Relation of intra-acinar arteries and their regression with changes of pulmonary artery pressure and blood gas values

Pulmonary hypertension (PAH) induced by monocrotaline in thirteen rhesus monkeys, seven of them treated by hydralazine to reduce PAH. In hypertensive animals the PAP and PaCO2 increased, the PaO2 decreased. The structural changes in intra-acinar artery manifested mainly by an increase in number of muscular artery resulting from muscularization of precursor cells (pericytes and intermediate cells) located within partially muscular and nonmuscular arterial wall to smooth muscle cell, and by the medial wall thickened due to hypertrophy and hyperplasia of smooth muscle cells as well as accumulation of a large amount of collagen, especially the type 1 collagen. In treated animals the PAPm dropped concomitantly with blood gas values reversing to normal level. The remodelled arteries showed clearly structural regressions: The medial wall thickness was decreased in which the hypertrophied smooth muscles became slender or disappeared, the amount of extracellular matrix, especially the volume density of collagen, decreased. Most of muscularized arteries reversed to nonmuscular arteries leading to an increase in number of nonmuscular artery and a decrease in number of muscular artery. It is concluded that the intra-acinar artery remodelling and their regression closely correlated with the changes of PAP and blood gas values.