Cordier J F
Hôpital cardiovasculaire et pneumologique Louis-Pradel, Université Claude-Bernard, Lyon.
Rev Prat. 1991 Jun 11;41(17):1534-40.
Pulmonary hypertension results from many causes: left cardiac failure, increased pulmonary blood flow, proximal vascular obstruction, decrease of the distal vascular bed (by loss of vessels, narrowing of their luminal diameter, or endoluminal obstruction). A part from passive hemodynamic responses, active processes contribute to pulmonary hypertension by vasomotricity and remodeling of the vascular wall. The biopathology of vasomotor mediators, as well as of endothelial and smooth muscle cell interactions just begins to be understood.
左心衰竭、肺血流量增加、近端血管阻塞、远端血管床减少（因血管丧失、管腔直径变窄或腔内阻塞）。除了被动血流动力学反应外，主动过程通过血管舒缩和血管壁重塑导致肺动脉高压。血管运动介质以及内皮细胞和平滑肌细胞相互作用的生物病理学才刚刚开始被了解。
