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Results for “Autonomic Pathways”

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At least 397 records · Page 22Linked to original sources
PubMed1997

Effect of cisapride on the isolated guinea pig gall bladder and common bile duct.

1. In this study, the effect of cisapride on the isolated guinea pig gall bladder (GB) and common bile duct (CBD) motility was investigated. 2. Cisapride, up to a certain concentration, produced an increase in tone of the GB (EC50 1.35 x 10(-8) M) and the CBD (EC50 2.75 x 10(-9) M), whereas, at concentrations higher than 3 x 10(-5) M for the GB and 5 x 10(-6) M for the CBD, it produced a transient increase in tone followed by a sustained decrease in tone or in the contraction amplitude or in both. 3. The cisapride-induced increase in tone was antagonized by atropine on both the GB and the CBD. 4. Cisapride up to 2 x 10(-5) M for the GB and 3 x 10(-6) M for the CBD did not modify, whereas, at concentrations higher than 2.8 x 10(-5) M for the GB and 4 x 10(-6) M for the CBD, it antagonized, noncompetitively, the concentration-response curve to exogenously applied acetylcholine. The IC50 values for cisapride on the EC50 of acetylcholine on the GB and the CBD were 9.4 x 10(-5) M and 8.2 x 10(-6) M, respectively. 5. In conclusion, on the guinea pig GB and CBD, low concentrations of cisapride produce a stimulating effect, probably of cholinergic origin, whereas higher concentrations produce a transient stimulating effect, probably of cholinergic origin, followed by a sustained relaxing effect, which may involve both cholinergic and noncholinergic pathways.

Acetylcholine↗
PubMed1993

Autonomic cardiovascular state after severe brain injury and brain death in children.

OBJECTIVE: To study and compare the autonomic cardiovascular state of children after severe brain injury and brain death. DESIGN: Prospective clinical study. SETTING: Pediatric ICU. PATIENTS: Pediatric patients suffering severe brain injury caused by trauma, anoxia, or hemorrhage. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: We analyzed cardiorespiratory parameters, heart rate power spectra, plasma catecholamine concentrations, and the response to the cold pressor test in nine brain-dead patients and compared the results with the test findings of 11 patients with severe brain injury. Low-frequency total heart rate power (p < .03), peak amplitude (p < .02), and plasma catecholamine concentrations (p < .001) were different with no overlap of values between groups. Cold pressor testing in patients with severe brain injury showed changes in respiratory rate and low-frequency heart rate power that were +/- 20% to 100% from baseline values; however, there were no measurable changes in brain-dead patients. CONCLUSIONS: Our results support the concept of a damaged sympathetic cardiovascular system in severe brain injury and complete interruption of the autonomic cardiovascular pathways in brain death. Since determination of brain death may be difficult, our findings have implications for corroborating brain death using autonomic cardiovascular testing.

Brain Death↗
PubMed1985

The influence of the autonomic system upon atrio-ventricular accessory pathways conductive performance.

In this report, the influence of the autonomic nervous system on the accessory pathway (Kent and Mahaim fibers) is discussed, based on electrophysiological and centrifuge examination results in two military pilots. We demonstrated that catecholamines reduce the effective refractory period (ERP) and improve conductivity in both the atrio-ventricular node (A-V node) and the accessory pathway. We concluded that the pattern of intermittent preexcitation may be connected with phenomenon of the 3rd and 4th phase block of the functional potential in the accessory pathway, and that in some cases the +Gz gravitoinertial tolerance test performed on the human centrifuge may help in distinguishing subjects with the intermittent preexcitation syndrome. Finally we concluded that all pilots with preexcitation syndrome should be dismissed from flying.

Adult↗
PubMed2003

Effects of chronic blockade of N-methyl-D-aspartate receptors by MK-801 on neuroplasticity of the micturition reflex pathway after partial urethral obstruction in the rat.

PURPOSE: To determine the role of N-methyl-D-aspartate (NMDA) glutamatergic receptors in the development of functional bladder changes after partial urethral obstruction we investigated the effects of repeat injection of MK-801, a noncompetitive NMDA receptor antagonist, on the micturition reflex in conscious obstructed rats. MATERIALS AND METHODS: In 9 female Wistar rats 1.0 mg/kg MK-801 was injected intramuscularly once weekly just prior to the creation of partial urethral obstruction until 5 weeks after obstruction. Five to 7 days after the last injection of MK-801 conscious filling cystometry was performed and compared with that in 9 obstructed rats treated with vehicle (saline). Conscious filling cystometry was also compared in 9 and 7 sham operated rats treated with repeat injection of MK-801 and vehicle, respectively. RESULTS: Partial urethral obstruction caused a significant increase in bladder weight. However, chronic MK-801 treatment did not affect bladder weight in obstructed or sham operated rats. In the obstructed/MK-801 vs the obstructed/vehicle group chronic treatment with MK-801 significantly increased bladder capacity (2.29 +/- 0.12 vs 1.73 +/- 0.16 ml, p <0.01) and voided volume (2.00 +/- 0.10 vs 1.56 +/- 0.17 ml, p <0.05) without changes in voiding efficiency (87.5% +/- 1.6% vs 87.8% +/- 1.7%) or micturition pressure (55.8 +/- 2.3 vs 56.4 +/- 3.0 cm water). Interestingly neither the frequency nor amplitude of premicturition contractions during filling was different in the groups. In sham operated rats chronic MK-801 treatment did not change bladder capacity, voided volume, voiding efficiency or micturition pressure significantly. CONCLUSIONS: The results in the current study suggest that bladder outlet obstruction causes NMDA receptor mediated alterations in bladder afferent pathways in the rat.

Animals↗
PubMed2005

Neural mechanisms of autonomic, affective, and cognitive integration.

Influential theoretical models propose a central role for afferent information from the body in the expression of emotional feeling states. Feedback representations of changing states of bodily arousal influence learning and facilitate concurrent and prospective decision-making. Functional neuroimaging studies have increased understanding of brain mechanisms that generate changes in autonomic arousal during behavior and those which respond to internal feedback signals to influence subjective feeling states. In particular, anterior cingulate cortex is implicated in generating autonomic changes, while insula and orbitofrontal cortices may be specialized in mapping visceral responses. Independently, ventromedial prefrontal cortex is recognized to support processes of internal (self-) reference that predominate in states of rest and disengagement and which putatively serve as a benchmark for dynamic interactions with the environment. Lesion data further highlight the integrated role of these cortical regions in autonomic and motivational control. In computational models of control, forward (efference copies) and inverse models are proposed to enable prediction and correction of action and, by extension, the interpretation of the behavior of others. It is hypothesized that the neural substrate for these processes during motivational and affective behavior lies within the interactions of anterior cingulate, insula, and orbitofrontal cortices. Generation of visceral autonomic correlates of control reinforce experiential engagement in simulatory models and underpin concepts such as somatic markers to bridge the dualistic divide.

Afferent Pathways↗
PubMed1996

Sympathetic nerve trajectories to rat orbital targets: role of connective tissue pathways.

The trajectories of sympathetic nerves projecting to orbital targets were determined in adult rats with intact innervation and following acute sympathetic denervation, neonatal unilateral superior cervical ganglionectomy, or unilateral ganglionectomy on postnatal day 30. Sympathetic nerves were identified by using immunofluorescence for the noradrenergic transmitter enzyme dopamine beta-hydroxylase and by using catecholamine histofluorescence. In rats with intact innervation, sympathetic fibers travel to the orbit in association with the abducens, trochlear, and Vidian nerves. Within the retroorbital and retroocular connective tissue, the fibers redistribute to become associated with sensory-nerve branches of the trigeminal nerve, the orbital vasculature, and the periorbital sheath. Fibers reach their targets by traversing variable amounts of connective tissue of the periorbitum, the orbital septa, and the striated muscle epimysia. Following neonatal ganglionectomy, intracranial fibers of contralateral origin enter the orbit by traveling through connective tissue of the optic nerve meninges and lining the anterior lacerated foramen. These fibers travel independent of the trochlear, abducens, and Vidian nerves, but, otherwise, they use the same orbital pathways as those employed in the intact animal. In animals ganglionectomized on postnatal day 30, fibers enter the posterior portion of the orbit primarily via the optic foramen; they travel only short distances and end blindly in the periorbital sheath. These findings indicate that fascial structures are a major component of the pathways that guide sympathetic fibers to their appropriate targets both in normal development and during reinnervation following neonatal ganglionectomy. Because orbital connective tissues are termination sites of abortive fiber sprouting in older rats, developmental changes in the properties of these tissues may contribute to the absence of pathway formation in the mature animal.

Adrenergic Fibers↗
PubMed1990

Role of visceral afferent mechanisms in functional bowel disorders.

This report analyzes the clinical and physiological evidence supporting a role for altered visceral afferent mechanisms in the pathogenesis of two functional bowel syndromes: noncardiac chest pain and the irritable bowel syndrome. Considerable recent evidence indicates that increased contractility is present only in a minority of patients and that hypercontractile episodes are not temporally related to abdominal pain. In contrast, altered sensation and motor reflexes in response to physiological stimuli, such as mechanical distention or acid, is common when appropriately investigated. The vagal and spinal afferent innervation mediates visceral sensation and is involved in multiple reflex loops regulating gastrointestinal effector function, such as motility and secretion. Sensory input can be modulated peripherally at the afferent nerve terminal, at the level of prevertebral ganglia, the spinal cord, and the brainstem. An up-regulation of afferent mechanisms would result both in altered conscious perception of physiological stimuli and in altered motor reflexes. Current evidence is consistent with an alteration in the peripheral functioning of visceral afferents and/or in the central processing of afferent information in the etiology of altered somatovisceral sensation and motor function observed in patients with functional bowel disease.

Afferent Pathways↗
PubMed2000

In vivo changes in free choline level induced by autonomic agonists in mouse organs, including three major salivary glands.

Whether free choline levels are changeable in vivo in response to different types of autonomic agonists was examined in several mouse organs. Upon one subcutaneous injection of isoproterenol, phenylephrine and pilocarpine, choline levels in whole organ decreased, increased and decreased, respectively, in various organs within 30 min and returned to initial levels in a day. In the three major salivary glands, a delayed choline elevation also appeared on day 2 after one isoproterenol injection and subsided by day 6. Only in the three salivary glands more choline was accumulated after 10 once-a-day injections of isoproterenol than after one isoproterenol injection. Neither phenylephrine nor pilocarpine induced comparable choline accumulation in any organs examined. Isoproterenol injection repeated at a 2-day interval augmented the subsequent, delayed choline elevation. Examination with dobutamine and the adenylyl cyclase activator 6-(3-dimethylaminopropionyl)forskolin suggested that isoproterenol-induced immediate choline lowering was down-stream of cAMP synthesis and linked to cAMP more tightly than the choline accumulation, though both choline changes occurred via beta1-adrenergic receptors. Choline levels in the salivary glands also changed depending on the form of diet given and particularly in the parotid gland in parallel with gland weights. These results provide the first evidence for the autonomic control of intracellular choline levels; intracellular choline levels might be an integral part of the autonomic signalling pathway.

Adrenergic alpha-Agonists↗