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The inheritance pattern for susceptibility to spontaneous (noninduced) aortic atherosclerosis in pigeons was determined by crossbreeding and backcrossing experiments with atherosclerosis-susceptible White Carneau and atherosclerosis-resistant Show Racer breeds. Susceptibility, assessed by the presence of grossly visible lesions at the celiac bifurcation of the aorta at 3 years of age, demonstrated an inheritance pattern consistent with an autosomal recessive Mendelian trait. Cell culture studies indicated that susceptibility is a constitutive property of aortic cells as evidenced by vacuole formation and lipid content in smooth muscle cells from various tissues in susceptible pigeons.

A 12-year-old, neutered female, Siberian Husky dog presented with a hind limb weakness of one month duration. To facilitate making a diagnosis multiple imaging modalities were performed. These modalities included radiography, ultrasonography, magnetic resonance imaging (MRI), magnetic resonance angiography (MRA) and selective angiography of the abdominal aorta. In this dog, the MRI/MRA studies provided the first documentation of the external iliac thrombi and the collateral circulation via the lumbar arteries. At necropsy, an aortoiliac thrombus caused by a mineralized arteriosclerotic plaque was noted.

The chemotactic activity of turkey peritoneal macrophages in response to an atherosclerotic plaque extract from a hypertensive strain of turkeys was determined. Atherosclerotic plaque extract stimulated macrophage chemotaxis, whereas normal aortic extract did not stimulate macrophage chemotaxis. However, differences were not revealed by sodium dodecyl sulfate-polyacrylamide gel electrophoretic analysis of extracts of atherosclerotic plaque and normal aorta. Chemotactic activity was diminished with pronase treatment, suggesting the chemo-attractant is a protein. Seemingly, atherosclerotic plaque of turkeys contains a macrophage chemotaxin.

Two experiments were conducted to determine the effects of physical training on the turkey cardiovascular system. Sexually mature (Experiment 1) and immature (Experiment 2) Large White turkeys were used. Equal numbers of genetically hypertensive and hypotensive birds were used in each experiment. In each experimental group, birds were randomly divided into exercise and control treatments. Assessments were made with regard to training effects and differences associated with genetic blood pressure strain. Exercise had no significant effect on the severity of atherosclerosis or serum lipid levels in either experiment. Significantly greater hematocrits were recorded among birds exercised in Experiment 1; however, hemoglobin concentration did not follow this trend. Exercise was also associated with increased cardiac dimensions (Experiment 1) and increased body weight (Experiment 2). Genetic hypertension was associated with accelerated atherogenesis and higher serum cholesterol levels in immature birds, and in mature birds cardiac enlargement was associated with hypertension. Differences in behavior response to exercise were observed between the two experiments. Sexually mature hypertensive turkeys showed less endurance to the walking regimen than the hypotensive turkeys, but no such differences were observed in immature hypertensive or hypotensive birds.

Lesions in the abdominal aorta were found in 36 of 40 mature female rhesus monkeys given various oral contraceptive steroids and in 8 of 10 monkeys of a non-treated control group. The lesions consisted of proliferation of subendothelial smooth muscle cells and collagen, often with fragmentation of the internal elastic lamina, forming a plaque. These occurred also, in order of descending frequency, in thoracic aorta, aortic arch, femoral and iliac arteries, and the carotid and pulmonary arteries. They appear statistically unrelated to steroid treatment and lack correlation with body weight and blood cholesterol levels.

The aorta and coronary arteries of two tortoise species, Testudo graeca ibera and Emys orbicularis are investigated. The elastic aorta of the first species showed minimal focal intimal thickenings while the muscular aorta of the second presented marked diffuse hyperplasia narrowing the caliber of the vessel. The author discusses this striking finding of the aortic structural differences between the two species investigated as well as the significance of such lesions for atherosclerosis development.

Arterial lesions were investigated in 48 adult wild Carpathian deers (Cervus elaphus). Aortas from 36 animals and fragments from the main coronary trunks of all the animals were studied histologically and histochemically. In 44.4% of the animals the specimens studied presented gross intimal lesions in the aorta consisting histologically of fibrous plaques (especially situated in the thoracic segment) and/or intimal musculo-elastic thickenings with lipid deposits or fatty streaks (especially in the abdominal segments). In only 5 of the 48 animals the coronary arteries presented slight intimal thickenings, free of lipids. The results obtained are discussed in relation with the possible effect of natural nutrition.

Of 223 histologically examined aortas of rabbits 24 showed spontaneous calcifying medial sclerosis. Spontaneous lesions found in the aorta of rabbits are histologically similar to those in other mammals and experimentally induced lesions following the action of vitamin D, adrenalin and orthostatic collaps as well as lesions of the arteriopathia calcificans infantum. Pathogenetically, it is reasonable to assume that primary media cell necrosis and secondary malregeneration of smooth muscle cells account for spontaneous medial sclerosis in the rabbit. Electron microscopical examination of the lesions showed the cells within the area of the lesions to represent forms of transformation of the smooth muscle cell.

This is a step section study of 3 fibrous plaques from the abdominal aorta of an ostrich. The distribution of gelatinous like lesions in these plaques suggested that the gelatinous lesions were formed by the influx of plasma at the plaque shoulders. Two gelatinous lesions extended like tunnels into the center of one of the plaques. The presence of focal necrosis and large cholesterol crystals in one of these gelatinous tunnels deep within the plaque suggested that gelatinous lesions might represent one mechanism by which fibrous plaques are converted to atheromatous plaques.

Heart, aorta, and sciatic arteries were collected from 157 wild male turkeys (Meleagris gallopavo silvestris) by hunters in 9 states during the spring 1983 and 1984 hunting seasons. In descending order of extent and severity, intimal vascular changes were observed in the left sciatic artery, aorta at the celiac region, cranial abdominal portion of the aorta, sciatic bifurcation, caudal abdominal portion of the aorta, coronary arteries, and thoracic portion of the aorta. Only the aorta from the celiac region and right sciatic artery had significant differences (P less than 0.05) among turkeys from various locations. Turkeys from Indiana had significantly (P less than 0.05) larger plaque scores in the celiac region than did those from Alabama, Missouri, and South Carolina. Turkeys from Indiana also had significantly (P less than 0.05) greater plaque scores in the right sciatic artery than did turkeys from Arkansas. When all tissues were considered, tissues from turkeys from Michigan had the highest plaque scores and those from Iowa had the lowest. Plaque scores for turkeys from Michigan were significantly (P less than 0.05) higher overall (including all blood vessels) than were plaque scores for turkeys from Alabama, Arkansas, Iowa, and South Carolina. Few significant (P less than 0.05) correlations were detected among plaque scores in turkeys from within states of origin (geographic location). Also, only a few significant (P less than 0.05) correlations were determined between age or body weight and atherosclerosis for blood vessels from turkeys within various states.

Aortas of 334 sheep 6 months to 6 years old were stained with Sudan IV. Sudanophilic lesions resembling early fatty streaks of man were detected in 50% of these aortas. Metastatic calcification was seen in eight (2.3%) aortas.

Ten laying hens with low plasma cholesterol levels and no signs of fatty liver syndrome were examined at necropsy. Liver coloration and deposition of body fat were not abnormal in such hens. Eleven nonlaying hens had signs of fatty liver syndrome. They were out of production for 1 to 3 months and had elevate plasma cholesterol levels. At necropsy, such hens had yellow livers, heavy deposits of body fat, and several involuted egg yolks, which were dark yellow. Intimal plaques were observed by light microscopy in the abdominal aortas of hens with low plasma cholesterol levels; the plaques contained little or no lipid and were composed of three or four rows of modified smooth-muscle cells. Aortic intimal plaques of hens with high plasma cholesterol levels were composed of 16 to 18 rows of modified smooth-muscle cells when examined by light microscopy. The plaques contained intracellular and extracellular lipid, indicating aortic atherosclerosis. Electron-microscopic observations of the abdominal aortas of both groups of hens were similar to light-microscopic observations, except that lipid, including cholesterol clefts, was seen both intracellularly and extracellularly in the thickened tunica intima of hens with high plasma cholesterol values. Thus, the presence of aortic atherosclerosis was confirmed by electron microscopy. It is suggested that the endogenous hypercholesterolemia and cessation of egg production, characteristic of severe fatty liver syndrome, originated from the reabsorption of involuted egg yolks and that such reabsorption caused the development of aortic atherosclerosis and deposition of excess body fat.