Speaker
Description
Heavy menstrual bleeding (HMB) is linked to dysregulated inflammatory signaling and abnormal spiral artery function. However, the mechanism connecting endometrial inflammation and vascular response is not well understood. To address this, we are extending an existing mechanistic ordinary differential equation model of the menstrual cycle. Our expanded framework incorporates the inflammatory modulation of spiral artery dynamics, specifically mediated by prostaglandin activity.
Our model investigates the relationship between hormone-regulated prostaglandin production in endometrial tissue and the resulting vascular dynamics, including spiral artery constriction, vasodilation, and breakdown throughout the menstrual cycle. We utilize local and global sensitivity analyses to assess the impact of various inflammatory parameters on vascular stability and predicted blood loss. This allows us to quantify how changes in tissue-level inflammatory signaling ultimately affect outcomes at the vascular scale.
This study establishes a multiscale mechanistic framework for investigating inflammation-driven vascular dysfunction. Key prostaglandin-related parameters that govern spiral artery reactivity were identified through preliminary results, which also pinpointed structurally sensitive model components. The sensitivity analysis highlights areas where greater cellular-scale detail may be necessary. This work provides a crucial foundation for future integration with clinical data
