Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0599766 (functional recovery)
 13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Canine bladders were distended for 4 h at 100 cm H2O to study the effects of distension on bladder function and structure. A micturition study was performed before overstretching, immediately after distension and 5 days after it. Bladder function was impaired immediately after distension, compliance and residual urine were increased and the maximum pressure during voiding decreased. The function returned to normal after 5 days. Overstretching caused diffuse or focal submucosal haemorrhages, only rarely fibrosis or necrosis of bladder wall. Electron microscopic changes of the bladder peripheral nerves were slight, the consistent finding being oedema in areas of outer mesoaxons and between cytoplasmic processes of Schwann cells. This change was sometimes accompanied by a rupture of the surrounding basement membrane. Axonal lysis was observed in one case. It is concluded that these anatomical changes, although found at the moment of functional recovery, may be linked to impaired conductivity of nerves in the bladder wall causing, at least partly, its impaired function. This may further decrease bladder instability and after urinary retention cause prolonged micturition problems. Functional recovery occurs, however, quite rapidly in healthy bladders.
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PMID:Effect of distension on function and nervous ultrastructure in the canine urinary bladder. 367 57

In order to understand the influence of obstruction duration on the recovery of obstructed bladders, a functional study of 36 obstructed rabbit bladders after relief of outlet obstruction was done. Bladder outlets were obstructed by placing a 5-mm inner diameter polyethylene cuff around the urethra. Obstructions were kept in place for varying periods: 1 day, 3 days, 1 week, 2 weeks, 4 weeks, 6 weeks and 8 weeks. The obstructions were then released and functional studies were performed after a recovery period of 2 weeks (experimental groups). Using results of another study of obstructed bladders as a basis, the bladder weight of the experimental groups decreased from an initial increase after obstruction, but stabilized at a 2.5-fold increase 8 weeks after release compared with the control bladders. In vitro whole bladder responses to electrical and carbachol stimulations were also studied. Significant functional recovery was noted in the experimental bladders of less than 4 weeks' obstruction, whereas in those of 6 weeks' and 8 weeks' obstruction, no definite functional improvement was noted after relief of outlet obstruction. The expulsion ability was not significantly better in the experimental bladders than in the obstructed bladders. A slight decrease in expulsion ability was noted in the experimental bladders as the obstructive duration increased but the difference was not statistically significant. An obstructive duration of up to 8 weeks did not have a significant influence on the functional recovery of the rabbit bladders. Applying these results to the management of humans with benign prostatic hyperplasia, surgical intervention seems indicated only in those patients with symptomatic outlet obstruction. Stable, mild obstruction can probably be treated conservatively.
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PMID:Recovery of bladder function after relief of mild outlet obstructions of different durations in rabbits. 877 54

Transplanting neuronal and glial restricted precursors (NRP/GRP) into a midthoracic injury 9 d after contusion improved bladder and motor function, diminished thermal hypersensitivity, and modified lumbosacral circuitry compared with operated controls (OP-controls). Histological analysis showed that NRP/GRP survived, filled the lesion site, differentiated into neurons and glia, and migrated selectively. Volume of spinal cord spared was increased in NRP/GRP recipients, suggesting local protection. Bladder areflexia developed in both operated groups, but NRP/GRP recipients exhibited an accelerated recovery, with decreased micturition pressure and fewer episodes of detrusor hyperreflexia. Because noradrenergic receptors proliferate after spinal injury and descending noradrenergic pathways contribute to regulation of bladder control, we examined the effects of administering an alpha-1A-adrenergic antagonist, Tamsulosin, on urodynamics. This improved all cystometric parameters in both operated groups, and micturition pressure in NRP/GRP rats recovered to normal levels. Both operated groups initially showed increased sensitivity to a thermal stimulus applied to the tail; the NRP/GRP rats showed significant improvement over time. NRP/GRP grafts also produced greater recovery of hindlimb function in several tests, although both groups showed persistent and similar deficits in locomotion on a grid. Because bladder, hindlimb, and tail sensory and motor functions are organized through lumbosacral cord, we examined descending and primary afferent projections at L6-S1. The density of serotonergic, noradrenergic, and corticotrophin releasing factor-positive fibers increased in the NRP/GRP group compared with OP-controls, suggesting some sparing and/or sprouting of these modulatory pathways. Immunocytochemical staining density of dorsal root axons in the dorsal horn increased in the OP-controls but appeared normal in the NRP/GRP group. Synaptophysin immunoreactivity in the lumbosacral dorsal horn was similar among groups, consistent with restoration of synaptic density in both groups of operated animals but by different pathways. We suggest that local protection provided by NRP/GRP resulted in increased sparing/sprouting of descending pathways, which prevented sprouting by dorsal root axons, and that this modification in lumbosacral circuitry contributes to the recovery of function.
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PMID:Transplantation of neuronal and glial restricted precursors into contused spinal cord improves bladder and motor functions, decreases thermal hypersensitivity, and modifies intraspinal circuitry. 1623 67

The aim of this study was to examine the expression profile of the vesicular acetylcholine transporter (VAChT), which is a cholinergic pre-synaptic marker, in the lower neural tract following spinal cord injury (SCI) and its effect on coordination of micturition. In adult female Sprague-Dawley rats, SCI was induced by complete transection of the spinal cord at T9. At various time points, 3, 7, 14 and 28 days, after SCI, cystometry was performed on conscious rats. Bladder areflexia was observed during the first week. Twenty-eight days after SCI the rats showed reflex contractions and voiding. The expression of VAChT was examined with immunohistochemistry. The number of VAChT-positive nerve terminals, which were surrounding neuronal soma, was transiently decreased in pelvic ganglion and spinal cord (L1, L2, L6 and S1). In particular VAChT terminals surrounding motor neurons in the ventral horn and autonomic pre-ganglion cells were dramatically decreased from 3 to 14 days after SCI. Similarly, and the number of VAChT-positive fibers in the bladder wall was also decreased. The intensity of VAChT terminals recovered in all above regions in conjunction with recovery of bladder function. These observations indicate that the transient decrease of the VAChT-positive nerve might cause a failure of cholinergic neuronal transmission along the urinary bladder tract after SCI. As the cholinergic system was recovered at least in rat, the functional recovery of neurogenic bladder syndrome in SCI patients may become possible by further understanding the mechanism underlying the recovery of cholinergic system in rat.
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PMID:Transient suppression of the vesicular acetylcholine transporter in urinary bladder pathways following spinal cord injury. 1722 8

Cylophosphamide (CYCL) is a strong anticancer and immunosuppressive agent but its urotoxicity presents one of the major toxic effects that limit its wide usage particularly in high dose regimens. Therefore, this study aimed to investigate Acacia Senegal gum exudate ,Gum Arabic (GA), for its possible role as a natural, nontoxic agent against CYCL-induced urotoxicity. Male Swiss albino rats were exposed to CYCL (150 mg/kg BW, once i.p) with or without GA oral supplementation (7.5 g/kg/day for 6 days) through drinking water. Glutathione (GSH), Malondialdehyde (MDA) and Nitric oxide (NO) bladder contents were assessed. Responsiveness of the bladder rings to acetylcholine (ACh) in vitro, microscopic and macroscopic features are also investigated. CYCL produced pronounced harmful effects on bladder urothelial lining with significant increases in (MDA) and NO levels in the tissue homogenates. Bladder-GSH content is dropped by over 60% following CYCL injection. Bladder contractility, as measured by its responsiveness to ACh, recorded a marked reduction. The isolated bladders exhibited such macroscopic changes as severe edema, inflammation and extravasation. The bladder weight increased as well. Histological changes were evident in the form of severe congestion, petechial hemorrhage and chronic inflammatory reaction in the lamina propria accompanied with desquamated epithelia. GA, a potential protective agent, produced an almost complete reversal of NO induction, lipid peroxidation or cellular GSH bladder contents in the GA+CYCL-treated group. Likewise, bladder inflammation and edema were reduced. Bladder rings showed a remarkable recovery in their responsiveness to ACh. Bladder histological examination showed a near normal configuration and structural integrity, with a significant reduction in inflammation and disappearance of focal erosions. These remarkable effects of GA may be attributed to its ability to neutralize acrolein, the reactive metabolite of CYCL and/or the resultant reactive oxygen metabolites, through a scavenging action. GA may limit the cascading events of CYCL -induced damage, initiating a cytoprotective effect leading to structural and functional recovery of the bladder tissues.
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PMID:Acacia Senegal gum exudate offers protection against cyclophosphamide-induced urinary bladder cytotoxicity. 2071 6

Following peripheral nerve injury, restoration of function may occur via the regeneration of injured axons or compensatory sprouting of spared axons. Injury to visceral nerves that control urogenital organs is a common consequence of pelvic surgery, however their capacity to reinnervate organs is poorly understood. To determine if and how sensory and motor connections to the bladder are re-established, a novel surgical model of visceral nerve injury was performed unilaterally in adult male Wistar rats. Bladder-projecting motor and sensory neurons in pelvic ganglia and lumbosacral dorsal root ganglia, respectively, were identified and characterised by retrograde tracing and immunofluorescence. Application of tracers ipsi- and contralateral to injury distinguished the projection pathways of new connections in the bladder. In naive animals, the majority of sensory and motor neurons project ipsilaterally to the bladder, while ~20 % project contralaterally and ~5 % bilaterally. Injured axons of motor neurons were unable to regenerate by 4weeks after transection. In contrast, by this time many injured sensory neurons regrew axons to reform a substantial plexus within the detrusor and suburothelial tissues. These regeneration responses were also indicated by upregulation of activating transcription factor-3 (ATF-3), which was sustained in motor neurons but transient in sensory bladder-projecting neurons. Axotomy had little or no effect on the survival of bladder-projecting sensory and motor neurons. We also found evidence that uninjured motor and sensory neurons develop additional projections to the denervated bladder tissue and return connectivity, likely by undergoing compensatory growth. In conclusion, our results show that visceral sensory and motor neurons have a different capacity to regenerate axons following axotomy, however in both components of the circuit uninjured bladder neurons spontaneously grow new axon collaterals to replace the lost terminal field within the organ. For a full functional recovery, understanding the environmental and cellular mechanisms that reduce the ability of pelvic ganglion cells to undergo axonal regeneration is needed.
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PMID:Regeneration of sensory but not motor axons following visceral nerve injury. 2572 51