Myocardial function during acute hypoxia in the calf.
Hemodynamics and myocardial contractility were evaluated in five unanesthetized calves during acute hypocapnic and isocapnic hypoxia and during acute hypocapnic hypoxia with beta-adrenergic blockade. Both hypocapnic and isocapnic hypoxia, with mean PaO2 levels of 33.1 and 39.1 mm Hg respectively, produced a decline in stroke volume and index, while cardiac output and index were maintained at normoxic control levels by an increase in heart rate. Evaluation of myocardial contractility indices suggested an augmentation of left ventricular contractility during both hypocapnic and isocapnic hypoxia. Beta-adrenergic blockade effectively eliminated the increase in left ventricular contractility during hypocapnic hypoxia, suggesting an important role of the adrenergic nervous system in the genesis of the cardiovascular response of the calf to acute hypoxia. Right ventricular contractility indices failed to demonstrate a clear-cut augmentation of contractility during hypocapnic and isocapnic hypoxia when the concurrent increase in afterload was considered. Mean pulmonary arterial blood pressure rose significantly during hypocapnic and isocapnic hypoxia. The pulmonary pressor response to hypocapnic hypoxia was significantly augmented by beta blockade, indicating that the autonomic nervous system is capable of modifying the hypoxic pulmonary pressor response in this species.
Myocardial function during acute hypoxia in the calf. Hemodynamics and myocardial contractility were evaluated in five unanesthetized calves during acute hypocapnic and isocapnic hypoxia and during acute hypocapnic hypoxia with beta-adrenergic blockade. Both hypocapnic and isocapnic hypoxia, with mean PaO2 levels of 33.1 and 39.1 mm Hg respectively, produced a decline in stroke volume and index, while cardiac output and index were maintained at normoxic control levels by an increase in heart rate. Evaluation of myocardial contractility indices suggested an augmentation of left ventricular contractility during both hypocapnic and isocapnic hypoxia. Beta-adrenergic blockade effectively eliminated the increase in left ventricular contractility during hypocapnic hypoxia, suggesting an important role of the adrenergic nervous system in the genesis of the cardiovascular response of the calf to acute hypoxia. Right ventricular contractility indices failed to demonstrate a clear-cut augmentation of contractility during hypocapnic and isocapnic hypoxia when the concurrent increase in afterload was considered. Mean pulmonary arterial blood pressure rose significantly during hypocapnic and isocapnic hypoxia. The pulmonary pressor response to hypocapnic hypoxia was significantly augmented by beta blockade, indicating that the autonomic nervous system is capable of modifying the hypoxic pulmonary pressor response in this species.