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In animals examined prenatally (100 \u00b1 2 days gestation) the total incidence of ventricular septal defects (VSD) was 40% in cynomolgus monkeys, 18% in rhesus monkeys, and 23% in baboons. The majority of VSD involved the muscular portion of the septum. No dose response was evident and there were no other cardiac or extracardiac defects found except for one baboon fetus with multiple defects. No defects were observed in cynomolgus monkeys administered Bendectin for 4\u2010day periods between 22 and 41 days of gestation. There was no association of Bendectin treatment with any noncardiac defect. In cynomolgus and rhesus monkeys examined at term there was one mitral valve defect and no incidence of VSD. The increased incidence of VSD observed prenatally in all three species and the absence of defects in macaques at term suggests a delay in closure of the ventricular septum in treated animals. The Bendectin\u2010treated monkey may be a suitable model for the study of the pathogenesis of VSD and the mechanism of spontaneous closure of the defect.<\/jats:p>","DOI":"10.1002\/tera.1420320205","type":"journal-article","created":{"date-parts":[[2005,6,11]],"date-time":"2005-06-11T14:53:14Z","timestamp":1118501594000},"page":"179-189","source":"Crossref","is-referenced-by-count":26,"title":["Evaluation of Bendectin embryotoxicity in nonhuman primates: I. Ventricular septal defects in prenatal macaques and baboon"],"prefix":"10.1002","volume":"32","author":[{"given":"A. 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