Acceleration of blood in the aorta: a parameter useful for evaluating cardiotonic and afterload reducing substances

Peak acceleration of blood in the aorta was measured in chloralose-urethane anesthetized open-chest cats with an electromagnetic flow probe around the aortic root. The effects of substances used in the treatment of chronic congestive heart failure were evaluated in this model. Isoprenaline, noradrenaline, and ouabain increased peak acceleration dose-dependently, while blood pressure, cardiac output, and heart rate were influenced differently by each drug. Nitroglycerin and nitroprusside sodium, afterload reducing agents used for the treatment of congestive heart failure, also increased peak acceleration; an effect that in the case of nitroprusside sodium was shown to be mediated by beta-receptors and probably attributable to baroreceptor activation. This simple model was judged to be suitable for evaluating positive inotropic and afterload reducing substances as long as its low sensitivity to heart rate increasing interventions is correctly appreciated.