Sodium salicylate has no effect on cerebrospinal fluid [H+] in dogs with normal acid-base balance

The experiments described here were designed to investigate the possibility that central stimulation of respiration by salicylates may be due to changes in [H⁺] of cerebral fluids. Two groups (n=6 in each) of anesthetized, paralyzed, and mechanically ventilated dogs were studied for 6 hr. Renal pedicles were ligated to maintain blood salicylate level constant. Group II received 150 mg/kg Na salicylate intravenously at 0 hr after samples had been obtained. Group I (control) received equal volume of half-normal saline. Mean plasma salicylate levels were 18.9, 18.4, and 19.6 mg % at 0.5, 3, and 6 hr after administration of Na salicylate. Respective cisternal cerebrospinal fluid (CSF) levels were 3.2, 4.8, and 5.9 mg %. Salicylate-induced hyperthermia was prevented by peritoneal cold dialysis, and a rise in PaCO₂ was prevented by increasing ventilation. During the 6 hr of relatively normal systemic acid-base balance, cisternal CSF mean PCO₂ values were 45.3, 43.6, and 49.3 mm Hg at 0, 3, and 6 hr in the control group; in group II, respective values were 46.9, 45.7, and 47.7 mm Hg. Cisternal CSF [H⁺] were 44.4, 45.2, and 50.5 nEq/L in group I at 0, 3, and 6 hr. Respective values in group II were 45.0, 47.5, and 50.6 nEq/L. These values were similar and statistically insignificant from those in group I. In both groups cisternal CSF [HCO ₃ ⁻ ] fell about 2 and CSF lactate concentration rose about 1 mEq/L at 6 hr. We conclude that at the dose used in the present study, Na salicylate increases metabolic rate but does not significantly influence cisternal CSF [H⁺] up to 6 hr in dogs with normal systemic acid-base balance.