Howell Katherine, Ooi Henry, Preston Rob, McLoughlin Paul
Department of Human Anatomy and Physiology, Conway Institute of Biomolecular and Biomedical Research, Dublin Molecular Medicine Centre, University College Dublin, Ireland.
Exp Physiol. 2004 Jan;89(1):66-72. doi: 10.1113/expphysiol.2003.026765.
Exposure to chronic hypoxia causes pulmonary hypertension and pulmonary vascular remodelling. In chronic lung disease, chronic hypercapnia frequently coexists with hypoxia and is associated with worsening of pulmonary hypertension. It is generally stated that pulmonary hypertension in these conditions is secondary to hypoxic vascular remodelling and that hypercapnia augments this remodelling thus worsening the hypertension. We review recent evidence which shows that although chronic hypoxia causes thickening of the walls of pulmonary arterioles, these changes do not lead to structural narrowing of the lumen by encroachment. Moreover, hypoxia leads to new vessel formation within the pulmonary vasculature and not loss of vessels as formerly thought. Such neovascularization may provide a beneficial adaptation by increasing the area of the gas exchange membrane. These novel structural findings are supported by recent reports that inhibitors of the RhoA pathway can acutely reduce pulmonary vascular resistance in chronically hypoxic lungs to near normal values, demonstrating that structural changes are not the dominant mechanisms underling hypoxic pulmonary hypertension. Chronic hypercapnia inhibits the development of hypoxic pulmonary hypertension, pulmonary vascular remodelling and hypoxia-induced angiogenesis. This last effect might be maladaptive, as it would prevent the potentially beneficial increase in gas exchange membrane area. These findings suggest that structural narrowing of the vascular lumen of resistance vessels is not the mechanism by which hypoxia and hypercapnia cause pulmonary hypertension in chronic lung disease.
长期暴露于低氧环境会导致肺动脉高压和肺血管重塑。在慢性肺部疾病中,慢性高碳酸血症常与低氧血症并存,并与肺动脉高压的加重相关。一般认为,这些情况下的肺动脉高压继发于低氧性血管重塑,而高碳酸血症会加剧这种重塑,从而使高血压恶化。我们回顾了近期的证据,这些证据表明,尽管长期低氧会导致肺小动脉壁增厚,但这些变化并不会通过压迫导致管腔结构变窄。此外,低氧会导致肺血管系统内新血管形成,而不是像以前认为的那样导致血管丢失。这种新血管形成可能通过增加气体交换膜面积提供有益的适应性变化。这些新的结构发现得到了近期报告的支持,即RhoA通路抑制剂可将慢性低氧肺中的肺血管阻力急性降低至接近正常水平,这表明结构变化并非低氧性肺动脉高压的主要机制。慢性高碳酸血症会抑制低氧性肺动脉高压、肺血管重塑以及低氧诱导的血管生成。最后这种效应可能是适应不良的,因为它会阻止气体交换膜面积潜在的有益增加。这些发现表明,阻力血管管腔的结构变窄并非低氧和高碳酸血症在慢性肺部疾病中导致肺动脉高压的机制。