What Effect Does ADX Have on Atherosclerosis Article

What Effect Does ADX Have on Atherosclerosis - Article Example Image 1 the image above shows the pathway by which the Adrenal glands respond to the signal triggered by the brain.1 When the adrenal glands are removed, there is a sudden decrease in the epinephrine, norepinephrine and hormones. This could lead to disastrous effects in the body. Reasons for an adrenalectomy could be due to an adrenal mass (incidental adenoma), pheochromocytoma, Conn’s Syndrome (aldostrenoma) and Cushing’s syndrome.2 Atherosclerosis is a stress inducing disease. The adrenal glands respond to the development of atherosclerosis and release hormones to reduce the further developing. In atherosclerosis the Low Density Lipoproteins (LDL) enter the endothelial cells in the cell wall where they are oxidized. Oxidized LDL is toxic and induces inflammation. The monocytes, in the blood passing through the artery, respond to the inflammation and engulf the macrophages (cholesterol rich oxidized LDL). These form foam cells, filled with lipid. The cells die (apoptos is) and leave a lipid core. The body’s attempt to heal forms a fibrous cap over the lipid core. LDL growth continues causing the elastic membrane to stretch outward. Arterial remodeling takes place to maintain the artery’s shape, however if the lesion continues to grow the growth will continue inwards when it cannot stretch outward anymore. This narrows the diameter making it less easy for the blood to pass through, and the fibrous cap is now very thin after is has been stretched which increases chances of lesion rupture. Glucocorticoids are stress-response hormones; the hormone is released in response to stress in the body by the adrenal glands. Glucocorticoids also play a role in the further developing of atherosclerosis. The glucocorticoids inhibit the colony growth of macrophages; this is beneficial to reducing atherosclerosis. However, glucocorticoids have side effects which could increase the chances of developing atherosclerosis, such as high blood pressure, ind uction on hypercholesterolemia, impairment of glucose tolerance, hypertriglyceridemia, imbalance of thrombosis and fibronolysis.3 In the present study, I hypothesized that an adrenalectomy will lead to further the development of atherosclerosis in the LDL-knockout mice. To test this hypothesis, the levels of stress was compared to the development of atherosclerosis in both sham operated and adrenalectomized (ADX) mice. The genetic differences were compared after the sham operation and the adrenalectomy took place. This study demonstrates the effect of ADX on atherosclerosis. Methods: In this experiment 12 week old female LDL-receptor knockout mice were used. Supplied by, my supervisor Menno Hoekstra. The mice were caged in groups of four or five. The drink bottles contained a saline solution, from which the mice could drink at any time, also during fasting. Diet N is made up of cholesterol, fat and cholic acid. The experiment took place as follows; the mice were 6 weeks old when the ADX and SHAM operations took place. This is week 0. At two weeks the mice gained strength after being fed the chow diet. Blood was drawn at two weeks. At six weeks the mice were put on diet N and blood was drawn again. At 8 weeks the mice were sacrificed after blood was drawn. Sacrificing: The adrenalectomy takes place when