Cardiopulmonary response to sodium fluoride infusion in the dog

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Abstract
Because humans are occasionally acutely exposed to high levels of fluoride (F‐), and cardiac and especially pulmonary 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 arterial 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 μM in the “low” group of 6 animals, and 1300 μM 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 in a decreased PCO2 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.