GUT ISCHEMIA
GUT ISCHEMIA
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DOI：
10.1136/gut.35.1_suppl.s73
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发表时间：
1994-01-01
期刊：
影响因子：
24.5
通讯作者：
HAGLUND, U
中科院分区：
文献类型：
--
作者：
HAGLUND, U
局部缺血导致的肠粘膜损伤可通过早期肠通透性增加，随后出现形态学、组织学和生化异常来检测。局部适应机制（例如增加氧提取）可以科普高达50%的血流量减少，这可能发生在感染性休克或心脏压塞发作期间。那么为什么会发生缺氧损伤呢？绒毛特殊的血管解剖结构允许在血流较低时在其基部发生氧气短路。虽然总的氧提取效率可能很高，但绒毛尖端的局部缺氧可能会矛盾地发生。再灌注损伤的严重程度取决于先前缺氧的持续时间。通过次黄嘌呤黄嘌呤氧化酶系统产生的自由基在介导细胞损伤中是重要的。此外，如早期研究所示，管腔侵袭因子（例如胰腺蛋白酶）可能导致粘膜损伤。最近对猪的研究表明，胰管结扎只是延迟，但不能防止肠道再灌注损伤的发展。肠内营养对缺血性肠的患者有益，因为与完全肠外营养相比，肠内营养可刺激局部血流，减轻粘膜损伤。没有随机试验来验证这一点，但使用眼压计监测局部缺血可能有助于解决这个问题。
Intestinal mucosal injury that results from local ischaemia can be detected by early increases in gut permeability, followed by later morphological, histological, and biochemical abnormalities. Local adaptive mechanisms (for example increased oxygen extraction) can cope with reductions in blood flow of up to 50%, as may occur during episodes of septic shock or cardiac tamponade. Why then does hypoxic injury develop? The peculiar vascular anatomy of the villi allows for oxygen short circuiting to occur at their base, when blood flow is low. Although overall oxygen extraction efficiency may be high, regional hypoxia at the villus tip may, paradoxically occur. The severity of reperfusion injury depends on the duration of preceding hypoxia. Free radical generation through the hypoxanthine xanthine oxidase system is important in mediating cellular damage. In addition, luminal aggressive factors (for example, pancreatic proteases) may cause mucosal damage, as suggested by earlier studies. More recent studies in pigs suggests that pancreatic duct ligation merely delays, but does not prevent development of gut reperfusion injury. Enteral nutrition should benefit patients with the ischaemic intestine because in comparison with total parental nutrition, it stimulates regional blood flow, and attenuates mucosal injury. There are no randomised trials to verify this, but use of tonometry to monitor local ischaemia may help resolve the issue.