Regional blood flow and metabolite levels in the left ventricular free wall and septum during aortic insufficiency: implications for the development of asymmetric septal hypertrophy.
Asymmetric septal hypertrophy is considered by many to be pathologic but its presence in a number of states associated with left ventricular overload indicates that it may develop as an adaptive feature in the overloaded heart. This hypothesis implies that initially in these states a greater systolic stress and thus energy metabolism occurs in the ventricular septum than in the left ventricular free wall. It was previously demonstrated that in the early stages of ischemia regional differences in energy metabolism could be determined by comparisons of tissue high energy phosphate depletion and lactate accumulation. In the present study these measurements were made in an animal model of left ventricular overload. In open chest dogs aortic insufficiency was produced, which served to provide both volume overload to the left ventricle and regional myocardial ischemia. In addition to regional metabolite levels, measurements of regional blood flow were determined using radioactive microspheres. Tissue samples were taken from the left ventricle and interventricular septum, freeze clamped, divided transmurally into thirds and analyzed for creatine phosphate, adenosine triphosphate and lactate. Animals with myocardial ischemia after aortic insufficiency were classified into two groups: those in which ischemia was limited to the inner left ventricle and left side of the septum and those with more extensive ischemia transmurally. In the latter group, creatine phosphate depletion and lactate accumulation were greater in the septum, but myocardial blood flow was also more depressed in the septum than in the left ventricle. In the former group, where ischemia was more restricted, metabolite changes were also more severe in the left septum than in the inner left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001022:Aortic Valve Insufficiency / Q000503:physiopathology*; D001794:Blood Pressure; D006332:Cardiomegaly / Q000209:etiology*; D004285:Dogs; D004734:Energy Metabolism; D006346:Heart Septum; D007773:Lactates / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism
D007773:Lactates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate