It is generally accepted that a vasoconstrictive mechanism participates in transient pulmonary hypertension observed in miliary embolism, in addition to the mechanical blockade of pulmonary vascular tree. For the explanation, some neural and humoral factors, especially those released from adhesion-aggregation process of platelets, have been emphasized. In our previous reports, we have stressed the importance of some local vascular factors in this vasoconstrictive mechanism. Present study was undertaken to elucidate those local factors extensively. Miliary pulmonary embolism in the isolated perfused canine lung lobe was produced by injecting lycopodium spore suspension in saline, in which hepalinized autologous blood and three different artificial solutions were employed as the perfusate. Although each perfusate made a slight difference in perfusing condition, probably owing to its viscosity and oncotic pressure, all preparations showed definite response to embolization. After each embolization, pulmonary inflow pressure was raised rapidly and reached to a maximal level after 30-60 sec., then fell gradually. Repeated embolization at an interval of 6 min., before pulmonary inflow pressure returned to the control level, produced a cumulative effect. There was no significant difference between perfusations with autologous blood and artificial perfusates at the first and the second embolizations, but it was more distinct in those with autologous blood at the third and the fourth embolizations. The results have showed that the initial pulmonary pressure elevation in miliary embolism is observed apparently even under the bloodless and denervated conditions. It was concluded that "Myogenic Factor" (existing locally in the pulmonary arterial and arteriolar endothelium-smooth muscle) must play a very important role as to initial elevation in pulmonary arterial pressure induced by miliary embolizations. Further advanced studies on the myogenic factor is expected.