Ileus in critical illness: mechanisms and management.
Ileus in critical illness: mechanisms and management.
复制标题
DOI：
10.1097/00075198-200204000-00011
复制
发表时间：
2002-04-01
影响因子：
3.3
通讯作者：
Kalff, Jorg C
中科院分区：
文献类型：
--
作者：
Bauer, Anthony J;Schwarz, Nicolas T;Kalff, Jorg C
非梗阻性肠梗阻，意味着协调推进的肠道动力受损，仍然是开放腹部手术和败血症的常见且几乎不可避免的后果。尽管肠梗阻的频率和对发病率和死亡率的主要影响，但这一重要临床难题的确切潜在分子和细胞机制仍不清楚。动物模型显示肠肌层内的神经性和局部炎症反应对肠梗阻有机械性的作用。神经机制似乎涉及抑制运动神经元释放一氧化氮的增强。同样，炎症细胞(巨噬细胞和单核细胞)通过一氧化氮合酶(INOS)和环氧合酶-2的诱导释放一氧化氮和前列腺素。最近，初步数据证实人类患者在手术过程中存在局部肌层炎症反应。
Nonobstructive ileus, signifying the impairment of coordinated propulsive intestinal motility, remains a frequently documented and almost inevitable consequence of open abdominal surgery and sepsis. Despite the frequency and major impact of ileus on morbidity and mortality, the exact underlying molecular and cellular mechanisms of this important clinical conundrum are still ill defined. Animal models suggest that both neuronal and local inflammatory responses within the intestinal muscularis mechanistically contribute to intestinal ileus. The neuronal mechanism appears to involve the enhanced release of nitric oxide from inhibitory motor neurons. Likewise, nitric oxide and prostaglandins are released from inflammatory cells (macrophages and monocytes) via the induction of nitric oxide synthase (iNOS) and cyclooxygenase-2. Recently, preliminary data have confirmed the existence of an intraoperative local muscularis inflammatory response during surgery in human patients.