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 language | English (US) |
|---|---|
| Pages (from-to) | 645-652 |
| Number of pages | 8 |
| Journal | Journal of Gastrointestinal Surgery |
| Volume | 8 |
| Issue number | 6 |
| DOIs | |
| State | Published - Sep 10 2004 |
| Externally published | Yes |
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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 journal › Article
}
TY - JOUR
T1 - Mesenteric lymph collected during peritonitis or sepsis potently inhibits gastric motility in rats
AU - Glatzle, Jörg
AU - Leutenegger, Christian M.
AU - Mueller, Mario H.
AU - Kreis, Martin E.
AU - Raybould, Helen E
AU - Zittel, Tilman T.
PY - 2004/9/10
Y1 - 2004/9/10
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.
KW - cytokines
KW - gastric motility
KW - Mesenteric lymph
KW - peritonitis
KW - sepsis
UR - http://www.scopus.com/inward/record.url?scp=4444341581&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=4444341581&partnerID=8YFLogxK
U2 - 10.1016/j.gassur.2004.05.009
DO - 10.1016/j.gassur.2004.05.009
M3 - Article
C2 - 15358323
AN - SCOPUS:4444341581
VL - 8
SP - 645
EP - 652
JO - Journal of Gastrointestinal Surgery
JF - Journal of Gastrointestinal Surgery
SN - 1091-255X
IS - 6
ER -