Access to abstract permanently restricted to Ball State community only / Access to thesis permanently restricted to Ball State community only / Department of Physiology and Health Science

Autoantibodies generated against M proteins can cause post-streptococcal disorders such as Rheumatic Fever. A severe complication of rheumatic fever is rheumatic heart disease which may involve both cardiomyopathy and valvulitis. Rheumatic fever has been associated with the class I M protein epitope of Group A streptococcus (GAS). This epitope can be recognized by monoclonal antibodies (mAbs) 10B6 and 10F5. Previously, we demonstrated binding of streptococcal mAb10F5 in the heart tissue (apex, atria, and valves) of Lewis rats as compared to anti-myosin binding. To determine if mAb10F5 binding in the heart is due to virulence of the antibody or antibody subtype, rats were injected with control IgG2 antibodies and euthanized after 24, 48, or 72 hrs. Hearts were harvested and immunofluorescence was used to analyze the hearts. The immunofluorescence intensities for IgG2b were compared to mAb10F5 using previously acquired data. Control IgG2b rats showed significantly less immunofluorescence intensities in the heart regions than mAb10F5 injected rats at the 48 and 72 hr time points. These findings reaffirm mAb10F5 as an anti-cardiac antibody thatbinds heart tissue due its own virulence. To differentiate between the two IgG subtypes, binding intensities of IgG2a were compared to the binding intensities of IgG2b. The binding intensities of IgG2a increased with time. This finding was supported by previous work in our laboratory suggesting IgG2a remained in the bloodstream longer than the IgG2b. / Access to thesis permanently restricted to Ball State community only. / Department of Physiology and Health Science

Athletes have continually sought to improve their physical performance. In order to accomplish this, athletes experiment with performance enhancing drugs, which are readily available to the athlete today. Cocaine, being one of them, is traditionally and popularly believed to increase muscular endurance and possess anti-fatiguing properties. The scientific literature as to whether cocaine is truly a performance enhancing drug is inconclusive. Moreover, few if any studies have been conducted on exercise performance following long term, repeated cocaine administration. The purpose of the present study was to determine the effects of 35 days of cocaine administration (25 mg/kg/day) on maximal endurance exercise capacity. Data were collected from six untrained male Sprague-Dawley rats. Resting and exercise heart rate and body temperature were recorded via radio telemetery. Running time to exhaustion was recorded via one weekly maximal treadmill exercise bout to exhaustion (26 m/min, at a 10% grade). Compared to saline controls, cocaine significantly decreased run time to exhaustion, following acute and chronic administration. Cocaine administration also significantly decreased maximal exercise heart rate. Chronic cocaine had minimal effects on resting heart rate and resting and exercise body temperature during maximal exercise conditions. These data indicate that daily, chronic cocaine administration significantly reduces endurance exercise capacity, and suggests that the decreased physical work capacity following cocaine is related to a decreased ability of the heart to function under maximal exercise conditions.