Dr. Ross' laboratory has been devoted to physiologic studies in animal models of disease, most recently with studies in small animals including mice, rats, and rabbits. For these investigations we have recently developed miniaturized videoangiographic techniques, as well as echocardiography, to study cardiac size and function in these species, along with high fidelity pressure measurements, coupled with studies on cell morphometry and collaborative studies on selected gene responses.
Current work is focused on heart failure.
Studies in normal rats have showed reduction of hypertrophy by IGF-1 and GH, and current experiments are addressing whether or nor added hypertrophy is beneficial or detrimental using angiographic, hemodynamic and morphometric techniques. The nature of the induced hypertrophy is also being examined in terms of collagen deposition and capillary density. Loss of a gp130 cardiac muscle cell survival pathway is a critical event in the onset of heart failure during biomechanical stress. Cardiac-specific overexpression of RhoA results in sinus and atrioventricular nodal dysfunction and contractile failure. Ross J Jr. Progressive cardiac dysfunction and fibrosis in the cardiomyopathic hamster and effects of growth hormone and angiotensin-converting enzyme inhibition.