Mesenteric lymph collected during peritonitis or sepsis potently inhibits gastric motility in rats

Jörg Glatzle, Christian M. Leutenegger, Mario H. Mueller, Martin E. Kreis, Helen E Raybould, Tilman T. Zittel

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Gastrointestinal motility is strongly inhibited during peritonitis or sepsis and proinflammatory cytokines released into mesenteric lymph during an acute gastrointestinal insult mediate systemic responses. We investigated whether mesenteric lymph collected during peritonitis or sepsis inhibits gastric motility and gastric emptying. Mesenteric lymph was collected for 12 hours from three experimental groups: vehicle (saline, 1 ml, intraperitoneally [ip], control lymph), peritonitis (0.5% acetic acid, 1ml, ip, peritonitis lymph), and sepsis (lipopolysaccharide [LPS], 5 mg/kg, 1 ml, ip, sepsis lymph). Gastric motility and gastric emptying were measured in recipient rats in response to lymph injections into the jugular vein. Quantitative polymerase chain reaction (PCR) for tumor necrosis factor α (TNFα) gene expression in the jejunum and in lymph cells were measured during sepsis. Mesenteric lymph flow significantly increased during peritonitis or sepsis (lymph flow [ml] per 60 minutes; control 2.45 ± 0.04; peritonitis 2.67 ± 0.07; sepsis 3.25 ± 0.1, p < 0.01 vs. control). Injection of peritonitis or sepsis lymph (1 ml) produced a significant and prolonged inhibition of gastric motility in recipient rats (decrease in intragastric pressure and duration: control lymph -0.14 ± 0.05 cm H 2O, 1.89 ± 1.31 minutes; peritonitis lymph: -0.56 ± 0.06 cm H 2O, 9.9 ± 0.9 minutes; sepsis lymph: -0.51 ± 0.05 cm H 2O, 6.9 ± 0.6 minutes; p < 0.001 vs. control for all comparisons). Gastric emptying was significantly inhibited by continuous infusion of sepsis lymph (3 ml per 60 minutes; gastric emptying: saline 81% ± 4%; control lymph: 80% ± 6%; sepsis lymph: 44% ± 10%; p < 0.001 vs. control). TNFα gene expression in the gut wall of the jejunum increased during sepsis over 90-fold within the first 2 hours and decreased continuously thereafter (relative TNFα mRNA transcription: basal 1.0 ± 0.05; LPS 2 hours: 91.9 ± 2.6, p < 0.001 vs. basal; 12 hours: 24.7 ± 16.8, not significant [NS]; 24 hours: 7.0 ± 3.4, NS). In conclusion, mediators in mesenteric lymph, possibly cytokines, may be responsible for the inhibition of gastric motility during peritonitis or sepsis. Because the composition of mesenteric lymph probably reflects the interstitial fluid of the gut wall, monitoring visceral lymph might be an extremely beneficial tool to determine mediators released during impaired gut wall function.

Original languageEnglish (US)
Pages (from-to)645-652
Number of pages8
JournalJournal of Gastrointestinal Surgery
Volume8
Issue number6
DOIs
StatePublished - Sep 10 2004
Externally publishedYes

Fingerprint

Lymph
Peritonitis
Sepsis
Stomach
Gastric Emptying
Tumor Necrosis Factor-alpha
Jejunum
Lipopolysaccharides
Cytokines
Gene Expression
Injections
Gastrointestinal Motility
Extracellular Fluid
Jugular Veins

Keywords

  • cytokines
  • gastric motility
  • Mesenteric lymph
  • peritonitis
  • sepsis

ASJC Scopus subject areas

  • Surgery

Cite this

Mesenteric lymph collected during peritonitis or sepsis potently inhibits gastric motility in rats. / Glatzle, Jörg; Leutenegger, Christian M.; Mueller, Mario H.; Kreis, Martin E.; Raybould, Helen E; Zittel, Tilman T.

In: Journal of Gastrointestinal Surgery, Vol. 8, No. 6, 10.09.2004, p. 645-652.

Research output: Contribution to journalArticle

Glatzle, Jörg ; Leutenegger, Christian M. ; Mueller, Mario H. ; Kreis, Martin E. ; Raybould, Helen E ; Zittel, Tilman T. / Mesenteric lymph collected during peritonitis or sepsis potently inhibits gastric motility in rats. In: Journal of Gastrointestinal Surgery. 2004 ; Vol. 8, No. 6. pp. 645-652.
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abstract = "Gastrointestinal motility is strongly inhibited during peritonitis or sepsis and proinflammatory cytokines released into mesenteric lymph during an acute gastrointestinal insult mediate systemic responses. We investigated whether mesenteric lymph collected during peritonitis or sepsis inhibits gastric motility and gastric emptying. Mesenteric lymph was collected for 12 hours from three experimental groups: vehicle (saline, 1 ml, intraperitoneally [ip], control lymph), peritonitis (0.5{\%} acetic acid, 1ml, ip, peritonitis lymph), and sepsis (lipopolysaccharide [LPS], 5 mg/kg, 1 ml, ip, sepsis lymph). Gastric motility and gastric emptying were measured in recipient rats in response to lymph injections into the jugular vein. Quantitative polymerase chain reaction (PCR) for tumor necrosis factor α (TNFα) gene expression in the jejunum and in lymph cells were measured during sepsis. Mesenteric lymph flow significantly increased during peritonitis or sepsis (lymph flow [ml] per 60 minutes; control 2.45 ± 0.04; peritonitis 2.67 ± 0.07; sepsis 3.25 ± 0.1, p < 0.01 vs. control). Injection of peritonitis or sepsis lymph (1 ml) produced a significant and prolonged inhibition of gastric motility in recipient rats (decrease in intragastric pressure and duration: control lymph -0.14 ± 0.05 cm H 2O, 1.89 ± 1.31 minutes; peritonitis lymph: -0.56 ± 0.06 cm H 2O, 9.9 ± 0.9 minutes; sepsis lymph: -0.51 ± 0.05 cm H 2O, 6.9 ± 0.6 minutes; p < 0.001 vs. control for all comparisons). Gastric emptying was significantly inhibited by continuous infusion of sepsis lymph (3 ml per 60 minutes; gastric emptying: saline 81{\%} ± 4{\%}; control lymph: 80{\%} ± 6{\%}; sepsis lymph: 44{\%} ± 10{\%}; p < 0.001 vs. control). TNFα gene expression in the gut wall of the jejunum increased during sepsis over 90-fold within the first 2 hours and decreased continuously thereafter (relative TNFα mRNA transcription: basal 1.0 ± 0.05; LPS 2 hours: 91.9 ± 2.6, p < 0.001 vs. basal; 12 hours: 24.7 ± 16.8, not significant [NS]; 24 hours: 7.0 ± 3.4, NS). In conclusion, mediators in mesenteric lymph, possibly cytokines, may be responsible for the inhibition of gastric motility during peritonitis or sepsis. Because the composition of mesenteric lymph probably reflects the interstitial fluid of the gut wall, monitoring visceral lymph might be an extremely beneficial tool to determine mediators released during impaired gut wall function.",
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AU - Zittel, Tilman T.

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N2 - Gastrointestinal motility is strongly inhibited during peritonitis or sepsis and proinflammatory cytokines released into mesenteric lymph during an acute gastrointestinal insult mediate systemic responses. We investigated whether mesenteric lymph collected during peritonitis or sepsis inhibits gastric motility and gastric emptying. Mesenteric lymph was collected for 12 hours from three experimental groups: vehicle (saline, 1 ml, intraperitoneally [ip], control lymph), peritonitis (0.5% acetic acid, 1ml, ip, peritonitis lymph), and sepsis (lipopolysaccharide [LPS], 5 mg/kg, 1 ml, ip, sepsis lymph). Gastric motility and gastric emptying were measured in recipient rats in response to lymph injections into the jugular vein. Quantitative polymerase chain reaction (PCR) for tumor necrosis factor α (TNFα) gene expression in the jejunum and in lymph cells were measured during sepsis. Mesenteric lymph flow significantly increased during peritonitis or sepsis (lymph flow [ml] per 60 minutes; control 2.45 ± 0.04; peritonitis 2.67 ± 0.07; sepsis 3.25 ± 0.1, p < 0.01 vs. control). Injection of peritonitis or sepsis lymph (1 ml) produced a significant and prolonged inhibition of gastric motility in recipient rats (decrease in intragastric pressure and duration: control lymph -0.14 ± 0.05 cm H 2O, 1.89 ± 1.31 minutes; peritonitis lymph: -0.56 ± 0.06 cm H 2O, 9.9 ± 0.9 minutes; sepsis lymph: -0.51 ± 0.05 cm H 2O, 6.9 ± 0.6 minutes; p < 0.001 vs. control for all comparisons). Gastric emptying was significantly inhibited by continuous infusion of sepsis lymph (3 ml per 60 minutes; gastric emptying: saline 81% ± 4%; control lymph: 80% ± 6%; sepsis lymph: 44% ± 10%; p < 0.001 vs. control). TNFα gene expression in the gut wall of the jejunum increased during sepsis over 90-fold within the first 2 hours and decreased continuously thereafter (relative TNFα mRNA transcription: basal 1.0 ± 0.05; LPS 2 hours: 91.9 ± 2.6, p < 0.001 vs. basal; 12 hours: 24.7 ± 16.8, not significant [NS]; 24 hours: 7.0 ± 3.4, NS). In conclusion, mediators in mesenteric lymph, possibly cytokines, may be responsible for the inhibition of gastric motility during peritonitis or sepsis. Because the composition of mesenteric lymph probably reflects the interstitial fluid of the gut wall, monitoring visceral lymph might be an extremely beneficial tool to determine mediators released during impaired gut wall function.

AB - Gastrointestinal motility is strongly inhibited during peritonitis or sepsis and proinflammatory cytokines released into mesenteric lymph during an acute gastrointestinal insult mediate systemic responses. We investigated whether mesenteric lymph collected during peritonitis or sepsis inhibits gastric motility and gastric emptying. Mesenteric lymph was collected for 12 hours from three experimental groups: vehicle (saline, 1 ml, intraperitoneally [ip], control lymph), peritonitis (0.5% acetic acid, 1ml, ip, peritonitis lymph), and sepsis (lipopolysaccharide [LPS], 5 mg/kg, 1 ml, ip, sepsis lymph). Gastric motility and gastric emptying were measured in recipient rats in response to lymph injections into the jugular vein. Quantitative polymerase chain reaction (PCR) for tumor necrosis factor α (TNFα) gene expression in the jejunum and in lymph cells were measured during sepsis. Mesenteric lymph flow significantly increased during peritonitis or sepsis (lymph flow [ml] per 60 minutes; control 2.45 ± 0.04; peritonitis 2.67 ± 0.07; sepsis 3.25 ± 0.1, p < 0.01 vs. control). Injection of peritonitis or sepsis lymph (1 ml) produced a significant and prolonged inhibition of gastric motility in recipient rats (decrease in intragastric pressure and duration: control lymph -0.14 ± 0.05 cm H 2O, 1.89 ± 1.31 minutes; peritonitis lymph: -0.56 ± 0.06 cm H 2O, 9.9 ± 0.9 minutes; sepsis lymph: -0.51 ± 0.05 cm H 2O, 6.9 ± 0.6 minutes; p < 0.001 vs. control for all comparisons). Gastric emptying was significantly inhibited by continuous infusion of sepsis lymph (3 ml per 60 minutes; gastric emptying: saline 81% ± 4%; control lymph: 80% ± 6%; sepsis lymph: 44% ± 10%; p < 0.001 vs. control). TNFα gene expression in the gut wall of the jejunum increased during sepsis over 90-fold within the first 2 hours and decreased continuously thereafter (relative TNFα mRNA transcription: basal 1.0 ± 0.05; LPS 2 hours: 91.9 ± 2.6, p < 0.001 vs. basal; 12 hours: 24.7 ± 16.8, not significant [NS]; 24 hours: 7.0 ± 3.4, NS). In conclusion, mediators in mesenteric lymph, possibly cytokines, may be responsible for the inhibition of gastric motility during peritonitis or sepsis. Because the composition of mesenteric lymph probably reflects the interstitial fluid of the gut wall, monitoring visceral lymph might be an extremely beneficial tool to determine mediators released during impaired gut wall function.

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