持续存在的消化道黏膜低度炎症是感染后肠易激综合征（PI-IBS）发病的主要病理生理学基础，而内脏高敏感是PI-IBS症状产生的核心机制。脊髓传入神经通路神经元兴奋性增高所致感觉易化是内脏伤害性感受异常的最关键动因，但其机制未明。综合新近研究提示，慢性炎症状态下，脊髓传入神经背根神经节（DRG）神经元细胞膜处的大电导Ca2+激活K+通道（BKCa）可通过改变神经元兴奋性而参与胃肠内脏感觉的调控，在PI-IBS内脏高敏感反应机制中发挥重要作用。

The persistent low-grade mucosal inflammation in the gastrointestinal tract is a main pathophysiological basis of the pathogenesis of post-infectious or inflammatory irritable bowel syndrome (PI-IBS) and visceral hypersensitivity is the core mechanism of PI-IBS. The sensory facilitation caused by the increase of neuronal excitation of spinal afferent nerve pathway plays the most important role in abnormal visceral nociception, but the underlying mechanisms have not been fully understood. Review of recent studies suggests that under the condition of chronic inflammation, the large conductance calcium-activated potassium channel (BKCa) of the cell membrane of neurons of spinal afferent nerve in dorsal root ganglions is vital in the reaction mechanism of visceral hypersensitivity of PI-IBS by changing the excitation of neurons and involving the regulation of gastrointestinal sensitivity.