Editorial Focus Rodent models of PAH: are we there yet?

analogs, endothelin receptor antagonists, and phosphodiester-ase type 5 inhibitors in severe pulmonary arterial hypertension (PAH) from 1990 to 2005 shows that although the pharmaco-logical agents moderately improve symptoms and hemody-namic parameters, none significantly reduces mortality (13). These disappointing results are not predicted by animal model studies, which show these classes of drugs largely prevent, and in some cases reverse, chronic hypoxia- and monocrotaline-induced pulmonary hypertension in rats (e.g., 6, 25, 29, 30). The limitations of using chronically hypoxic or monocrotaline-injected rats as models of human PAH have been previously noted (9, 28, 39, 42). It is apparent that preventing or reversing sustained constriction and neomuscularization of pulmonary arteries in these rodent models (15, 31) is not equivalent to “dissolving ” obstructive neointimal and other complex vascu