Masters Degrees (Physiological Sciences)
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Browsing Masters Degrees (Physiological Sciences) by Subject "Anabolic steroids -- Health aspects"
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- ItemThe effect of androgenic anabolic steroids on the susceptibility of the rat heart to ischaemia and reperfusion injury(Stellenbosch : Stellenbosch University, 2002-12) Rossouw, Ellen; Du Toit, E. F.; Van Rooyen, J.; Stellenbosch University. Faculty of Science. Dept. of Physiological Sciences.ENGLISH ABSTRACT: Background: Athletes use androgenic anabolic steroids (AAS) to enhance their physical performance. The abuse of AAS is however associated with a host of side effects including sudden death due to cardiac arrest. The use of AAS leads to myocardial hypertrophy, which possibly makes the heart more prone to ischaemia/reperfusion injury, since it often develops in the absence of proper vasculature development. Chronic AAS use also disrupts myocardial p-adrenoreceptor function and possibly cAMP, signalling in the heart. Drugs increasing cAMP and decreasing cGMP levels in the ischaemic myocardium exacerbate myocardial ischaemia/reperfusion injury. We also know that AAS causes coronary artery disease secondary to the deleterious alteration of lipid profiles by increasing the LOL cholesterol and decreasing the HOLcholesterol levels. AAS treatment may increase systemic TNFa levels by stimulating lymphocyte TNFa secretion that has been implicated in the depression of myocardial function, myocardial hypertrophy and the worsening of ischaemia/reperfsuion injury. Aims: To determine whether chronic AAS treatment in trained and untrained rats influences: 1) heart function and susceptibility to ischaemia/reperfusion injury, 2) myocardial cyclic nucleotide levels (cAMP and cGMP) and 3) myocardial TNFa levels. Material and methods: Male Sprague-Dawley rats (n=100) were divided into 4 groups: sedentary vehicle (placebo) treated group, sedentary AAS treated group, exercise vehicle (placebo) treated group, and exercise AAS treated group. Steroid treated animals received an intramuscular injection of nandrolone laureate (0.375 mg/kg) once a week, for six weeks. Training consisted of swim sessions 6 days a week for 6 weeks. Swim time was incrementally increased up to a maximum of 50 minutes a day. For biometric parameters heart weight and body weight were documented. Hearts were mounted on a l.anqendorff perfusion apparatus and left ventricular developed pressure (LVDP), heart rate (HR) and coronary flow (CF) was monitored. The hearts were subjected to a period of 20 minutes of global ischaemia, followed by 30 minutes of reperfusion. Functional parameters was again monitored and documented. For biochemical analysis, blood was collected for the determination of serum lipid levels and myocardial tissue samples were collected before, during and after ischaemia for the determination of myocardial TNFa, cGMP and cAMP levels and p38 activity. Conclusions: Results obtained would suggest that AAS exacerbate exercise induced myocardial hypertrophy. It also prevents the exercise-induced improvement in cardiac function. AAS use reduces reperfusion function in treated hearts, which may suggest that AAS exacerbates ischaemie and reperfusion injury. Furthermore it was seen that AAS elevates basal (preischaemie) cyclic nucleotide levels and basal (pre-ischaemic) as well as reperfusion TNFa levels. This may also contribute to the exacerbation of ischaemic and reperfusion injury.