Improved nutrition for mammals and birds at the Philadelphia Zoological Garden has been followed by continued increases in the frequency of arteriosclerosis and by changes in the character and location of the lesions. During the first decade after diets were improved the large atheromata of the proximal aorta and brachiocephalic arteries of birds were replaced by smaller, more compact lesions, usually of the abdominal aorta. At the same time many species of mammals developed atheromata of the aorta, whereas earlier these lesions had been found chiefly in baboons and monkeys (Cercopithecidae). During the second decade of adequate nutrition, and especially since 1950, arteriosclerosis of the coronary arteries has become relatively common in both mammals and birds. Usually this lesion has developed in the distal, intramural segments of the coronary arteries, as intimal thickening and occlusion. Most frequently it has been associated with myocardial fibrosis, but it also has led to myocardial infarction and sudden death in both mammals and birds. Present evidence suggests that this lesion reflects a response of adequately nourished animals to population densities.

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In 1956 MARGOLIS and associates introduced a new experimental model (39,60) for the study of the pathogenesis of the injury to the nervous system produced by contrast media used in diagnostic angiology. Employing retrograde abdominal aortography in the dog, and using the spinal cord as the site of study they described, for the first time in experimental animals, the full evolution of the contrast medium lesion. From these observations it was manifest that existing concepts of the injury as a transient vascular disorder were no longer adequate and had to be revised to include a severe necrotizing effect.Continuing their studies with this model (41, 42), they described in association with the injury a severe irreversible disruption of the circulation of the cord, immediate in onset, and characterized by an abrupt arrest of the toxic injection mass, an immediate impairment of vascular permeability barriers, torpid blood flow with development of severe sludging, and a persistent elevation of vascular resistance in the area of injury. The changes took place in the absence of demonstrable vasospasm. These disturbances in vasomotion were so severe as to constitute, in their opinion, a formidable obstacle to any therapeutic 388 at Harvard Libraries on June 30, 2015 acr.sagepub.com Downloaded from