Division of Cardiology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Compr Physiol. 2011 Jan;1(1):123-39. doi: 10.1002/cphy.c090004.
Hemodynamic stress in the pulmonary vessel is directly linked to the development of vascular remodeling and dysfunction, ultimately leading to pulmonary hypertension. Recently, some advances have been made in our molecular understanding of the exogenous upstream stimuli that initiate hemodynamic pertubations as well as the downstream vasoactive effectors that control these responses. However, much still remains unknown regarding how these complex signaling pathways connect in order to result in these characteristic pathophysiological changes. This chapter will describe our current understanding of and needed areas of research into the clinical, physiological, and molecular changes associated with pressure/volume overload in the pulmonary circulation.
肺血管中的血流动力应激与血管重构和功能障碍的发展直接相关，最终导致肺动脉高压。最近，我们在分子水平上对外源性上游刺激物的理解有了一些进展，这些刺激物引发血流动力学紊乱，下游的血管活性效应物控制这些反应。然而，对于这些复杂的信号通路如何连接以导致这些特征性的病理生理变化，我们仍然知之甚少。本章将描述我们目前对与肺循环压力/容量过载相关的临床、生理和分子变化的理解，以及需要研究的领域。
