Mechanism of cardiac output response to hypertonic sodium chloride infusion in dogs

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Abstract
Hypertonic NaCl solution and tris(hydroxymethyl)aminomethane hydrochloride (Tris HCl) (0.3 mmol/kg .cntdot. min) were infused i.v. into chloralose-anesthetized dogs over a 20 min period. Cardiac output, maximum left ventricular dP/dt [rate of pressure rise], and (dP/dt)/P [ratio of dP/dt to developed left ventricular pressure of 50 mm Hg] increased by 55, 33 and 23%, respectively, during NaCl infusion, but Tris HCl infusion had no effects. NaCl infusion did not change heart rate or left ventricular end-diastolic pressure. Mean systemic and pulmonary arterial blood pressures increased; total peripheral and pulmonary vascular resistances decreased. Responsiveness of cardiac .beta.-adrenergic receptors, as determined by serial i.v. injections of epinephrine, was not affected by NaCl infusion. Plasma catecholamine concentration increased during NaCl infusion. The increases in cardiac output, maximum left ventricular dP/dt and (dP/dt)/P were abolished by prior treatment with practolol, a cardioselective .beta.-adrenergic receptor blocking agent. The hemodynamic effects of NaCl infusion were possibly caused, at least in part, by the inotropic action of catecholamines.