Mesenteric lymph reperfusion exacerbates spleen injury caused by superior mesenteric artery occlusion shock.
The intestinal lymph pathway plays an important role in the pathogenesis of organ injury following superior mesenteric artery occlusion (SMAO) shock. We hypothesized that mesenteric lymph reperfusion (MLR) is a major cause of spleen injury after SMAO shock. To test this hypothesis, SMAO shock was induced in Wistar rats by clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h. Similarly, MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h, followed by reperfusion for 2 h. In the MLR+SMAO group rats, both the SMA and MLD were clamped and then released for reperfusion for 2 h. SMAO shock alone elicited: 1) splenic structure injury, 2) increased levels of malondialdehyde, nitric oxide (NO), intercellular adhesion molecule-1, endotoxin, lipopolysaccharide receptor (CD14), lipopolysaccharide-binding protein, and tumor necrosis factor-α, 3) enhanced activities of NO synthase and myeloperoxidase, and 4) decreased activities of superoxide dismutase and ATPase. MLR following SMAO shock further aggravated these deleterious effects. We conclude that MLR exacerbates spleen injury caused by SMAO shock, which itself is associated with oxidative stress, excessive release of NO, recruitment of polymorphonuclear neutrophils, endotoxin translocation, and enhanced inflammatory responses.
Institute of Microcirculation, Hebei North University, Zhangjiakou, Hebei, China.
L L
LL
Li
Institute of Microcirculation, Hebei North University, Zhangjiakou, Hebei, China.
C H
CH
Zhang
Institute of Microcirculation, Hebei North University, Zhangjiakou, Hebei, China.
J C
JC
Liu
Institute of Microcirculation, Hebei North University, Zhangjiakou, Hebei, China.
L N
LN
Yang
Institute of Microcirculation, Hebei North University, Zhangjiakou, Hebei, China.
C Y
CY
Niu
Institute of Microcirculation, Hebei North University, Zhangjiakou, Hebei, China.
Z G
ZG
Zhao
D000209:Acute-Phase Proteins / Q000032:analysis; D000251:Adenosine Triphosphatases / Q000032:analysis; D000818:Animals; D002352:Carrier Proteins / Q000032:analysis; D004731:Endotoxins / Q000032:analysis; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D007422:Intestines / Q000098:blood supply; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D008196:Lymph / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D008562:Membrane Glycoproteins / Q000032:analysis; D017538:Mesenteric Artery, Superior; D008641:Mesenteric Vascular Occlusion / Q000150:complications*; D009569:Nitric Oxide / Q000032:analysis; D019001:Nitric Oxide Synthase / Q000032:analysis; D009195:Peroxidase / Q000032:analysis; D017208:Rats, Wistar; D015424:Reperfusion / Q000009:adverse effects*; D015427:Reperfusion Injury / Q000209:etiology*; D013154:Spleen / Q000293:injuries* / Q000473:pathology; D013482:Superoxide Dismutase / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D000099231:Lipopolysaccharide-Binding Protein
D000209:Acute-Phase Proteins; D000251:Adenosine Triphosphatases; D002352:Carrier Proteins; D004731:Endotoxins; D018799:Intercellular Adhesion Molecule-1; D018950:Lipopolysaccharide Receptors; D008315:Malondialdehyde; D008562:Membrane Glycoproteins; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D009195:Peroxidase; D013482:Superoxide Dismutase; D014409:Tumor Necrosis Factor-alpha; D000099231:Lipopolysaccharide-Binding Protein