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PubMed2001

Determination of reduced, protein-unbound, and total concentrations of N-acetyl-L-cysteine and L-cysteine in rat plasma by postcolumn ligand substitution high-performance liquid chromatography.

A high-performance liquid chromatographic assay was developed for the quantitative determination of the sulfur-containing amino acids N-acetyl-L-cysteine (NAC) and L-cysteine (Cys) in rat plasma. The thiols were separated by reverse-phase ion-pair chromatography, and the column eluent was continuously mixed with an iodoplatinate-containing solution. The substitution of sulfur of the thiol compound with iodide was quantitatively determined by measuring changes in the absorption at 500 nm. The low-molecular-weight disulfides and mixed disulfide conjugates of thiols with proteins were entirely reduced to the original reduced compounds by dithiothreitol. By reducing these two types of disulfides separately during sample pretreatment, the reduced, protein-unbound, and total thiol concentrations could also be determined. Validation testing was performed, and no problems were encountered. The limit of detection was approximately 20 pmol of thiol on the column. The present method was used to measure the plasma concentrations of NAC and Cys in the rat after a bolus intravenous administration of NAC, focusing on disulfide formation. The binding of NAC to protein through mixed disulfide formation proceeds in a time-dependent and reversible manner. Moreover, this "stable" covalent binding might limit total drug elimination, while the unbound NAC is rapidly eliminated. Consequently, the analytical method described in this study is very useful for the determination of plasma NAC and Cys, including disulfide conjugates derived from them.

Acetylcysteine↗
PubMed1991

Atracurium decay and the formation of laudanosine in humans.

Several groups of investigators have reported that the plasma concentrations of laudanosine, a metabolite of atracurium, are high immediately after administration of atracurium and thereafter decline. Such a time profile of a metabolite in plasma is very unusual. The authors describe a model of atracurium decay and laudanosine disposition that satisfactorily explains these data. The model reveals the following: 1) each atracurium molecule is degraded into two of laudanosine; 2) the generation of laudanosine occurs through two processes--a rapid one, involving approximately 31% of the atracurium dose and proceeding with a half-life of 0.25 min, and a slower one, involving the residual 69% and proceeding with a half-life of 51 min; 3) atracurium degradation by Hofmann elimination proceeds in the central and the noncentral compartments; 4) laudanosine formed from atracurium gains access to its central compartment and disappears from plasma in a biexponential pattern; 5) in cirrhotic patients, only 18% of the atracurium dose is degraded rapidly and laudanosine is disposed of more slowly. The authors propose that the rapid degradation of atracurium in plasma proceeds through a nucleophilic substitution reaction, with plasma nucleophiles substituting for the laudanosine moiety in atracurium. Because both laudanosine moieties in atracurium are required to establish and sustain plasma concentrations of laudanosine, excretion of atracurium or its degradation through pathways not generating laudanosine must be small.

Atracurium↗
PubMed1988

Salivary concentrations of hexamethylene bisacetamide (HMBA) in patients receiving 5-day continuous infusions.

Salivary and plasma concentrations of hexamethylene bisacetamide (HMBA) were studied to determine (1) how the concentrations of HMBA achieved in saliva compared with those required to induce differentiation in vitro, and (2) whether saliva might substitute for plasma as a biologic fluid on which to base dosage adjustment. Plasma and expectorated saliva were collected concomitantly from 16 patients receiving 5-day continuous infusions of HMBA. The concentrations of HMBA in each fluid were determined by gas chromatography. The patients displayed a range of periodontal disease from gingivitis to complete edentia, but periodontal disease status did not appear to influence the salivary behavior of HMBA, which mirrored that of the drug in plasma, with concentrations of HMBA increasing in both fluids during the first 12-16 h of infusion. Between 24 and 120 h, HMBA concentrations in saliva and plasma remained constant. In some patients, salivary HMBA concentrations lagged behind those in plasma during the first 6-8 h of infusion, but after that the salivary HMBA concentrations approximated those in the plasma. Salivary concentrations of HMBA between 0.96 and 2.56 mM were associated with nontoxic plasma concentrations of HMBA. Therefore, in patients with restricted venous access, saliva might be a suitable substitute for plasma if adaptive control-dosing schemes for HMBA are employed. Moreover, the concentrations of HMBA in saliva bathing the oral cavity are quantitatively comparable to those required for induction of cell differentiation in vitro.

Acetamides↗