Small intestinal transit in the portal hypertensive rat

Reilly, James; Quigley, Eamonn Martin; Forst, Curtis F.; Rikkers, Layton F.

doi:10.1016/0016-5085(91)80010-7

Cited by 59 publications

(35 citation statements)

References 14 publications

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“…In our study, cirrhotic animals showed a slower intestinal transit than controls, although a significant relationship between this dismotility and BT could not be established. The lack of this statistic correlation may be due to the non-direct nature of the method used to assess intestinal transit compared with the more precise methods used in other studies (55,56).…”

Section: Discussionmentioning

confidence: 98%

Role of intestinal bacterial overgrowth and intestinal motility in bacterial translocation in experimental cirrhosis

Sánchez

Casafont

Guerra

et al. 2005

Rev. esp. enferm. dig.

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Background: intestinal bacterial overgrowth (IBO) is related to small bowel motility and has been involved in the pathogenesis of bacterial translocation (BT) in experimental models, and both overgrowing gut flora and translocating bacteria to mesenteric lymph nodes are common features in cirrhosis.Objectives: the aims of this study were to analyze cecal aerobic bacteria and intestinal transit in cirrhotic rats, and their relationship with BT, evaluating the role of intestinal bacterial overgrowth and small bowel dismotility in the development of BT in experimental cirrhosis.Material and methods: we included twenty-seven male Sprague-Dawley rats with carbon tetrachloride-induced cirrhosis without ascites and ten controls. Cultures of mesenteric lymph nodes (MLN), peripheral and portal blood, liver, spleen and cecal samples were carried out. Small intestinal transit was determined in ten cirrhotic rats and in ten control rats.Results: the prevalence of bacterial translocation was 56%. Total cecal aerobic bacteria count was significantly higher in cirrhotic rats than in control rats (p < 0.001). Cirrhotic rats with translocated bacteria had higher total aerobic intestinal counts than culture-negative MLN bacteria (p < 0.05). The prevalence of total intestinal bacterial overgrowth in cirrhotic animals was 67%, and 0% in control animals (p < 0.001). According to BT, total IBO was more frequent in cirrhotic rats with BT versus those without BT (93 vs. 33%) (p < 0.001). Of the translocating bacteria, 95.6% were found to be overgrown in the cecum. The smallintestinal transit was slower in cirrhotic rats (60.5 ± 12.7 cm vs. 81.2 ± 5.7 cm) than in control animals (p < 0.001).Conclusions: these results suggest that the increase of intestinal aerobic bacteria in experimental cirrhosis is associated with translocation. In addition, IBO is frequent in cirrhotic rats, and is supposed to play an important role in the development of BT. Impaired motility of the small intestine is a common feature in cirrhosis and may be implicated in the pathogenesis of IBO.

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Section: Discussionmentioning

confidence: 98%

Role of intestinal bacterial overgrowth and intestinal motility in bacterial translocation in experimental cirrhosis

Sánchez

Casafont

Guerra

et al. 2005

Rev. esp. enferm. dig.

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“…Therefore, reduction of PH is expected to increase hepatic processing of IgAIC. PH also decreases small intestinal motility promoting bacterial overgrowth [31,32] , while in the same time increases intestinal permeability [33] . In this regard, increased circulating IgA and IgAIC may represent an exaggerated response of immune system to excess gut antigen exposure [34,35] , resulting from diminished mucosal integrity and spillage of IgA into the circulation.…”

Section: Discussionmentioning

confidence: 99%

Association of liver cirrhosis related IgA nephropathy with portal hypertension

Kalambokis

Christou²,

Stefanou³

et al. 2007

WJG

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A high incidence of IgA nephropathy has been reported in patients with liver cirrhosis, though, clinically evident nephrotic syndrome is very uncommon. Impaired hepatic clearance of circulating IgA immune complexes and subsequent deposition in renal glomeruli has been considered principally in the pathogenesis of liver cirrhosis associated IgA nephropathy. Here we report on a patient with cryptogenic liver cirrhosis and splenic vein thrombosis, who presented with nephrotic syndrome. Renal biopsy showed findings consistent with IgA nephropathy. Lower endoscopy showed features of portal hypertensive colopathy. Following initiation of propranolol and anticoagulant treatment to reduce portal pressure, a gradual decrease of proteinuria and hematuria to normal range was noted. The potential p a t h o g e n e t i c ro l e o f p o r t a l hy p e r t e n s i o n i n t h e development of IgA nephropathy in cirrhotic patients is discussed.

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“…Intestinal hypomotility had not been previously reported in rats with cirrhosis, but our finding agrees with the observation of prolonged small intestinal transit in rats with portal vein stenosis and in patients with cirrhosis. 11,18,22 Moreover, cirrhotic patients with a history of SBP show higher incidence of IBO and more severe small intestine dismotility than cirrhotic patients without a history of SBP. 11 The pathogenesis of these abnormalities in small bowel motility remains speculative and is probably of multifactorial origin.…”

Section: Discussionmentioning

confidence: 99%

“…Intestinal transit was assessed by measuring the distribution of 51 Cr throughout the intestine, as previously described. 17,18 Once both ends of the small intestine were ligated, special care was taken during intestine handling to avoid movement of intestinal contents. The small intestine was mobilized from the ileum to the duodenum, freed from the mesentery, removed from the abdomen, placed longitudinally on a moist gauze, and divided into 5-cm segments.…”

Section: Methodsmentioning

confidence: 99%

Effect of propranolol on the factors promoting bacterial translocation in cirrhotic rats with ascites

et al. 2000

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Bacterial translocation appears to be an important mechanism in the pathogenesis of spontaneous infections in cirrhosis. Cirrhotic patients are commonly treated with ␤-adrenoceptor blockers, but the impact of this treatment in the factors promoting bacterial translocation has not been investigated. This study was aimed at investigating in cirrhotic rats with ascites the effect of propranolol on intestinal bacterial load, transit, and permeability of the bowel and on the rate of bacterial translocation. Bacterial translocation to mesenteric lymph nodes and intestinal bacterial overgrowth, permeability (urinary excretion of 99m Tc-diethylenetriaminepentaacetic acid [ 99m Tc-DTPA]), and transit (geometric center ratio of 51 Cr) were assessed in 29 rats with carbon tetrachloride (CCl 4 ) cirrhosis and 20 controls. These variables were then measured in 12 placebo-and in 13 propranolol-treated ascitic cirrhotic rats. Bacterial translocation was present in 48% of the cirrhotic rats and in none of the controls. Cirrhotic rats with intestinal bacterial overgrowth had a significantly higher rate of translocation and slower intestinal transit than those without it. Among the 15 rats with overgrowth and a 99m Tc-DTPA excretion greater than 10%, 15 had translocation and 2 had bacterial peritonitis. Only 1 of the 14 rats with either intestinal overgrowth or a 99m Tc-DTPA excretion greater than 10% presented translocation. Compared with the placebo group, propranolol-treated animals had significantly lower portal pressure, faster intestinal transit, and lower rates of bacterial overgrowth and translocation. In ascitic cirrhotic rats, bacterial translocation results from intestinal overgrowth and severe damage to gut permeability. In this setting, intestinal overgrowth is associated with intestinal hypomotility. Propranolol accelerates the intesti- Cirrhotic patients are prone to bacterial infections, with spontaneous bacterial peritonitis (SBP) being the most characteristic. Clinical and experimental evidence indicates that translocation of bacteria from the intestinal lumen to the bloodstream is directly involved in the pathogenesis of these spontaneous infections. SBP is caused predominantly by enteric organisms, 1 and selective intestinal decontamination lowers the rate of first or recurrent SBP in cirrhotic patients. 2 Studies in carbon tetrachloride (CCl 4 )-induced cirrhotic rats have shown the frequent, simultaneous presence of bacterial translocation (BT) and SBP caused by enteric organisms, 3-5 a higher rate of BT in ascitic than in nonascitic animals, 6 frequent genotype identity between ileal flora and bacteria colonizing the mesenteric lymph nodes (MLN), 7 and a reduction, by selective intestinal decontamination, in the incidence of BT after hemorrhagic shock. 8 The factors that favor BT in cirrhosis are incompletely understood. Proposed mechanisms include disruption of the equilibrium of normal intestinal bacterial flora, increased permeability of the intestinal mucosal barrier, and deficiencies in host immune def...

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Small intestinal transit in the portal hypertensive rat

Cited by 59 publications

References 14 publications

Role of intestinal bacterial overgrowth and intestinal motility in bacterial translocation in experimental cirrhosis

Role of intestinal bacterial overgrowth and intestinal motility in bacterial translocation in experimental cirrhosis

Association of liver cirrhosis related IgA nephropathy with portal hypertension

Effect of propranolol on the factors promoting bacterial translocation in cirrhotic rats with ascites

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