Ischemia/reperfusion-induced disruption of rat small intestine transit is reversed by total enteral nutrition

Grossie, V. Bruce; Weisbrodt, Norman W.; Moore, Frederick A.; Moody, Frank G.

doi:10.1016/s0899-9007(01)00668-2

Cited by 41 publications

(16 citation statements)

References 27 publications

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“…Consistent with this general observation, ischemia/reperfusion injury causes pathological changes in gastrointestinal motility (Udassin et al 1995;Grossie et al 2001;Hakgüder et al 2002;Türler et al 2002). Intestinal ischemia can occur when the intestine is transplanted and because transplantation is being increasingly used to treat patients with severe disorders that are refractory to parenteral feeding (Fryer 2005), it is important to investigate the nature and mechanisms of neuronal damage.…”

Section: Introductionmentioning

confidence: 87%

“…Loss of descending inhibition in the human colon results in stasis, as in Hirschsprung's disease (Swenson 2002) and in experimental animals, antagonism of transmission from NOS neurons inhibits transit (Ferens et al 2005). Thus, the damage to NOS neurons could contribute to the inhibition of transit that has been observed after I/R damage (Udassin et al 1995;Grossie et al 2001;Hakgüder et al 2002;Türler et al 2002;Calcina et al 2005). Because neurons die and neuronal damage outlasts the period of ischemia and the immediate reperfusion, it is likely that I/R damage to neurons contributes to sustained functional impairment.…”

Section: Possible Roles Of Neuronal Damagementioning

confidence: 99%

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Deleterious effects of intestinal ischemia/reperfusion injury in the mouse enteric nervous system are associated with protein nitrosylation

et al. 2011

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Changes in intestinal function, notably impaired transit, following ischemia/reperfusion (I/R) injury are likely to derive, at least in part, from damage to the enteric nervous system. Currently, there is a lack of quantitative data and methods on which to base quantitation of changes that occur in enteric neurons. In the present work, we have investigated quantifiable changes in response to ischemia of the mouse small intestine followed by reperfusion from 1 h to 7 days. I/R caused distortion of nitric oxide synthase (NOS)-containing neurons, the appearance of a TUNEL reaction in neurons, protein nitrosylation and translocation of Hu protein. Protein nitrosylation was detected after 1 h and was detectable in 10% of neurons by 6 h in the ischemic region, indicating that reactive peroxynitrites are rapidly produced and can interact with proteins soon after reperfusion. Apoptosis, revealed by TUNEL staining, was apparent at 6 h. The profile sizes of NOS neurons were increased by 60% at 2 days and neurons were still swollen at 7 days, both in the ischemic region and proximal to the ischemia. The distribution of the enteric neuron marker and oligonucleotide binding protein, Hu, was significantly changed in both regions. Hu protein translocation to the nucleus was apparent by 3 h and persisted for up to 7 days. Particulate Hu immunoreactivity was observed in the ganglia 3 h after I/R but was never observed in control. Our observations indicate that effects of I/R injury can be detected after 1 h and that neuronal changes persist to at least 7 days. Involvement of NO and reactive oxygen species in the changes is indicated by the accumulation of nitrosylated protein aggregates and the swelling and distortion of nitrergic neurons. It is concluded that damage to the enteric nervous system, which is likely to contribute to functional deficits following ischemia and re-oxygenation in the intestine, can be quantified by Hu protein translocation, protein nitrosylation, swelling of nitrergic neurons and apoptosis.

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Section: Introductionmentioning

confidence: 87%

Section: Possible Roles Of Neuronal Damagementioning

confidence: 99%

Deleterious effects of intestinal ischemia/reperfusion injury in the mouse enteric nervous system are associated with protein nitrosylation

et al. 2011

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“…Studies that have investigated changes up to 48 h after superior mesenteric artery occlusion indicate that intestinal transit is slowed, and that motility is inhibited (Udassin et al 1995;Hierholzer et al 1999;Grossie et al 2001;Hakgüder et al 2002;Calcina et al 2005). The prolonged changes in motility that are observed after intestinal transplant are considered to be attributable to I/R damage, which adversely effects neuro-muscular control (Türler et al 2002a).…”

Section: Introductionmentioning

confidence: 99%

Damaging effects of ischemia/reperfusion on intestinal muscle

et al. 2010

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Periods of ischemia followed by restoration of blood flow cause ischemia/reperfusion (I/R) injury. In the intestine, I/R damage to the mucosa and neurons is prominent. Functionally, abnormalities occur in motility, most conspicuously a slowing of transit, possibly as a consequence of damage to neurons and/or muscle. Here, we describe degenerative and regenerative changes that have not been previously reported in intestinal muscle. The mouse small intestine was made ischemic for 1 h, followed by re-perfusion for 1 h to 7 days. The tissues were examined histologically, after hematoxylin/eosin and Masson's trichrome staining, and by myeloperoxidase histochemistry to detect inflammatory reactions to I/R. Histological analysis revealed changes in the mucosa, muscle, and neurons. The mucosa was severely but transiently damaged. The mucosal surface was sloughed off at 1-3 h, but re-epithelialization occurred by 12 h, and the epithelium appeared healthy by 1-2 days. Longitudinal muscle degeneration was followed by regeneration, but little effect on the circular muscle was noted. The first signs of muscle change were apparent at 3-12 h, and by 1 and 2 days, extensive degeneration within the muscle was observed, which included clear cytoplasm, pyknotic nuclei, and apoptotic bodies. The muscle recovered quickly and appeared normal at 7 days. Histological evidence of neuronal damage was apparent at 1-7 days. Neutrophils were not present in the muscle layers and were infrequent in the mucosa. However, they were often seen in the longitudinal muscle at 1-3 days and were also present in the circular muscle. Neutrophil numbers increased in the mucosa in both I/R and sham-operated animals and remained elevated from 1 h to 7 days. We conclude that I/R causes severe longitudinal muscle damage, which might contribute to the long-term motility deficits observed after I/R injury to the intestine.

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“…The MMC cycle length and MI in the 90% PHx ϩ saline group did not differ from those in the 90% PHx group, although the MMC cycle length tended to decrease at 1 day after surgery in the 90% PHx ϩ saline group compared with the 90% PHx group, which may have been associated with systemic volume expansion and/or local stimulation of the gut by saline administration (Table 1, Fig. 4) [11]. …”

Section: Effect Of Saline Administration On Ileal Motility Induced Bymentioning

confidence: 87%

Role of Bile in Intestinal Motility After Massive Liver Resection in Conscious Rats

Shimura

Suehiro

et al. 2008

Journal of Surgical Research

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Ischemia/reperfusion-induced disruption of rat small intestine transit is reversed by total enteral nutrition

Cited by 41 publications

References 27 publications

Deleterious effects of intestinal ischemia/reperfusion injury in the mouse enteric nervous system are associated with protein nitrosylation

Deleterious effects of intestinal ischemia/reperfusion injury in the mouse enteric nervous system are associated with protein nitrosylation

Damaging effects of ischemia/reperfusion on intestinal muscle

Role of Bile in Intestinal Motility After Massive Liver Resection in Conscious Rats

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