Abstract
During chloralose-urethan anesthesia of 4 hr duration with spontaneous respiration the pulmonary artery pressure tended to rise, the cardiac output tended to fall; the pulmonary vascular resistance rose. Thus, anesthesia produced an unsteady state. Hypoxia (9.8-12.5% oxygen), superimposed on anesthesia, lead in only approximately 50% to a significant rise in pulmonary artery pressure and cardiac output. The hypoxia-induced rise in pulmonary vascular resistance could not be differentiated from the increase seen with anesthesia alone. Respiratory minute voluem, respiratory rate, oxygen consumption, systemic blood pressure, and heart rate remained constant during prolonged anesthesia; hypoxia-induced changes were similar to those reported for unanesthetized human subjects or dogs. Anesthesia eliminated in almost all the animals the fast rise (1-8 min) in pulmonary artery pressure and pulmonary vascular resistance which is typical for unanesthetized dogs exposed to acute hypoxia. Changes in pulmonary artery pressure and pulmonary vascular resistance did not have a significant relationship to any other of the studied parameters, in particular arterial oxygen partial pressure.