Inhibition by ketamine and amphetamine analogs of the neurogenic nitrergic vasodilations in porcine basilar arteries.

The abuse of ketamine and amphetamine analogs is associated with incidence of hypertension and strokes involving activation of sympathetic activities. Large cerebral arteries at the base of the brain from several species receive dense sympathetic innervation which upon activation causes parasympathetic-nitrergic vasodilation with increased regional blood flow via axo-axonal interaction mechanism, serving as a protective mechanism to meet O2 demand in an acutely stressful situation. The present study was designed to examine effects of ketamine and amphetamine analogs on axo-axonal interaction-mediated neurogenic nitrergic vasodilation in porcine basilar arteries using techniques of blood-vessel myography, patch clamp and two-electrode voltage clamp, and calcium imaging. In U46619-contracted basilar arterial rings, nicotine (100µM) and electrical depolarization of nitrergic nerves by transmural nerve stimulation (TNS, 8Hz) elicited neurogenic nitrergic vasodilations. Ketamine and amphetamine analogs concentration-dependently inhibited nicotine-induced parasympathetic-nitrergic vasodilation without affecting that induced by TNS, nitroprusside or isoproterenol. Ketamine and amphetamine analogs also concentration-dependently blocked nicotine-induced inward currents in Xenopus oocytes expressing α3ß2-nicotinic acetylcholine receptors (nAChRs), and nicotine-induced inward currents as well as calcium influxes in rat superior cervical ganglion neurons. The potency in inhibiting both inward-currents and calcium influxes is ketamine>methamphetamine>hydroxyamphetamine. These results indicate that ketamine and amphetamine analogs, by blocking nAChRs located on cerebral perivascular sympathetic nerves, reduce nicotine-induced, axo-axonal interaction mechanism-mediated neurogenic dilation of the basilar arteries. Chronic abuse of these drugs, therefore, may interfere with normal sympathetic-parasympathetic interaction mechanism resulting in diminished neurogenic vasodilation and, possibly, normal blood flow in the brainstem.

Improvement of the Diagnostic Method for the Detection of Parasite Eggs Using the Formalin Ethyl Acetate Concentration Technique.

PURPOSE: The formalin-ethyl acetate (FEA) concentration method is commonly used in routine clinical practice to detect parasite eggs in feces. This procedure involves extraction of oil with the organic solvent ethyl acetate (EA), which reduces fecal sediment and provides a cleaner background for microscopic analysis. However, clinically, some sediment failed to float after EA treatment. METHODS: Hexane, commonly used in the food oil extraction from oilseeds did not float the feces. Gas chromatography-mass spectrometry (GC-MS) analysis showed that neither the amount of the oil nor the classes of the oil determined was differed whether hexane or EA was used to float the feces. Oil red, Bodipy and Calcofluor staining showed that the unabsorbed oil droplets in the fecal sediment were trapped within the leaf structure. HCl or acetic acid was added to see if the acid residue could dissolve the cellulose of the leaf to promote the bulk float. RESULTS: Our result showed that the fecal bulk contained the loosened mesophyll cell wall. The addition of acid residues improved fecal bulk float. The proximity of cellulose fiber to EA, but not hexane, may enhance the efficacy of oil extraction from cellulose. CONCLUSION: This is the first report that the interaction of cellulose with ethyl acetate in fecal solution has an effect on bulk float. This study improves the understanding of fecal bulk flotation and may assist in the visualization of parasite eggs in clinical practice with non-floating fecal samples in the FEA concentration method.