【作者】 郑巧芬；

【导师】 曹定睿；

【作者基本信息】 山西医科大学 ， 麻醉学， 2011， 硕士

【摘要】 目的通过研究舒芬太尼对肠缺血再灌注大鼠肺组织及血清中肿瘤坏死因子-α(TNF-α)和肺组织中核因子-κB(NF-κB)的影响,探讨舒芬太尼后处理对大鼠肠缺血再灌注时肺组织的影响及可能机制,以期为临床提供实验依据。方法将32只健康成年雄性Wistar大鼠,随机分为4组:假手术组(S组)、肠缺血再灌注组(I/R组)、肠缺血后处理组(I-post组)及1ug/kg舒芬太尼后处理组(SP组)。每组各8只。①假手术组:仅行开腹,分离肠系膜上动脉(SMA)不夹闭;②缺血-再灌注组:采用夹闭肠系膜上动脉60min后再灌注120min的方法制备肠I/R模型;③缺血后处理组:缺血60 min后即刻行3个循环的灌注30 s/阻断30 s,余同I/R组。④舒芬太尼后处理组:将1ug/kg舒芬太尼稀释到0.3ml在再灌注即刻经股静脉用微量注射泵泵入0.1ml/30S,期间间断30s,如此循环3次(共0.3ml),余同I/R组。于再灌注120min时处死8只大鼠。HE染色观察大鼠肺组织病理改变。采用放射免疫法测定血清及肺组织中TNF-α的含量;采用免疫组织化学法测定肺组织中NF-κB表达水平。结果(1)HE检测病理变化:①S组:未发现明显病理变化,肺泡大小均匀,结构完整,壁薄,未见出血水肿及炎性细胞浸润;②I/R组可见肺泡大小不均,完整性破坏,肺泡腔有蛋白样渗出物,肺泡壁增厚,间隔增宽,肺间质和肺泡水肿,大量炎细胞浸润、充血、出血明显。③I-post组、SP组上述病理变化均较轻,肺泡腔内蛋白渗出减少,肺泡壁增厚、炎细胞浸润减轻(。2)TNF-α、NF-κB检测:与S组相比,其余各组TNF-α增加、NF-κB表达上调( );与I/R组相比,I-post组及SP组NF-κB表达下调、TNF-α减少( P ?0.05);I-post组及SP组比较上述指标差异无统计学意义( )。结论(1)小肠缺血再灌注可以导致严重的肺损伤。(2)肠缺血再灌注肺损伤机制复杂,其发生和发展可能与TNF-α和NF-κB有关。(3)舒芬太尼后处理对肠缺血再灌注导致的肺损伤有保护作用,可抑制肺组织中NF-κB的表达,减轻大鼠肠缺血再灌注时血清及肺组织中TNF-α的含量。更多还原

【Abstract】 Objective Research sufentanil on intestinal ischemia-reperfusion rat lung tissue and serum tumor necrosis factor-α(TNF-α) and lung tissue nuclear factor-κB (NF-κB), and investigate the effects of Sufentanil post-conditioning (SP) acute lung injury induced by ischemia-reperfusion in rats and possible mechanisms, In order to provide experimental basis for clinical.Methods Thirty-two healthy male Wistar rats were randomly divided into four group (n=8): Sham-operation group (S group),I/R group(I/R group),intestinal ischemic Post-conditioning group(I-post group) and 1ug/kg Sufentanil post-conditioning group (SP group).Each group of 8.(1)S group :Superrior mesenteric artery was only isolated but not blocked.(2)I/R group was established by clamping superior mesenteric artery(SMA)for 1 hour and reperfusing for 2 hours.(3) Line immediately after 60 min ischemia and 3 cycles of reperfusion 30 s / block 30 s, more than with the I / R group. (4) The 1ug/kg sufentanil diluted to 0. 3ml immediately after reperfusion through the femoral vein with a syringe pump pump 0.1ml/30S, during the intermittent 30s, so the cycle 3 times (a total of 0.3ml), than with the I / R Group. The animals were killed at 2 h of reperfusion respectively (n=8). HE dyed observe lung tissue pathology changes in rats. TNF-αin the serum and lung tissue were determined using radio-immunifaction method .Expression of NF-κB P65 in the lung tissue was assessed by immunohistichemical method.Results (1) HE detection pathological changes:①S group: not found significant pathological changes, alveolar size uniform, complete structure, wall thin, did not see the bleeding edema and inflammatory cells infiltrating;②I/R group visible alveolar size is uneven and integrity damage, alveolar exudate of cavity have protein samples, the alveolar wall thickening widened, the interval, interstitial lung and alveolar edema, a lot of inflammatory cell, congestion, bleeding obvious.③I-post group and SP group are lighter the pathological changes, the alveolar lumen protein, the alveolar exudate is reduce thickened wall, inflammatory cell ease.Compared with the sham-operated control group, serum and lung TNF-a lever was increased significantly in the other groups ( ), and NF-kB p65 protein in the lung was increased (P<0.05). Compared with the I/R group, TNF-αin the serum and lung tissues were decreased significantly following Sulfentanil treatment ( ), and the expression of lung NF-κB was markedly ameliorated (P<0.05).There were no significant difference between I-post group and SP group( ). Conclusion (1)This study demonstrated that intestinal ischemia-reperfusion l may result in sincerely lung damage.(2) The mechanism of lung injury induced by intestinal ischemia-reperfusion is complicated, and its occurrence and development may be related to TNF-αand NF-KB related.(3) sulfentanil post-conditioning on intestinal ischemia-reperfusion induced lung injury has a protective effect, can inhibit NF-κB in lung tissue expression of rat intestinal ischemia and reperfusion reduce the serum and lung tissue content of TNF-α.更多还原