Purpose: It has been suggested that inflammatory mediators such as cytokines released during intestinal ischemia and reperfusion increase permeability in the lungs. Cytokines exist at concentrations several hundred times higher at the site of inflammation than in the blood. When absorbed, the locally produced cytokines may affect multiple remote organs. We thus investigated whether the isolation of the intestine in a bag during ischemia and reperfusion can reduce subsequent lung injury.
Methods: Rats were divided into three groups: group 1, simple laparotomy (sham); group 2, intestinal ischemia and reperfusion (I/R); and group 3, intestinal ischemia and reperfusion with an intestinal bag (IB). Lung permeability was assessed using the Evans Blue leakage method. Cytokines (interleukin-1beta, tumor necrosis factor alpha, interleukin-8) in the plasma and ascites were measured by enzyme-linked immunosorbent assay.
Results: The increase in lung permeability of I/R significantly decreased in IB (1.73 +/- 0.48 vs 1.05 +/- 0.22, P < 0.01). The plasma cytokine concentrations were also lower in IB than in I/R. In addition, the cytokine levels in the intestinal bag fluid were extremely high.
Conclusion: The isolation of the intestine during ischemia and reperfusion was found to reduce the degree of subsequent lung injury, possibly due to the reduced absorption of locally produced cytokines via the parietal peritoneum.
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http://dx.doi.org/10.1007/s00595-004-2847-9 | DOI Listing |
Mol Cell Neurosci
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View Article and Find Full Text PDFGen Physiol Biophys
January 2025
Shanghai University of Traditional Chinese Medicine, Shenzhen Hospital, Shenzhen, Guangdong, China.
Cerebral ischemia-reperfusion (I/R) is a serious complication in patients with ischemic stroke. Senkyunolide A (SenA) can alleviate neuronal cell damage induced by cerebral I/R; however, the exact action mechanism remains unclear. An in vitro cellular injury model was established by inducing PC-12 cells with OGD/R.
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Oxidative stress and neuronal apoptosis could be an important factor leading to post-hemorrhagic consequences after germinal matrix hemorrhage (GMH). Previously study have indicated that relaxin 2 receptor activation initiates anti-oxidative stress and anti-apoptosis in ischemia-reperfusion injury. However, whether relaxin 2 activation can attenuate oxidative stress and neuronal apoptosis after GMH remains unknown.
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