Abstract
Male and female virgin rats with no arteriosclerosis and male and female breeder rats with preexisting arteriosclerosis were given daily injections 5 days/week (.15 mg/100 gm body weight) of the contraceptive drug Enovid (9.85 mg progestin (norethynodrel) and .15 mg estrogen (mestranol) for 4 8 and 12 weeks. There were a total of 864 animals 288 for each of the time intervals consisting of 48 controls 48 male and 48 female virgins 48 male breeders and 48 1-time and 48 4-5 time female breeders. After the 3-month period 1/3 of each group was autopsied. Examinations were made of the heart and vascular systems. Creatine phosphokinase (CPK) transaminases (SGOT SGPT) lactic dehydrogenase (LDH) triglycerides cholesterol free fatty acids glucose and blood urea nitrogen (BUN) were analyzed. All of the treated showed body weight loss adrenal glandular hypertrophy degranulation of pituitary gonadotrophic cells and testicular and ovarian atrophy. CPK SGOT SGPT and LDH were elevated and then their levels receded. The treated developed a fatty liver hypertriglycerdemia elevated free fatty acids and hypercholesterolemia. The treated were diabetic but eventually manifested hypoglycemia despite beta cells degranulation. Corticosterone levels were subnormal. Microscopic arterial lesions appeared in the previously nonarteriosclerotic virgin rats. There was no exacerbation of the arterial lesions in breeder rats with preexisting arteriosclerois. Lesions were in the aorta and its side branches consisting of intimal mucopolysaccharide collagen elastolytic changes and calcification. It was believed that the drug upset hypothalamic and gonadal hormone homeostasis which led to endogenous hormonal-metabolic alterations favoring the pathogenesis of cardiovascular disease in both male and female rats.(Authors modified)
Published Version
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