Calcium and phospholipase A2 appear to be involved in the pathogenesis of hemorrhagic shock-induced mucosal injury and bacterial translocation.
Calcium and phospholipase A2 appear to be involved in the pathogenesis of hemorrhagic shock-induced mucosal injury and bacterial translocation.
复制标题
钙和磷脂酶 A2 似乎参与失血性休克引起的粘膜损伤和细菌移位的发病机制。
DOI：
10.1097/00003246-199501000-00021
复制
发表时间：
1995
影响因子：
8.8
通讯作者：
Deitch,EA
中科院分区：
文献类型：
--
作者：
Xu,D;Lu,Q;Deitch,EA
失血性休克损伤肠道并导致细菌移位的机制仍不完全确定。由于细胞游离钙水平和磷脂酶A2活性的增加可导致细胞损伤，并且在某些休克状态下都有记录，因此对钙或磷脂酶A2可能在失血性休克诱导的肠粘膜损伤和细菌移位中发挥作用的假设进行了测试。设计
ObjectiveThe mechanism by which hemorrhagic shock injures the gut and leads to the translocation of bacteria remains incompletely determined. Since increased free cellular calcium levels and phospholipase A 2 activity can lead to cellular injury and both have been documented in certain shock states, the hypothesis that calcium or phospholipase A 2 may play a role in hemorrhagic shock-induced gut mucosal injury and bacterial translocation was tested.Design