• P R Silva, A Fonseca-Costa, W A Zin, A Böddener, and T M Pinto.
• Braz. J. Med. Biol. Res. 1986 Jan 1; 19 (2): 279-86.

AbstractThis paper examines the mechanism responsible for hyperventilation and accompanying respiratory alkalosis during acute salicylism. Sodium salicylate (250 mg/kg) was administered to 8 spontaneously breathing anesthetized dogs (alpha-chloralose, 50 mg/kg, and urethane, 500 mg/kg, iv). The trachea was sectioned and connected to a pneumotachograph. A catheter was placed in the cisterna magna for sampling cerebrospinal fluid (CSF) and a femoral artery was cannulated for blood sampling and pressure determinations. Once the cardiorespiratory steady-state was obtained, air flow, tidal volume, arterial pressure, ECG and rectal temperature were measured for baseline control. The measurements were repeated 8 times during 100 min after salicylate infusion. Simultaneous determinations of CSF and plasma salicylate showed that plasmatic levels were maximal just after infusion, diminishing with time. CSF concentration increased gradually as the salicylate diffused through the blood-brain barrier. Minute ventilation increased to more than 600% of control values and was maximal between 60-100 min after salicylate infusion. Respiratory alkalosis and hyperthermia (up to 40.3 degrees C) followed the time-course of hyperventilation. Only a small part of hyperventilation can be attributed to the temperature increase. A high correlation coefficient (r = 0.974) was obtained by regression analysis of the values for ventilation and CSF salicylate. We conclude that the central action of salicylate is much more important for increasing ventilation than effects related to oxidative phosphorylation uncoupling.

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