The excretion of tolbutamide in saliva of diabetic patients receiving single intravenous doses of 1 gm tolbutamide is described. Gas chromatography with electron capture was used for analysis. Pharmacokinetic parameters could be obtained from either salivary or plasma tolbutamide levels. There was a good linear relationship between tolbutamide concentration in saliva and in plasma; salivary levels were 1.2% of plasma levels. Equations are presented that account for the excretion in saliva based on extent of protein binding and degree of ionization of tolbutamide in plasma and saliva. Correlation of the saliva to plasma concentration ratio was extended to data in the literature on two other drugs.

Amphetamine was administered to healthy subjects as the racemic mixture and as (+)- and (-)-isomers under conditions of urine acidification and alkalinization. Plasma and saliva concentration of each isomer was measured and the kinetics of the individual isomers were determined. (+)-amphetamine was eliminated more rapidly than the (-)-isomer. The difference in half-life between isomers was maximal under basic urinary pH conditions. Saliva amphetamine levels were higher than plasma levels and in the postabsorptive phase were predictably proportional to plasma drug levels.

The pharmacokinetics of SH‐methotrexate were studied in 22 patients with malignancies. Following the intravenous administration of 30 mg methotrexate (Mtx) per square meter, the plasma disappearance was triphasic with half‐lifes of 0.7.5 ± 0.11,3.49 ± 0 . .55, and 26.99 ± 4.44 hours, respectively. The urinary excretion of radioactivity paralleled the plasma data for most patients. A metabolite was found in urine that eluted before Mix when chromatographed on a diethylaminoethyl (DEAE) cellulose column. The excretion of this metabolite reached steady state and accounted for 20 (14 to 37) per cent of the radioactivity in urine after 30 hours. Our observation that Mtx has a long terminal half‐life may explain the high incidence of tOXicity in patients receiving chronic low‐dose Mtx therapy.

I The pharmacokinetics of intravenous and oral atenolol (50 mg) in six healthy volunteers was studied. Plasma, saliva and urine were collected up to 24 h after each dose.2 There was no significant difference in atenolol half-life when administered by the two routes. Bioavailability of the orally administered atenolol was 50%.3 Atenolol levels in saliva required about 2 h to reach equilibrium with plasma drug levels. 4 A comparison between the pharmacokinetics and pharmacology of atenolol was made in twelve healthy subjects.5 Dose-independent pharmacokinetics were observed. Reductions in resting heart rate and arterial blood pressure were proportional to either the logarithm of dose or area under the plasma concentration time curve or cumulative urinary atenolol excretion. 6 Plasma elimination half-life in five subjects with renal failure was prolonged.