Measurements of intracranial liquor pressure were made during i.v. molsidomine administration in pentobarbital anaesthetized beagle dogs without thoracotomy, and compared with those after nitroglycerin. The administration of 100 micrograms/kg molsidomine decreased blood pressure by 14 mmHg and increased intracranial pressure by 3.7 cm H2O (P less than 0.05). No changes in heart rate and the alveolar end-tidal CO2 concentration were noted. The i.v. administration of 5 micrograms/kg nitroglycerin, however, decreased systolic blood pressure by 41 mmHg (p less than 0.05), increased heart rate by 40 bpm (p less than 0.01), elevated intracranial pressure by 3.2 cm H2O (p less than 0.05), and caused marked hyperventilation indicated by increased end-tidal CO2 concentration. Larger increases in intracranial pressure were related to larger pressure reductions. Thus, molsidomine produced significant increase in intracranial liquor pressure of longer duration (60 to 90 min of observation time). Nitroglycerin increased liquor pressure with a short duration of action and was about twenty time more effective with respect to intracranial pressure increase. In contrast to molsidomine, this was accompanied by significant decrease in systolic peripheral blood pressure.