscles) we could not demonstrate improvement (P=0.274). CONCLUSION: This study showed that nordic walking is a simple, well-tolerated and effective physical activity for older people in Hungary. Based on the findings of our studies, the nordic walking will play an important role in geriatric physiotherapy in order to improve or maintain the functional abilities of this growing population.

Trigeminal ganglion innervates the auditory brainstem.

A neural connection between the trigeminal ganglion and the auditory brainstem was investigated by using retrograde and anterograde tract tracing methods: iontophoretic injections of biocytin or biotinylated dextran-amine (BDA) were made into the guinea pig trigeminal ganglion, and anterograde labeling was examined in the cochlear nucleus and superior olivary complex. Terminal labeling after biocytin and BDA injections into the ganglion was found to be most dense in the marginal cell area and secondarily in the magnocellular area of the ventral cochlear nucleus (VCN). Anterograde and retrograde labeling was also seen in the shell regions of the lateral superior olivary complex and in periolivary regions. The labeling was seen in the neuropil, on neuronal somata, and in regions surrounding blood vessels. Retrograde labeling was investigated using either wheatgerm agglutinin-horseradish peroxidase (WGA-HRP), BDA, or a fluorescent tracer, iontophoretically injected into the VCN. Cells filled by retrograde labeling were found in the ophthalmic and mandibular divisions of the trigeminal ganglion. We have previously shown that these divisions project to the cochlea and middle ear, respectively. This study provides the first evidence that the trigeminal ganglion innervates the cochlear nucleus and superior olivary complex. This projection from a predominantly somatosensory ganglion may be related to integration mechanisms involving the auditory end organ and its central targets.

Direct evidence of trigeminal innervation of the cochlear blood vessels.

This paper provides the first detailed description of the trigeminal innervation of the inner ear vasculature. This system provides a newly discovered neural substrate for rapid vasodilatatory responses of the inner ear to high levels of activity and sensory input. Moreover, this discovery may provide an alternative mechanism for a set of clinical disturbances (imbalance, hearing loss, tinnitus and headache) for which a central neural basis has been speculated. Iontophoretic injections of biocytin were made via a glass microelectrode into the trigeminal ganglion in guinea-pigs. Tissue for histological sections was obtained 24 h later. Labeled fibers from the injection site were observed as bundles around the ipsilateral spiral modiolar blood vessels, as individual labeled fibers in the interscala septae, and in the ipsilateral stria vascularis. The dark cell region of the cristae ampullaris in the vestibular labyrinth was also intensively labeled. No labeled fibers were observed in the neuroepithelium of the cristae ampullaris or the semicircular canals. These results confirm and localize an earlier indirect observation of the trigeminal ganglion projection to the cochlea. This innervation may play a role in normal vascular tone and in some inner ear disturbances, e.g., sudden hearing loss may reflect an abnormal activity of trigeminal ganglion projections to the cochlear blood vessels.

Co-localization of the vanilloid capsaicin receptor and substance P in sensory nerve fibers innervating cochlear and vertebro-basilar arteries.

Evidence suggests that capsaicin-sensitive substance P (SP)-containing trigeminal ganglion neurons innervate the spiral modiolar artery (SMA), radiating arterioles, and the stria vascularis of the cochlea. Antidromic electrical or chemical stimulation of trigeminal sensory nerves results in neurogenic plasma extravasation in inner ear tissues. The primary aim of this study was to reveal the possible morphological basis of cochlear vascular changes mediated by capsaicin-sensitive sensory nerves. Therefore, the distribution of SP and capsaicin receptor (transient receptor potential vanilloid type 1-TRPV1) was investigated by double immunolabeling to demonstrate the anatomical relationships between the cochlear and vertebro-basilar blood vessels and the trigeminal sensory fiber system. Extensive TRPV1 and SP expression and co-localization were observed in axons within the adventitial layer of the basilar artery, the anterior inferior cerebellar artery, the SMA, and the radiating arterioles of the cochlea. There appears to be a functional relationship between the trigeminal ganglion and the cochlear blood vessels since electrical stimulation of the trigeminal ganglion induced significant plasma extravasation from the SMA and the radiating arterioles. The findings suggest that stimulation of paravascular afferent nerves may result in permeability changes in the basilar and cochlear vascular bed and may contribute to the mechanisms of vertebro-basilar type of headache through the release of SP and stimulation of TPVR1, respectively. We propose that vertigo, tinnitus, and hearing deficits associated with migraine may arise from perturbations of capsaicin-sensitive trigeminal sensory ganglion neurons projecting to the cochlea.

Trigeminal ganglion innervation of the cochlea--a retrograde transport study.

Innervation patterns of sensory nerves from the trigeminal ganglion to the cochlear blood vessels were studied using retrograde transport of wheat germ agglutinin conjugated to horseradish peroxidase. Guinea-pigs (n=7) were unilaterally implanted with an osmotic pump and a cannula for cochlear delivery of 2% or 20% wheat germ agglutinin horseradish peroxidase (Group 1), 2% wheat germ agglutinin-horseradish peroxidase followed by 100 micromol capsaicin (Group 2), or vehicle alone. Histological sections of the trigeminal ganglia, the C1 and C2 dorsal ganglia, the superior and inferior ganglia of the glossopharyngeal nerve bilaterally, the midbrain and the brainstem were obtained after 48 h of infusion. In Group 1, a large number of labeled nerve cell bodies were observed in the anteromedial portion of the trigeminal ganglion and at the origin of the ophthalmic nerve. Some labeled cells were also found on the lateral side of the ophthalmic nerve, as well as on the medial side of the maxillary nerve root. Capsaicin pretreatment significantly reduced the density of labeled neurons in the trigeminal ganglion. A few labeled neurons were also found in the trigeminal brainstem nucleus complex and in certain auditory brainstem nuclei. No wheat germ agglutinin horseradish peroxidase-positive cells were observed in the spinal C1 or C2 cervical ganglia or in the superior or inferior glossopharyngeal ganglia. In contrast, wheat germ agglutinin-horseradish peroxidase application to the middle ear resulted in labeled cells in the middle posterolateral portion of the trigeminal ganglia and in the superior ganglia of the glossopharyngeal nerve. These results provide the first direct evidence that the trigeminal ganglion sends projections to the cochlea.

Capsaicin stimulation of the cochlea and electric stimulation of the trigeminal ganglion mediate vascular permeability in cochlear and vertebro-basilar arteries: a potential cause of inner ear dysfunction in headache.

Trigeminal neurogenic inflammation is one explanation for the development of vascular migraine. The triggers for this inflammation and pain are not well understood, but are probably vasoactive components acting on the blood vessel wall. Migraine-related inner ear symptoms like phonophobia, tinnitus, fluctuation in hearing perception and increased noise sensitivity provide indirect evidence that cochlear blood vessels are also affected by basilar artery migraine. The purpose of this investigation was to determine if a functional connection exists between the cochlea and the basilar artery. Neuronally mediated permeability changes in the cochlea and basilar artery were measured by colloidal silver and Evans Blue extravasation, following orthodromic and antidromic stimulation of the trigeminal ganglion innervating the cochlea. Capsaicin and electrical stimulation induced both dose- and time-dependent plasma extravasation of colloidal silver and Evans Blue from the basilar artery and anterior inferior cerebellar artery. Both orthodromic and antidromic activation of trigeminal sensory fibers also induced cochlear vascular permeability changes and significant quantitative differences between the treated and control groups in spectrophotometric assays. These results characterize a vasoactive connection between the cochlea and vertebro-basilar system through the trigeminal sensory neurons. We propose that vertigo, tinnitus and hearing deficits associated with basilar migraine could arise by excitation of the trigeminal nerve fibers in the cochlea, resulting in local plasma extravasation. In addition, cochlear "dysfunction" may also trigger basilar and cluster headache by afferent input to the trigeminal system.

Evidence for the role of nitric oxide in the circulation of the dental pulp.

Many authors have studied the hemodynamics of the dental pulp; however, there are scarcely any data regarding the involvement of the L-arginine/nitric oxide pathway in the regulatory mechanism. Thus, we have examined the physiological effects of (1) NG-nitro-L-arginine as an inhibitor of nitric oxide synthesis and (2) the nitric oxide donor 3-morpholinosydnonimine on blood flow and vascular resistance in the canines of anesthetized cats to study the potential involvement of nitric oxide in the regulation of dental vascular homeostasis. Mean arterial blood pressure, heart rate, blood gases, pH, cardiac output, and tissue blood flow were determined prior to and 15 min after i.v. administration of either NG-nitro-L-arginine (30 mg/kg, n = 9) or 3-morpholinosydnonimine (1 mg/kg, n = 7). Blood flow was measured by radioactive-labeled microspheres. There were no significant differences in baseline parameters between the two groups of cats. The dental pulp blood flow decreased to 53 +/- 13% (p < 0.01) of the control level after NG-nitro-L-arginine administration, while it decreased only slightly (to 82 +/- 12%) after 3-morpholinosydnonimine administration. The dental pulp's vascular resistance increased to 367 +/- 69% (p < 0.01) of the control level after NG-nitro-L-arginine, while it decreased to 73 +/- 10% (p < 0.05) of control after 3-morpholinosydnonimine. We found that the L-arginine/nitric oxide pathway plays an important role in the regulation of pulpal blood circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Capsaicin-induced release of substance P increases cochlear blood flow in the guinea pig.

Physiological evidence from several studies suggests that endogenous vasoactive peptides, such as substance P (SP), and their respective receptor populations may participate in the mechanisms that govern the autoregulatory capacity of the cochlear vascular system. However, these studies do not provide evidence regarding the origin or mechanism of action of SP. Capsaicin sensitivity has been used as a marker for sensory neurons, and the release of SP following capsaicin treatment suggests a sensory transmitter role for SP. The present investigation examines the relationship between the capsaicin-sensitive sensory neurons and SP in the regulation of cochlear blood flow (CBF). In 75 pigmented guinea pigs, the cochlea was surgically exposed and a laser Doppler flowmeter probe placed on the bony surface of the first turn to monitor CBF. Capsaicin solutions (2 microliters, 0.01%, 0.001% and 0.0001%) applied to the round-window membrane (RWM) resulted in a dose-related CBF increase, without change in the systemic blood pressure. This effect could be inhibited by application of a specific SP receptor antagonist, [D-Pro2,D-Trp7,9]-SP, after which none of the capsaicin concentrations used induced a change in CBF. Moreover, after RWM application of 50 nmol/2 microliters of SP there was a significant increase in CBF. No CBF change was observed with the lower concentrations of 10 nmol SP or 100 pmol SP. These results indicate a role of SP in CBF regulation and give indirect evidence that SP is released from capsaicin-sensitive primary sensory neurons.

Nitric oxide mediates capsaicin-induced increase in cochlear blood flow.

Capsaicin has been previously shown to increase cochlear blood flow (CBF) in a dose-dependent manner. The aim of this study was to define the role of nitric oxide (NO) in capsaicin-induced changes in CBF. This was investigated in the anesthetized guinea pig, utilizing laser Doppler flowmetry. Application of capsaicin (64.8 and 6.48 nmol in 2 microliters of saline) to the round window membrane (RWM) caused increases in CBF (34 +/- 2.8% of baseline (BL) and 28 +/- 2.3% BL, respectively (P < 0.001)). Application of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg intravenously or topically to the RWM) reduced blood flow in the cochlea, as previously reported. After pretreatment with i.v. L-NAME, the effect of capsaicin on CBF was significantly decreased. With the dose of capsaicin at 64.8 nmol, the increase in CBF fell from 34 +/- 2.8% BL to 6.9 +/- 1.5% BL (P < 0.001), and at 6.48 nmol it fell from 28 +/- 2.3% BL to 4.8 +/- 1.6% BL (P < 0.001). RWM L-NAME application also decreased the capsaicin vasodilatation effect. A capsaicin dose of 64.8 nmol resulted in only a 10 +/- 2.5% BL increase in CBF, and with 6.48 nmol capsaicin the increase was 7.8 +/- 2.2% of BL (P < 0.001). Capsaicin-sensitive sensory neurons in other systems are generally known to release substance P (SP), which in turn elicits release of endothelium derived relaxing factor (NO). The results of this study indicate that NO is a mediator of capsaicin-sensitive sensory neuronal function in CBF regulation.

Expression of Trk A receptors in the mammalian inner ear.

Tyrosine kinase receptors, including Trk A, Trk B and Trk C, participate in many different biological processes that are regulated by neurotrophic factors. Nerve growth factor (NGF)-triggered Trk A signaling is involved in growth, survival and differentiation of neurons in the central nervous system and in neural crest-derived cells. Trk A, Trk B and Trk C expression has been reported in the rat ventral cochlear nucleus. In the present study, we explored the immunocytochemical distribution of Trk A in the rodent inner ear. Rat and mouse cochleae were immunolabeled with a rabbit anti-Trk A polyclonal antibody (Chemicon) that has no reported cross-reactivity with Trk B and Trk C. In embryonic day 16 mice, no Trk A immunolabeling could be detected in the developing neuroepithelium. At postnatal day 6, weak Trk A labeling could be observed in both inner and outer hair cells. At postnatal day 12, enhanced punctate Trk A immunoexpression was present in hair cells. In adult mice and rats, intense Trk A labeling was observed in outer and inner hair cell bodies, in supporting cell bodies throughout the cochlea, and in spiral ganglion neurons. Trk A was not observed in stria vascularis, hair cell stereocilia, nor in the Trk B- and Trk C-rich cerebellum. This distribution pattern of Trk A suggests that its ligand, NGF, exerts significant trophic effects in the rodent inner ear.

The effect of a nitric oxide donor and an inhibitor of nitric oxide synthase on blood flow and vascular resistance in feline submandibular, parotid and pancreatic glands.

The aim was to examine whether (1) blood flow and vascular resistance are altered in response to exogenous nitric oxide and (2) whether endogenous synthesis of nitric oxide participates in the haemodynamic regulation of the submandibular, parotid and pancreatic glands. Experiments were performed on anaesthetized, artificially ventilated cats. Mean arterial blood pressure, heart rate, blood gases, cardiac output and tissue blood flow were determined before and 15 min after intravenous administration of either the nitric oxide donor SIN-1 (3-morpholinosydnonimine, 1 mg/kg, n = 10) or the competitive nitric oxide synthase inhibitor NOLA (NG-nitro-L-arginine, 30 mg/kg, n = 9) blood flow was measured by a radioactive-labelled microsphere method. In the SIN-1 group, in spite of a serious decrease in mean arterial blood pressure (p < 0.001), the blood flow in the glands remained unchanged. The vascular resistance decreased after SIN-1 in the submandibular and pancreatic glands (p < 0.001 and p < 0.05, respectively), and was slightly reduced in the parotid. The NOLA increased mean arterial blood pressure (p < 0.01) and reduced the blood flow in the submandibular and pancreatic glands (p < 0.01 and p < 0.001, respectively), but the decrease in the parotid was not significant. Vascular resistance increased after NOLA in all three glands (p < 0.05, p < 0.001 and p < 0.05). These findings suggest that basal nitric oxide production in these exocrine glands is sufficient to modulate vascular resistance. Moreover, the release of endogenous NO from the nerves and/or endothelium is probably involved in the regulation of vascular tone. The nitric oxide-dependent component of blood-flow regulation, however, seems to be less pronounced in the parotid gland.

Possible involvement of capsaicin-sensitive sensory nerves in the regulation of cochlear blood flow in the guinea pig.

Capsaicin-induced microcirculatory changes in the cochlea of anaesthetized guinea pigs were examined by laser-Doppler flowmetry. Close intraarterial capsaicin infusion into the anterior inferior cerebral artery at doses of 10-50 pmol/min was followed by dose-dependent vasodilatation. Capsaicin infused in a dose of 150-200 pmol/min or above resulted in vasoconstriction in the region examined. Topical capsaicin administration into the cochlea (50-150 pmol) resulted in very moderate vasodilation with a latency of 1-2 min. Perivascular capsaicin application onto the anterior inferior cerebellar artery elicited an elevated blood flow in the cochlea, too. It is concluded that the release of vasoactive substances from capsaicin-sensitive nerve fibres in the inner ear of the guinea pig may play a role in the control of the local microcirculation. These nerves may also be involved in the neurogenic inflammatory processes in the region.

Effect of endolymphatic hydrops on capsaicin-evoked increase in cochlear blood flow.

Capsaicin, which causes release of neuropeptides including substance P, has been shown to cause dose-related increases in cochlear blood flow (CBF). Since CBF regulation is altered in animal models with endolymphatic hydrops, this study was designed to examine the effect of hydrops on capsaicin-induced CBF changes. CBF responses to 0.01 and 0.001% capsaicin applied to the round window membrane were measured in normal and 12-week hydropic guinea pigs using laser Doppler flowmetry. With 0.01% capsaicin, CBF increased by only 13 +/- 7.8% in the hydropic ear, compared with 34% +/- 13% in the normal animal (p = 0.027). With 0.001% capsaicin, CBF increased by only 7.5 +/- 4.2% in the hydropic ear, compared with 28 +/- 16% in the normal ear (p < 0.001). These findings demonstrate a reduced responsiveness to capsaicin with endolymphatic hydrops and suggest that hydrops causes an alteration in the peptidergic sensory fibers of the inner ear or in the vascular smooth muscle or both. The results are consistent with previous reports of reduced vascular responsiveness in hydropic guinea pigs and provide further evidence for abnormal CBF regulation in hydrops.

[Computerized data base for recording information on patients with hypersensitivity to metals]. / Számítógéppel értékelhetö etiológiai adatlap fémérzékeny betegek adatainak rögzítésére.

The authors describe a computer analysable etiological card used for registration of data of Ni hypersensitive patients' with oral symptoms. The collection and evaluation of the data related to the pathological changes and predisposing factors can be useful in prevention of development of hypersensitivity or clinical symptoms of hypersensitivity in cases belonging to this risk group.

[Electrochemical properties of dental alloys (II)]. / Fogászati ötvözetek elektrokémiai jellemzöi (II. rész).

The studies were focused on the corrosion stability of dental alloys (containing NiCr and stainless steel), for a possible release of Nickel (Ni). The investigations were carried out in artificial saliva at 37 degrees C. The potential range, where Ni dissolution may occur, was determined by transient measurements. It has been established, that: 1. Under in vivo conditions the probability of the pitting corrosion is very low. 2. The Ni release takes place on the temporarily damaged, locally activated parts of the surfaces.