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Effects Of Lidocaine On Lung Injury Induced By Intestinal Ischemia-reperfusion In Young Rats

Posted on:2011-01-27Degree:MasterType:Thesis
Country:ChinaCandidate:W C QuFull Text:PDF
GTID:2194330335493573Subject:Academy of Pediatrics
Abstract/Summary:PDF Full Text Request
Obsjective:An intestinal ischemic reperfusion (Ⅱ/R) young rat model was established and the lidocaine injection was used to intervene for lung injury in the model. The aim of this study was to detect the expression of intercellular adhesion molecule-1, myeloperoxidase and malondialdehyde in the lung tissue and calculated the ratio of wet and dry weight and histological damage of lung tissue found in significant tissue for explorring the protective effect of lidocaine injection in young rats with intestinal ischemia-reperfusion injury in lung and paving the way for clinical experiment and guidance.Methods:80 Sprague Dawley (SD) rats at 4 weeks old were divided into 4 groups:(1) Sham-operated group (10 rats), only exposure to the superior mesenteric artery, no intestinal ischemia-reperfusion and infusion of lidocaine injection,1 hour after the death. (2) Ischemia group (I group,10 rats), expose the abdominal cavity, clamping the superior mesenteric artery, were sacrificed after 1 hour. (3) Ischemic reperfusion model group (Ⅱ/R group,30 rats), occlusion of the superior mesenteric artery 1 hour, before reperfusion of femoral vein injection of 0.5ml physiologic saline as control. (4) Lidocaine intervention group (Lid group,30 rats), occlusion of the superior mesenteric artery 1 hour, reperfusion after femoral vein before the injection of lidocaine 2mg-kg-1(diluted in 0.5 ml of physiologic saline). (3) and (4) groups after reperfusion 30 minute,60 minute,120 minute, each time point was sacrificed 10 animals. Animals were killed, lung tissue for pathological study.The expression of intercellular adhesion molecule-1 in the lung tissue were measured by enzyme-linked immunosorbent assay (ELISA). The expression of myeloperoxidase and malondialdehyde in the lung tissue was measured by spectrophotometer. Scale of lung tissue wet and dry weight to calculate the wet to dry weight ratio (W/D)。Data was managed on statistical analysis processing with SPSS 16.0 statistics software and expressed with mean±standard deviation (x±s). The data with the Kolmogorov-Smirnov method of normal inspection, results P greater than 0.05, test hypothesis was rejected, indicating data was not consistent with normal distribution. Therefore, the choice of rank-sum test method of testing, results showed statistically significant, heterogeneity of variance, using Dunnett's T3 test. Takeα= 0.05 level test. P<0.05 indicate statistical significance.Results:1. Sham- operated group was free as a result of superior mesenteric artery without clipping, no ischemia-reperfusion injury. Lungs were pale pink, no congestion, edema, hemorrhage and necrosis under naked eye. There was depth color, mild edema, but no obvious aspect foamy liquid in lung tissue compared with sham-operated group in ischemia group. Intestinal ischemia-reperfusion lung volume increases, congestion, edema, and see the point like or spotty bleeding, cut with pink or white foamy liquid overflow. Lidocaine pretreatment group showed lung congestion, edema, lighter, a small amount of foam-like liquid section.2. General HE staining showed that:Sham- operated group no significant pathological changes in lung tissue. Ischemia group lung interstitial lung congestion, edema, thickening, and no diffuse bleeding, no red blood cells or alveolar inflammatory cell infiltration. Intestinal ischemia-reperfusion group obvious pathological lung injury, pulmonary interstitial thickening, hyperemia, edema, inflammatory cell infiltration and erythrocyte exudation, alveolar infiltration of red blood cells can be seen clearly, with the reperfusion time, the damage gradually increase. Lidocaine pretreatment lung injury had the same trend of the injury in ischemia-reperfusion model, severer than sham- operated group, but lighter than intestinal ischemia-reperfusion group, similar with ischemic group.3. Measured lung wet to dry weight ratio results between the two groups, intestinal ischemia-reperfusion group at each time point of lung wet to dry weight ratio greater than lidocaine pretreatment group, sham-operated group and ischemia group lung wet to dry weight ratio (P<0.01). Lidocaine pretreatment group at all time points less than intestinal ischemia-reperfusion group (P<0.01), but compared with ischemia group, there were no significant difference (P>0.05). Lidocaine pretreatment reperfusion 30 minutes and 60minutes compared with the sham-operated group had no statistically significant (P>0.05). Lidocaine pretreatment reperfusion 120 minutes compared with the sham-operated group had statistically significant (P<0.05).4. enzyme-linked immunosorbent assay (ELISA) detection of lung tissue intercellular adhesion molecule-1 results showed that:(1) ischemia group lung tissue intercellular adhesion molecule-1 levels higher than sham-operated group, but lower than the ischemia-reperfusion group and the lidocaine intervention group, and intestinal ischemia-reperfusion group compared with other three time groups showed statistically significant (P<0.01). (2) Intestinal ischemia-reperfusion gradually increased to the reperfusion peak from 30 minutes to 60 minutes, and then gradually decreased, but still higher than sham-operated, ischemia group. Intestinal ischemia-reperfusion group at each time point lung tissue intercellular adhesion molecule-1 levels were significantly higher than the sham group, ischemic group and lidocaine group, after compared the results showed significantly (P<0.01). (3) Lidocaine pretreatment group lung tissue intercellular adhesion molecule-1 levels changing trends were the same with intestinal ischemic-reperfusion groups, and the intercellular adhesion molecule-1 levels were significantly lower than the intestinal ischemia-reperfusion group and the compared results had significant differences (P<0.01), but higher than sham-operated group and ischemia group (P<0.05). Lidocaine pretreatment group lung tissue intercellular adhesion molecule-1 levels higher than ischemia group, but the result had no significantly different (P>0.05) Lidocaine pretreatment group 60 minutes compared with the sham- operated group, the results were significantly different (P<0.01). (4) Intestinal ischemia-reperfusion 60min and 120min's lung tissue intercellular adhesion molecule-1 compared to intestinal ischemia-reperfusion 30min difference significant (P<0.01), but intestinal ischemia-reperfusion 60min compared to 120min comparison between the results was not significant (P>0.05). (5) The three time points of lid group had no significant difference between (P>0.05).5. Spectrophotometer results showed that:(1) Myeloperoxidase and malondialdehyde content measured in the ischemic group compared with the sham group, the difference was not statistically significant (P>0.05). (2) The lung tissues myeloperoxidase and malondialdehyde content in both intestinal ischemia-reperfusion group and lidocaine pretreatment group gradually increased from reperfusion 30 minutes, and it still going up until reperfusion 120 minutes, but in lidocaine pretreatment group the content of myeloperoxidase and malondialdehyde are all going up to the peak when reperfusion 60 minutes. Ischemia group lung tissue myeloperoxidase and malondialdehyde compared to sham-operated group was no significant difference (P>0.05).Lidocaine pretreatment group lung tissue myeloperoxidase and malondialdehyde content in the corresponding time points were lower than intestinal ischemia-reperfusion group (P<0.01). (3)Myeloperoxidase levels measured values between groups, compared lidocaine pretreatment group reperfusion 30 minutes and the ischemic group was no significant difference (P>0.05). The content of myeloperoxidase in both intestinal ischemia-reperfusion group and the lidocaine pretreatment 60 minutes group were higher than ischemic group (P<0.01). (4) Malondialdehyde levels measured values between groups, lidocaine pretreatment group at all time points measured were less than intestinal ischemia-reperfusion group. The content of malondialdehyde in lidocaine pretreatment reperfusion 60 minutes and 120 minutes groups compared with sham-operated group there were significant difference(P<0.05). Lidocaine pretreatment reperfusion 60 minutes group compared with the ischemic group there was significant difference(P<0.05). The content of malondialdehyde in both lidocaine pretreatment reperfusion 30 minutes and 120 minutes compared with ischemia group had no significant difference, and malondialdehyde content of lidocaine pretreatment reperfusion 30 minutes compared with the sham- operated group had no statistically significant (P>0.05). (5) Intestinal ischemia-reperfusion 60min and 120min's lung tissue myeloperoxidase, malondialdehyde compared to intestinal ischemia-reperfusion 30min difference significant (P<0.01), but intestinal ischemia- reperfusion 60min compared to 120min comparison between the results was not significant (P>0.05). (6) The three time points of lid group had no significant difference between (P>0.05). Conclusions:Intestinal ischemia - reperfusion injury in lung tissue caused by the pathological changes, the ratio of wet and dry weight increased and intercellular adhesion molecule-1, myeloperoxidase, and malondialdehyde content increased in lung tissue, lidocaine injection can reduce this pathological changes, and reduce intercellular adhesion molecule-1, myeloperoxidase and malondialdehyde expression, effects of lidocaine injection on the growth and development period of animal intestinal ischemia - reperfusion lung injury has a protective effect. As part of the pathogenesis is the intestinal tract, intestinal ischemia-reperfusion lung injury caused by the mechanism needs further study.
Keywords/Search Tags:Intestinal ischemia-reperfusion, Lung injury, Lidocaine, Intercellular adhesion molecule-1, Myeloperoxidase, Malondialdehyde, Rats
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