Study of intestinal ischemic disease in newborn patients

Northern印迹分析和逆转录聚合酶链式反应(RT-PCR)检测iNOS基因在组织中的表达，iNOS基因在注射内毒素后1h在食道、十二指肠、空肠、回肠、结肠等组织中表达，4h达高峰。地塞米松可抑制诱导型一氧化氮合酶mRNA的升高，地塞米松和一氧化氮合酶抑制剂L NAME均可改善内毒素诱导的肠粘膜通透性增加。我们的结果表明，iNOS mRNA在消化道中存在组织特异性表达。本实验研究了内皮型一氧化氮合酶(NOS-III)基因在体内的组织分布，并检测了其对内毒素攻击的反应。胃肠道粘膜中可见NOS-III基因和蛋白的表达。内毒素可下调大鼠胃肠黏膜中一氧化氮合酶-11基因的表达。在诱导诱导型一氧化氮合酶基因表达的同时，一氧化氮合酶-Ⅲ基因的表达降低，可能与脓毒症时内皮依赖的松弛功能受损和粘膜完整性受损有关。

We measured tissue expression of mRNA encoding iNOS by Northern blot analysis and reverse transcription PCR.The iNOS mRNA was detectable at 1 h, peaked at 4 h after endotoxin injection in esophagus, duodenum, jejunum, ileum arid colon. Pre-treatment with dexamethasone attenuated the rise of iNOS mRNA.Both dexamethasone and NOS inhibitor, L-NAME, ameliorated the endotoxin-induced increase in intestinal mucosal permeability. Our results indicate that there is tissue-specific expression of iNOS mRNA in the digestive tract. The maniprations that decrease NO production may have therapeutic potential in preserving intestinal mucosal integrity in sepsis.We characterized the tissue distribution of mRNA for endothelial nitric oxide synthase (NOS-III) and to examine its response to endotoxin challenge in vivo. The expression of NOS-III mRNA and protein in mucosa was demonstrated throughout the gastrointestinal tract. NOS-Ill mRNA expression in the gastrointestinal mucosa was down-regulated in rats treated with endotoxin. The decreased NOS-III mRNA, in parallel to induction of inducible NOS mRNA, may contribute to the impaired endothelium-dependent relaxation and damaged mucosal integrity during sepsis.