Both New World and Old World monkeys have been extensively evaluated for their ability to develop atherosclerotic lesions. Nonhuman primates develop atherosclerotic lesions that bear remarkable similarities to those of humans, including the ability to mineralize and undergo plaque rupture. Atheromatous formation in monkeys is modified by many of the same factors that influence human vascular disease—diet, gender, age, blood pressure, and genetics. Thus, nonhuman primates have many ideal characteristics for developing animal models of atherosclerosis. However, these advantages are mitigated by three major factors: regulatory issues that make it difficult to acquire and obtain monkeys for research; requirements for specialized housing and veterinary services; and the relatively long time-intervals required for atherosclerotic lesion development.
In spite of these challenges, nonhuman primates exhibit a number of remarkable features that favor their use for understanding the mechanisms of human vascular disease. For example, cynomolgus macaques have lipid profiles similar to humans, and exhibit sex differences in lesion formation that mimic what is observed in humans (Rudel et al., 1977). In addition, both cynomolgus and rhesus monkeys develop myocardial infarctions (Bond et al., 1980), which is otherwise a rare occurrence within the animal kingdom outside Homo sapiens. Localization of atherosclerotic lesions in monkeys is generally similar to that in humans, allowing analysis of disease in coronary, iliac, aortic, and intracranial vessels, all of which are major sources of disease in humans.
Arguably the best data linking diet and lifestyle changes with modulation of the risk of atherosclerosis have derived from nonhuman primate studies. Regression of atherosclerosis has been amply demonstrated to occur in conjunction with reductions in plasma cholesterol concentrations (Clarkson et al., 1984). This remains one of the few models in which true plaque regression can be observed, and given that therapeutic interventions to elicit plaque regression in humans are limited, this is a powerful advantage. In addition, monkeys are arguably the only model organisms in which human-type psychosocial stresses can be tested. A number of studies have now shown clearly that high levels of psychosocial stress associated with activation of the autonomic nervous system and neuroendocrine reactions to stress in monkeys result in acceleration of atherosclerotic lesion formation that at least in some cases can be modulated pharmacologically (Kaplan et al., 1987). Thus, it is unfortunate that logistical and practical reasons limit the utility of these models, which are becoming increasingly limited to a few specialized centers.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...