Objective. To evaluate the accuracy of pharmacy students compounding skills. Methods. Potassium permanganate aqueous solution (KMnO 4 ) and citrated caffeine syrup were compounded by 2 first-year pharmacy classes in 2 consecutive years.Results. Approximately 54% of the students prepared the KMnO 4 solution within ±10% of the nominal concentration at the first attempt. The "not pass" formulation errors ranged from -75% to >200%. For the citrated caffeine syrup, 78% of the students prepared the medicine within ±10% of the nominal concentration in the first attempt. The "not pass" formulation errors ranged from -89% to 269%. For the citrated caffeine syrup preparation, there was no significant difference between using an electronic digital balance or a torsion balance (p>0.05) with respect to accuracy. Conclusion. The results from this study were comparable with those reported for pharmacists across the country, both in the number of formulations failing potency analysis and in the range of error observed. Objective assessment of pharmacy student compounding skills should be employed to determine competency.
Barbiturates are widely used as anesthetics, anticonvulsants, and neuroprotective agents. However, barbiturates may also inhibit mitochondrial respiration, and mitochondrial inhibitors are known to potentiate NMDA receptor-mediated neurotoxicity. Here we used rat cortical cultures to examine the effect of barbiturates on neuronal mitochondria and responses to NMDA receptor stimulation. The barbiturates tested, secobarbital, amobarbital, and thiamylal, each potentiated NMDA-induced neuron death at barbiturate concentrations relevant to clinical and experimental use (100-300 microm). By using rhodamine-123 under quenching conditions, barbiturates in this concentration range were shown to depolarize neuronal mitochondria and greatly amplify NMDA-induced mitochondrial depolarization. Barbiturate-induced mitochondrial depolarization was increased by the ATP synthase inhibitor oligomycin, indicating that barbiturates act by inhibiting electron transport sufficiently to cause ATP synthase reversal. Barbiturates similarly amplified the effects of NMDA on cytoplasmic free calcium concentrations. The cell-impermeant barbiturate N-glucoside amobarbital did not influence mitochondrial potential or potentiate NMDA neurotoxicity or calcium responses. However, all of the barbiturates attenuated NMDA-induced calcium elevations and cell death when present at millimolar concentrations. Whole-cell patch-clamp studies showed that these effects may be attributable to actions at the cell membrane, resulting in a block of NMDA-induced current flux at millimolar barbiturate concentrations. Together, these findings reconcile previous reports of opposing effects on barbiturates on NMDA neurotoxicity and show that barbiturate effects on neuronal mitochondria can be functionally significant. Effects of barbiturates on neuronal mitochondria should be considered in experimental and clinical application of these drugs.
The methods of gas chromatography/Fourier transform infrared spectroscopy (GC/FTIR) and gas chromatography/infrared spectroscopy/mass spectrometry (GC/IR/MS) are evaluated for their ability to differentiate side chain isomers of amphetamine. It is found that absorption bands from 3000 to 2850 cm-1 and 900 to 650 cm-1 are most useful for differentiating the alkyl amines, while the bands from 1600 to 900 cm-1 are only useful for differentiating primary amines from the other substituted amines. The combination of GC/IR/MS is superior for differentiating these side chain isomers.
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