Myocardial performance and contractility were evaluated during standardized hemorrhagic shock in dogs and cats. Myocardial contractility, measured by utilizing V<sub>maχ</sub> 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 V<sub>maχ</sub>. This preservation of V<sub>maχ</sub> is probably related to stimulating factors in shock plasma, such as the catecholamines, which overshadow the presence of any myocardial depressant factors.