Obstruction of the thoracic aorta for 30 minutes can be accomplished without apparent damage to the animal.1 When the period of occlusion is greater than 30 minutes, spinal cord damage, manifested by hindlimb paralysis, ensues in a large percentage of cases. There is a progressive increase in the percentage mortality as the length of obstruction is prolonged. Although survival studies following prolonged aortic obstruction and autopsy reports have been presented, relatively few investigations have been conducted on the alterations in the cardiovascular functions. Studies of the hemodynamic and metabolic changes occurring consequent to prolonged occlusion of the thoracic aorta have been made and are being reported herein.
Eleven mongrel dogs, ranging in weight from 11.2 to 19.5 kg. (mean body weight, 14.9 kg.) were anesthetized with pentobarbital sodium (30 mg/kg. body weight) and heparinized (5 mg/kg. body weight). A single-lumen, bird's-eye-tip cardiac catheter was inserted into a branch