Job design and system redesign theory are applied to elucidate costs and benefits of alternative restructuring schemes. Strategies are outlined for nurse executives to use for successful reconceptualization of nursing positions.

Efficiency↗

PubMedDate not supplied

Effect of 3-methylcholanthrene pretreatment on glucuronidation and sulfation in perfused rat liver.

The metabolism of p-nitro[14C]phenol (PNP) was studied in perfused rat liver. Metabolites were identified in perfusate and bile. The perfusion system containing 0.5 mM PNP, at the start, converted the phenol within 2 hr to p-nitrophenyl glucuronide (PNPGA), 31.4% in perfusate and 21% in bile; p-nitrophenyl sulfate (PNPS), 22% in perfusate; and p-nitrophenyl glucoside (PNPG), between 2 and 4% perfusate. Biliary excretion of PNPS and PNPG accounted for less than 2% of PNP. An apparent maximal rate of PNPGA synthesis by the perfused liver, estimated from the rates of appearance of PNPGA in perfusate and bile, corresponded well to the glucuronyl-transferase activities determined in "native" liver homogenates. Sulfation of PNP in the perfused liver exhibited two apparent maximal rates of synthesis, as determined from the rates of appearance of metabolite in the perfusate. A slower rate (R1) occurred when PNP concentration was between 0.13 and 0.5 mM, and a faster rate (R2) when PNP was approximately between 0.025 and 0.13 mM in the perfusate. Possible significance of these findings is discussed. Pretreatment of rats with 3-methylcholanthrene (3MC) increased the apparent maximal rate of PNPGA production by the perfused liver by a factor of 1.7, and biliary excretion of PNPGA by a factor of 1.5. The latter increase was attributed to the increased rate of synthesis of the glucuronide rather than to an increase in the biliary transport maximum, since the 3MC treatment produced no significant effect on the biliary excretion of performed PNPGA added to the perfusate. The 3MC pretreatment increased 1.5-fold the rate of sulfation of PNP, as judged by the increase in R2.

Animals↗

PubMedDate not supplied

Gastric excretion of intravenously administered meperidine in surgical patients.

We have demonstrated sequestration of unchanged meperidine in gastric juice of humans following intravenous administration. Concentrations attained were as great as 360 times plasma concentration. The drug was first detected between 5 and 15 minutes after administration. This phenomenon appears to be due to ionization and ion trapping of meperidine in gastric juice.

Adult↗

PubMedDate not supplied

Renal N-oxidation of meperidine by the perfused kidney of the rat.

Isolated perfused kidneys of rats were used to determined renal metabolism of meperidine and its relation to meperidine excretion. Starting perfusate concentrations of meperidine were 18.4 and 190 micrograms/ml, and resulted in respective nonsaturation and saturation kinetics for removal of meperidine. Disposition of 14C-meperidine was followed and supplemented with measurements of meperidine by gas chromatography. A major renal metabolite was shown to facilitate the renal excretion of meperidine. This metabolite was identified by gas chromatography/mass spectrometry as the N-oxide of meperidine.

Animals↗

PubMedDate not supplied

Renal N-oxidation of meperidine.

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Animals↗