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Rodrigues, Cleonísio Leite; Gondim, Francisco de Assis Aquino; Leal, Paulo Roberto Lacerda; Camurça, Flávio Duarte; Freire, Caio Castro; Santos, Armênio Aguiar dos; Rola, Francisco H.

doi:10.1023/a:1010624730975

Cited by 19 publications

References 20 publications

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Autonomic Consequences of Spinal Cord Injury

Hou

Rabchevsky

2014

Comprehensive Physiology

179

112

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Spinal cord injury (SCI) results not only in motor and sensory deficits but also in autonomic dysfunctions. The disruption of connections between higher brain centers and the spinal cord, or the impaired autonomic nervous system itself, manifests a broad range of autonomic abnormalities. This includes compromised cardiovascular, respiratory, urinary, gastrointestinal, thermoregulatory, and sexual activities. These disabilities evoke potentially life-threatening symptoms that severely interfere with the daily living of those with SCI. In particular, high thoracic or cervical SCI often causes disordered hemodynamics due to deregulated sympathetic outflow. Episodic hypertension associated with autonomic dysreflexia develops as a result of massive sympathetic discharge often triggered by unpleasant visceral or sensory stimuli below the injury level. In the pelvic floor, bladder and urethral dysfunctions are classified according to upper motor neuron versus lower motor neuron injuries; this is dependent on the level of lesion. Most impairments of the lower urinary tract manifest in two interrelated complications: bladder storage and emptying. Inadequate or excessive detrusor and sphincter functions as well as detrusor-sphincter dyssynergia are examples of micturition abnormalities stemming from SCI. Gastrointestinal motility disorders in spinal cord injured-individuals are comprised of gastric dilation, delayed gastric emptying, and diminished propulsive transit along the entire gastrointestinal tract. As a critical consequence of SCI, neurogenic bowel dysfunction exhibits constipation and/or incontinence. Thus, it is essential to recognize neural mechanisms and pathophysiology underlying various complications of autonomic dysfunctions after SCI. This overview provides both vital information for better understanding these disorders and guides to pursue novel therapeutic approaches to alleviate secondary complications.

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Autonomic Consequences of Spinal Cord Injury

Hou

Rabchevsky

2014

Comprehensive Physiology

179

112

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Colonic Electrical Stimulation Regulates Colonic Transit Via the Nitrergic Pathway in Rats

Shi¹,

Chen²

2006

Dig Dis Sci

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Gastrointestinal electrical stimulation has been proposed for the treatment of gastrointestinal motor disorders. However, little is known about potential roles of colonic electrical stimulation (CES). The aim of this study was to evaluate the effect and mechanism of CES on colonic transit in conscious rats. Male rats (N = 14) were equipped with a pair of colonic serosal electrodes for stimulation and a catheter in the colon. Colonic transit was assessed in four randomized sessions with or without CES and with or without nitric oxide synthesis blocker, L-NNA, by calculating the output of phenol red from the anus every 10 min for 90 min. Results were as follows. (1) CES with trains of short pulses significantly enhanced colonic transit. Colonic emptying was 57.3 +/- 6.1% in the control session and 81.9 +/- 4.6% with CES at 90 min, reflecting a 43% increase. (2) L-NNA delayed colonic transit compared with saline and prevented the accelerative effect of CES on colonic transit. We conclude that CES has an excitatory effect on colonic transit and this excitatory effect may be mediated via the nitrergic pathway.

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On the Complex Autonomic Changes Involved in the Inhibition of Gastrointestinal Motility After Spinal Cord Injury (SCI)

et al. 2006

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We read with interest the paper published by Chen et al.(1) in a recent issue of Digestive Diseases and Sciences. The authors observed that the orocecal transit time (OCTT) of 36 patients with SCI was delayed, more significantly in quadraplegic than in paraplegic patients. SCI patients had a higher prevalence of gastrointestinal (GI) complaints and the OCTT was negatively correlated with the low frequency of heart rate variability. The authors concluded that the OCTT delay was probably due to loss of sympathetic activity.Decreased sympathetic activity resulting in hypotension is known to occur after SCI. Delayed lower GI motility has also been extensively reported in experimental animals and humans. Delayed upper GI motility has been well described in rats (2, 3), although as the authors pointed out, conflicting results have been found in humans (1). Therefore, it would not be surprising that both decreased sympathetic activity (evidenced by heart rate analysis) and delayed OCTT were found in SCI patients. Despite the negative correlation between sympathetic activity and OCTT, direct causality between the low sympathetic activity and the delayed OCTT cannot be established, since heart rate variability is a marker of cardiovascular sympathetic activity, which only indirectly reflects the overall activity in other systems, like the GI tract.The dichotomy of opposing sympathetic and parasympathetic activity resulting from an "autonomous nervous system," which was proposed in the early twentieth century, has been replaced by recent advances on the multiplicity of neurotransmitters and complex interactions between the so-called central regulators and vagus and spinal centers. In our experimental model of SCI, we observed that subdiaphragmatic vagotomy and celiac ganglionectomy + section of the splanchnic nerves or yohimbine prevented the inhibition of gastric emptying and GI transit after SCI (5). This indicated that rather than a loss of sympathetic activity, more complex phenomena are responsible for the inhibition of GI motility after SCI. More recently, we have also observed that the facilitation of inhibitory GI reflexes may be crucial for the development of upper GI motility in rats (6, 7). Further research is necessary to clarify this rather complex subject, but research focused on nonadrenergic, noncholinergic pathways is likely to clarify this matter and further help the management of the GI dysfunction in patients with SCI.

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Cited by 19 publications

References 20 publications

Autonomic Consequences of Spinal Cord Injury

Autonomic Consequences of Spinal Cord Injury

Colonic Electrical Stimulation Regulates Colonic Transit Via the Nitrergic Pathway in Rats

On the Complex Autonomic Changes Involved in the Inhibition of Gastrointestinal Motility After Spinal Cord Injury (SCI)

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