Letter: Amount of neostigmine needed to antagonize a gallamine-induced neuromuscular block.
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Biomedical subjects
Publications and source records attributed to R D Miller.
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The interaction between pancuronium, d-tubocurarine, polymyxin B, and neostigmine was studied in the rat diaphragm-phrenic nerve preparation. Polymyxin B (5 mug/ml) did not affect twitch tension alone but decreased the pancuronium ED50 from 0.8 mug/ml to 0.32 mug/ml and the d-tubocurarine ED50 from 0.25 mug/ml to 0.15 mug/ml. Neostigmine (0.2 to 10 mug/ml) antagonized pancuronium or d-tubocurarine-induced depression of twitch tension. In contrast, neostigmine (0.001 to 0.2 mug/ml) augmented polymyxin B depression. Similarly, neostigmine (0.1 mug/ml) augmented combined polymyxin B-pancuronium or polymyxin B-d-tubocurarine depression of twitch tension. The authors conclude that polymyxin B potentiates the neuromuscular blockade from pancuronium or d-tubocurarine and that neostigmine further augments this block.
Seven anesthetized patients were studied to determine the interaction between pancuronium and lincomycin and the ability of neostigmine and 4-aminopyridine to antagonize the block. Lincomycin 600 mg given IV alone did not decrease twitch tension. An 8 to 10% decrease in twitch tension occurred when lincomycin was given after neostigmine antagonism of pancuronium. Lincomycin augmented a partial pancuronium neuromuscular blockade. The combined lincomycin-pancuronium neuromuscular blockade was effectively antagonized by both neostigmine and 4-aminopyridine although the latter produced a slower rate of antagonism. The authros conclude that lincomycin, 600 mg IV, augments a pancuronium neurovascular blockade. 4-Aminopyridine offers no advantage over neostigmine and, in fact, may offer a disadvantage because of a slower rate of antagonism.
Antagonism by neostigmine of neuromuscular blockade produced by pancuronium or its metabolites was studied in the cat anterior or tibialis muscle-peroneal nerve preparation using constant infusions of muscle relaxants. The ED50 of neostigmine (dose which caused a 50% antagonism) was 16, 11, 29, and 26 micrograms/kg for pancuronium, 3-hydroxypancuronium, 17-hydroxypancuronium, and 3, 17-hydroxypancuronium, respectively. Times of onset of neostigmine action were shorter when antagonizing 17-hydroxypancuronium neuromuscular blockade. Duration of neostigmine action when antagonizing 17- or 3, 17-hydroxypancuronium blockade was shorter than with pancuronium or 3-hydroxypancuronium. We conclude that more neostigmine is required to antagonize 17- or 3,17-hydroxypancuronium neuromuscular blockade than is required to antagonize pancuronium. Conversely, less neostigmine was required to antagonize 3-hydroxypancuronium blockade.
Acute and chronic levodopa (L-dopa) administration alters halothane minimum alveolar concentration (MAC) in dogs. L-dopa 5, 10, and 25 mg./kg. intravenously (I.V.) reduced halothane MAC 15, 20, and 25 percent, respectively, 1 hour after injection, with return toward normal after 3 hours. Fifty mg./kg. increased halothane MAC 40 percent at 1 hour, but produced at 30 percent decrease from control MAC at 3 hours. Two groups of 4 dogs each given oral L-dopa in doses increasing from 50 mg./kg. daily the 1st week to 300 mg./kg. daily the 5th week, decreased MAC an insignificant 9.5 plus or minus 25.2 percent at 4 hours after the last dose and increased MAC 3.5 plus or minus 7.3 percent at 12 hours after the last dose. A small, insignificant decrease of 9 percent in MAC was measured in 4 dogs given I.V. L-dopa 25 mg./kg. q.i.d for 4 days.
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The inaccuracies of the casting and fitting processes associated with semiprecision intracoronal attachment systems may compromise the fit of the completed prosthesis. The objective of using metal prefabricated intracoronal semiprecision attachments is to improve the adaptation between the matching attachment surfaces used in the fabrication of removable partial dentures. In milled dovetail or waxed dowel rests, the attachment of one side is completed and the other is cast to match. The prefabricated attachment system presented uses a matching component cast directly against the precast metal rest-mandrel. This reduces the inaccuracies resulting from waxing, investing, and casting.
This paper summarizes the results of studies of the metabolic fate of laudanosine, a major degradation product of atracurium. Intravenous bolus doses of laudanosine (1-3 mg/kg) were administered to eight dogs and two rabbits anesthetized with halothane, and urine and bile samples were collected for up to 6 hr. Urine samples also were collected from two surgical patients given repetitive doses of atracurium. Metabolites were isolated from all samples using C18-Sep Paks. Treatment of the isolates with beta-glucuronidase followed by purification of the hydrolysate by preparative liquid chromatography provided metabolite fractions which were characterized by analytical liquid chromatography and capillary gas chromatography combined with nitrogen-phosphorus and/or electron ionization-mass spectrometric detection. Reference compounds were employed as chromatographic retention time markers. O-Trimethylsilyl, O-tert-butyldimethylsilyl, and N-trifluoroacetyl derivatives of the metabolites and reference compounds were used for gas chromatographic and mass spectrometric analysis. In all three species, the following metabolites of laudanosine were identified: pseudocodamine (4'-desmethyllaudanosine), pseudolaudanine (6-desmethyllaudanosine), laudanine (3'-desmethyllaudanosine), codamine (7-desmethyllaudanosine), N-norlaudanosine, N-norpseudocodamine, and N-norpseudolaudanine.
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