PULMONARY VASCULAR SMOOTH-MUSCLE - BIOCHEMICAL AND MECHANICAL DEVELOPMENTAL-CHANGES

To evaluate the developmental changes in pulmonary vascular smooth muscle contractile protein content, mechanical properties, and their contribution to the high resistance characteristic of the fetal and immediate neonatal period, we studied pulmonary vessels of fetal, newborn, and adult sheep, as well as newborn and adult pigs. Strips of the second- through fifth-generation vessels were dissected, and their content of tissue total smooth muscle cell protein, myosin, and actin-to-myosin ratio were measured; the mechanical properties of the second-generation vascular strips were also studied. For all ages the smooth muscle protein and myosin content of the second-generation vessels were significantly greater than for the lower pulmonary vascular orders (P < 0.05). The myosin content in fetal sheep (0.77 +/- 0.03-mu-g/mg wet tissue) was similar to that of the newborn (0.79 +/- 0.04) and adult (0.86 +/- 0.05). However, the smooth muscle protein content (7.94 +/- 0.21-mu-g/mg wet tissue) and the actin-to-myosin ratio of the pulmonary vascular tissue of the fetus (1.00 +/- 0.04) were lower (P < 0.01) in the fetal than in the newborn (9.16 +/- 0.26 and 1.60 +/- 0.12) and adult (9.38 +/- 0.3 and 1.60 +/- 0.11, respectively). No differences were observed for these parameters between the newborn and adult pig. Stress (16.5 +/- 1.7 mN/mm2) and the maximum shortening capacity (13.0 +/- 1.5% of optimal length) in the newborn pulmonary vascular strips were significantly greater than for the fetus (6.8 +/- 1.4 and 5.9 +/- 1.0, respectively) but similar to those of the adult sheep. The vascular muscle maximum velocity of shortening (0.065 +/- 0.013 optimal length/s) was significantly greater in the newborn (P < 0.01) than in the adult (0.010 +/- 0.003) and fetus (0.014 +/- 0.006). In conclusion, the fetal pulmonary vascular muscle has a reduced potential for vasoconstriction compared with the newborn and adult. Thus the higher pulmonary vascular resistance present prenatally is not the result of a greater pulmonary vascular muscle mass or of increased muscle contractility.