Pulmonary hypertension. Anatomic and physiologic correlates.
The types of pulmonary arterial hypertension described here all focus attention on the changes produced in the lung's microcirculation, particularly the precapillary unit. Although one senses intuitively that obliteration of resistance arteries is an effective cause of hypertension, we emphasize that cell metaplasia and adaptation by structural remodeling of the precapillary arterial wall is also effective in reducing the vascular bed. A question often asked is whether "pruning" is the cause of the hypertension . . . perhaps an inappropriate question. While the reduced cross-sectional area of the vascular bed is the basis for the rise in pulmonary vascular resistance and for its severity, the real question is what is the cause of the "pruning." Hypoxia, monocrotaline, and high flow each causes pulmonary artery hypertension--and pruning--but with differences in cell adaptation, timing, and severity that indicate different pathogenetic mechanisms and pathways. It is paradoxical that hypoxia, whose lesions are more reversible, produces a more severe hypertension and faster than the others. While the pathophysiologic aspects are important to clinical diagnosis and management, it is analysis of cause and pathways of pathogenesis that will give the keys to prevention and cure of the disease.
D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D006976:Hypertension, Pulmonary / Q000473:pathology / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology; D007231:Infant, Newborn; D008833:Microcirculation; D010547:Persistent Fetal Circulation Syndrome / Q000503:physiopathology; D011650:Pulmonary Alveoli / Q000098:blood supply; D011651:Pulmonary Artery / Q000033:anatomy & histology; D011655:Pulmonary Embolism / Q000503:physiopathology; D011667:Pulmonary Veins / Q000033:anatomy & histology; D014655:Vascular Resistance