Myocardial performance and contractility were evaluated during standardized hemorrhagic shock in dogs and cats. Myocardial contractility, measured by utilizing Vmaχ from the isovolumic force-velocity relation, was maintained despite a decline in cardiac performance and progression to irreversible shock. By contrast, in animals subject to β-adrenergic blockade, there was a significant decline of myocardial contractility, suggesting dependence of V on sympathetic neurohumoral support during shock. Plasma taken at hourly intervals from dogs in shock was assayed for inotropic effect utilizing a cat papillary muscle preparation. Fresh plasma taken during shock caused a small augmentation of contractility, while plasma taken at the same time, but frozen before assay, was depressant. It is concluded that in severe and irreversible hemorrhagic shock there is a dissociation between ventricular function as measured by cardiac output and filling pressure, and contractility as measured by Vmaχ. This preservation of Vmaχ is probably related to stimulating factors in shock plasma, such as the catecholamines, which overshadow the presence of any myocardial depressant factors.