Because humans are occasionally acutely exposed fluoride (F-), and cardiac and especially pulmonary to high levels of tissue accumulate higher concentrations of F- than do the other soft tissues, the present study was undertaken to investigate the effects of acute exposure to toxic plasma levels of F- on cardiopulmonary hemodynamics.
Anesthesized dogs were instrumented with right and left cardiac catheters to measure pulmonary ar terial and wedge pressures, left ventricular and aortic pressures, left ventricular dP/dt, and cardiac output. An intravenous loading dose of NaF followed by a 3-h infusion produced a plasma F- level of 800 uM in the “low” group of 6 animals, and 1300 uM in the “high” group. The mean pulmonary arterial pressure peaked at 1 h, 83% above preinfusion values in the high group, while that of the low group attained the same level by the end of the infusion period. Impaired pulmonary gas exchange, as indicated by an increased alveolar-arterial Po2 gradient occurred in half the animals, and an obvious hyperventilation was reflected i n a decreased Pc02 value; there was no change in arterial pH. ECG T-wave peaking was common. The central venous pressure declined steadily, while there were no significant changes from controls in systemic arterial pressure, heart rate, cardiac output, or myocardial contractility (dP/dt). Thus, pulmonary hemodynamics and the systemic capacitance vessels are more affected by acute exposure to F- than is cardiac function.