Mechanisms of Impaired Cardiac Function by Vasopressin

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Abstract
The mechanisms by which elevated levels of vasopressin (ADH) in man and animals cause serious myocardial dysfunction, evidenced by arrhythmias, reduction in cardiac output and coronary blood flow, are not settled. Experiments were conducted in 16 isolated working left ventricles of dogs to examine their metabolic and hemodynamic responses to the infusion of vasopressin and the combination of vasopressin and epinephrine. Contractile performance was evaluated by analysis of positive dP/dt [change in pressure with time], contractile element velocities and ventricular work-curves using stroke work/end-diastolic pressure. Relaxation parameters, including negative dP/dt and the early diastolic relaxation time constant, were also studied. Coronary blood flow was reduced 22% or less by vasopressin while cardiac output was maintained at a constant level. Myocardial O2 consumption, lactate and K balances were determined from arterial and coronary sinus concentrations. Vasopressin produced myocardial dysfunction indicated by decrements in contractile and relaxation indices, without evidence of global ischemia. Epinephrine restored the mechanical performance to normal without significant change in coronary blood flow, myocardial O2 consumption or lactate and K balance.