Thoracic epidural anesthesia has been used to manage intraoperative and postoperative pain for thoracic surgical patients with general anesthesia recently, And this combined anesthesia has been associated with less sedation, earlier ambulation, blunting of the stress response and better pain control in the post-operative period. But the effects of thoracic epidural anesthesia on pulmonary shunt, pulmonary vasoactivity and oxygenation are still unknown. The author has investigated the effects of thorarcic epidural anesthesia on pulmonary hypertension induced by acute diffuse alveolar hypoxia and N(W) -nitro-L-arginine(L-NNA) in 12 mongrel dogs. Acute diffuse alveolar hypoxia which is similar to the early stage of acute respiratory failure may induce the pulmonary hypertension. And L-NNA, inhibitor of endothelium derived relaxing factor(EDRF), may also induce pulmonary hypertension under hypoxic state. The measurements were made three times, the first was baseline at room air ventilation. Following baseline recordings, saline 4 ml(group A, n=6) or 2% lidocaine 4 ml(group B, n=6) was injected through the epidural catheter and ventilation was started with hypoxic gas mixture(10% O2, 90% N2). The seeond measurements was made 30 min after the hypoxic ventilation and third was 20 min after infusion of L-NNA(50 mg/kg mixed with distill water 50 ml, infusion rate is 50 ml/20min) under the continuous ventilation with hypoxic gas mixture. The results were as follows: 1) There were significant changes in mean pulmonary arterial pressure, pulmonary vascular resistance in group A(p<0.05) and in arterial and mixed venous oxygen tension, arterial and mixed venous oxygen content, intrapulmonary shunt in both groups(p<0.05) 30 minutes after hypoxia but there were not significant differences between groups. 2) There were significant changes in mean pulmonary arterial pressure, in group B (p<0.05) and pulmonary vascular resistance, systemic vascular resistance and mixed venous oxygen tension and content in both groups (p<0.05) 20 miniutes after infusion of L-NNA under the continuous ventilation with hypoxic gas mixture but there were not significant differences between groups. But there were significant changes in central venous pressure in group B(p<0.05) and significant differences between groups(p<0.05) at 20 miniutes after infusion of L-NNA. These results indicate that thoracic epidura1 anesthesia does not influence the pulmonary hypertension directly and does not praduce any unfavorable hemodynamic events during pulmonary hypertension induced by acute diffuse alveolar hypoxia and N(W)-nitro-L-arginine. Therefore thoracic epidural anesthesia shoud be valuable assistant to the general anesthesia for pulmonary hypertensive patients.