Subtotal nephrectomy inhibits the gastric emptying of liquid in awake rats

Graça, José Ronaldo Vasconcelos da; Parente, Cynara Carvalho; Fiuza, Robério Ferreira; Silva, Pedro Alberto Freitas da; Mota, Bruno Teixeira; Salles, Luiz Derwal; Silva, Camila Meirelles de Souza; Silva, Moisés Tolentino Bento da; Oliveira, Ricardo Brandt de; Santos, Armênio Aguiar dos

doi:10.14814/phy2.12291

Cited by 9 publications

(10 citation statements)

References 31 publications

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“…In the present study, we therefore chose this model, and used the charcoal transport assay to objectively assess the effect of CKD on intestinal motility. The results showed that CKD induced a progressive decrease in the intestinal transit at all investigated time points, reaching statistical significance level on postoperative weeks 8 and 10, indicating that CKD could indeed decrease intestinal motility, which were consistent with the results reported by others [4,31].…”

Section: Discussionsupporting

confidence: 92%

Chronic Kidney Disease Elicits an Intestinal Inflammation Resulting in Intestinal Dysmotility Associated with the Activation of Inducible Nitric Oxide Synthesis in Rat

et al. 2018

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This study was conducted to investigate whether chronic kidney disease (CKD) affects intestinal inflammation and intestinal motility and the underlying mechanisms. Rats were randomized into control group and uremic group. Uremia rats were induced by the 5/6 kidney resection, while the control went through the same procedures but without any kidney resection. Intestinal motility was assessed by charcoal transport assay; intestinal inflammation was assessed by analyses of levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 in the ileum tissue. The inducible nitric oxide synthesis (iNOS) activity was assessed in the ileum tissue. The results showed that the intestinal motility in uremic group was significantly decreased compared with that in the control group on postoperative weeks 8 and 10. Meanwhile, the uremic group presented significantly higher concentrations of TNF-α, IL-6, and IL-10 than control group on postoperative weeks 8 and/or 10, and higher gene expression on postoperative weeks 6, 8, and 10. Furthermore, the intestinal iNOS activity in the uremic group was significantly increased compared with that in control group on postoperative weeks 8 and 10. These results suggest that CKD could induce intestinal inflammation and lead to intestinal dysmotility, which may be associated with iNOS activation in the intestine.

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Section: Discussionsupporting

confidence: 92%

Chronic Kidney Disease Elicits an Intestinal Inflammation Resulting in Intestinal Dysmotility Associated with the Activation of Inducible Nitric Oxide Synthesis in Rat

et al. 2018

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“…The present results are in line with previous reports supporting a gut dysmotility in animal models or humans. Da Graça et al reported an impaired gastric emptying in 5/6 nephrectomized rats [ 14 ]. Acute renal failure results decreased motility of the duodenum and the distal colon in rats [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

“…Lefèvre et al demonstrated that duodeno-jejunal motility and colonic transit time were altered in dogs with moderate renal failure [ 12 ]. Rats with CKD (induced surgically by 5/6 subtotal nephrectomy) exhibited alteration of the interdigestive migrating complex (IMC), reduced gastric emptying and small intestinal transit [ 13 , 14 ]. However, limited data is available regarding the mechanisms that underlie gut dysmotility associated with renal failure.…”

Section: Introductionmentioning

confidence: 99%

Distal Colon Motor Dysfunction in Mice with Chronic Kidney Disease: Putative Role of Uremic Toxins

Hoibian

Florens

Koppe

et al. 2018

Toxins

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Although gastrointestinal complications are a common feature of patients with chronic kidney disease (CKD), the impact of uremia on bowel motility remains poorly understood. The present study was, therefore, designed to investigate the impact of uremia on gut motility. Kidney failure was induced in mice by chemical nephrectomy using an adenine diet (0.25% w/w). Gastrointestinal transit time and colon motility were explored in vivo and ex vivo. Colons from control mice were incubated with uremic plasma or uremic toxins (urea, indoxyl-sulfate or p-cresyl-sulfate) at concentrations encountered in patients with end-stage renal disease. Mice fed an adenine diet for 3 weeks exhibited a 3-fold increase in plasma urea (p < 0.001) evidencing kidney failure. The median gastrointestinal transit time was doubled (1.8-fold, p < 0.001) while a reduction in colonic propulsive motility was observed in CKD mice (3-fold, p < 0.001). Colon from CKD mice exhibited an abnormal pattern of contraction associated with a blunted maximal force of contraction. Control colons incubated with plasma from hemodialysis patients exhibited a blunted level of maximal contraction (p < 0.01). Incubation with urea did not elicit any difference but incubation with indoxyl-sulfate or p-cresyl-sulfate decreased the maximal force of contraction (−66% and −55%, respectively. p < 0.01). Taken together, these data suggest that uremia impairs colon motility probably through the retention of uremic toxins. Colon dysmotility might contribute to the gastrointestinal symptoms often reported in patients with CKD.

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“…Polyethylene glycol is commonly used for experimentally reducing plasma volume, causing acute dehydration in cells. In studies of gastric emptying in PNX animals, it was able to reverse gastric emptying reducing hypervolemia 11 . In this study, it was able to reverse colonic secretion of water and sodium by returning its absorptive capacity in partially nephrectomized animals (Figure 3).…”

Section: Discussionmentioning

confidence: 50%

“…Research on rats submitted to 5/6 nephrectomy has shown that there is a significant reduction in gastric emptying, and when submitted to bilateral nephrectomy they present intense intestinal secretion of water and electrolytes in the duodenal, jejunal and ileal segments 3 , 10 , 11 . Any kind of electrolyte imbalance is dangerous since the optimal functioning of the body depends on it.…”

Section: Introductionmentioning

confidence: 99%

Effect of Chronic Renal Dysfunction on the Permeability of the Colon to Water and Electrolytes: Experimental Study in Rats

Freire¹,

Albuquerque²,

Leal³

et al. 2019

ABCD, arq. bras. cir. dig.

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Background: Renal insufficiency is a disease that affects several organs by provoking hypervolemia and uremia. The disease reaches more than 500 million people worldwide and few studies bring their influence on the gastrointestinal tract. Aim: To evaluate the influence of 5/6 nephrectomy-induced hypervolemia on colonic permeability to water and electrolytes. Method: Sixty male Wistar rats weighing between 280-300 g were divided into three groups: 3, 7 and 14 days after nephrectomy, each one having a false-operated/control and partially nephrectomized. For colonic permeability they were submitted to colonic perfusion with a solution of Tyroad containing phenolphthalein. Differences among the concentrations of Na+, K+ and Cl- were used to calculate the rate of colonic permeability for the electrolytes. Phenolphthalein concentrations were used to evaluate the rate of secretion and water absorption. Results: The colonic secretion of water and electrolytes occurred expressively in the group seven days after nephrectomy. Hemodynamic and biochemical assessments determined the progression of renal failure in all three groups and polyethylene glycol was shown to be effective in reversing the secretory capacity of the colon. Conclusion: Hypervolemia established after 7 days post-nephrectomy 5/6 caused marked colonic secretion for water and electrolytes. The organism presents progressive colonic secretion as the blood volume increases; on the other hand, polyethylene glycol was able to revert this secretory framework of the colon to water and electrolytes by reversing the hypervolemia.

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Subtotal nephrectomy inhibits the gastric emptying of liquid in awake rats

Cited by 9 publications

References 31 publications

Chronic Kidney Disease Elicits an Intestinal Inflammation Resulting in Intestinal Dysmotility Associated with the Activation of Inducible Nitric Oxide Synthesis in Rat

Chronic Kidney Disease Elicits an Intestinal Inflammation Resulting in Intestinal Dysmotility Associated with the Activation of Inducible Nitric Oxide Synthesis in Rat

Distal Colon Motor Dysfunction in Mice with Chronic Kidney Disease: Putative Role of Uremic Toxins

Effect of Chronic Renal Dysfunction on the Permeability of the Colon to Water and Electrolytes: Experimental Study in Rats

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