Painful unanesthetized arterial puncture may produce transient hyperventilation, and this hyperventilation might alter resting values of arterial pH and PCO2. We investigated this possibility by comparing pH and PCO2 values of blood samples obtained by arterial puncture with values of arterialized venous blood obtained by a painless method. In 19 consecutive subjects, virtually no difference in pH or PCO2 resulted from an arterial puncture that could not be attributed to the inherent precision of the measuring instrument. Mean +/- SEM pH was identical (7.45 +/- 0.05) both before and during an arterial puncture, as was PCO2 (34.4 +/- 1.2 mm Hg). The variation (SD) in PCO2 within an individual subject was +/- 1.7 mm Hg, which was almost identical to the inherent precision of the Radiometer ABL-2 acid base laboratory (SD, +/- 1.32). We conclude that an unanesthetized arterial puncture provides an accurate measurement of resting pH and PCO2.
A specific high-pressure liquid chromatographic method for the determination of chlorpheniramine and pseudoephedrine in urine was developed and applied in a urinary excretion study of normal healthy subjects who received a sustained-release dosage form contianing 8 mgof chlorpheniramine maleate and 120 mg of pseudoephedrine hydrochloride. Five subjects received one dose on Day 1, followed by multiple dosing every 12 hr for 7 days without ammonium chloride administration. Four subjects received one dose of the sustained-release dosage form together with ammonium chloride. Urine samples were collected during the 1st day and at steady state. The method is specific and simultaneously determines choorpheniramine, two metabolites (mono- and di-desmethylchlorpheniramine), pseudoephedrine, and norpseudoephedrine. The assay recovery was less than 97% (0.06-3 microgram/ml) for chlorpheniramine maleate and less than 98% (1.5-75 microgram/ml) for pseudoephedrine hydrochloride. Excretion of chlorpheniramine and its two metabolites in urine was enhanced after ammonium chloride administration. At steady state, a change in urine pH from 5.69 to 6.46 resulted in more than a 25% decrease in chlorpheniramine and monodesmethylchlorpheniramine excretion. In spite of expected changes in its biological half-life, the overall amount of unchanged pseudoephedrine excreted in urine was not affected by urine pH, presumably because it is primarily excreted in urine as intact drug.