The effectiveness of orally administered pseudoephedrine in patients with acute or chronic nonsuppurative rhinitis was evaluated under double-blind conditions. Intranasally administered ephedrine which was given to all patients at the end of this study served as the positive control. Marked nasal decongestant effects of a single oral dose of pseudoephedrine (60 mg tablet), as determined by a modified passive anterior, rhinometric technique occurred within 30 minutes and were maintained for at least four hours. The mean nasal decongestant response (delta % of baseline) of 57.2% was associated with a mean peak, plasma pseudoephedrine level of 274 ng/ml. In addition, the maximum response to oral pseudoephedrine treatment was equivalent to the response produced by ephedrine nasal spray. These results suggest that pseudoephedrine is an orally, effective nasal decongestant.
Our present findings suggest that the COM is related to the presence of SCD. The roof of the temporal bone may become thin by the failure of postnatal bone development and susceptible to chronic brain pulsation and pressure exerted by the temporal lobe in COM ears.
In vitro generation of free radicals by xanthine oxidase acting on hypoxanthine as a substrate induced a decreased calcium uptake velocity and reduced calcium-dependent ATPase activity of isolated sarcoplasmic reticulum (SR) vesicles from canine masseter muscle at pH 7.0. At pH 5.5 calcium uptake velocity was also reduced but ATPase activity was unaffected. Application of arachidonic acid or prostaglandin G2 induced the depression of both calcium uptake velocity and ATPase activity. The effect of arachidonic acid and prostaglandin G2 on ATPase activity depended on the pH. At pH 7.0, ATPase activity was decreased, but at pH 5.5 it was unchanged. These effects were reversed by superoxide dismutase (SOD) at pH 7.0, and by SOD plus mannitol at pH 5.5. Prostaglandin H2, prostaglandin E2 and 11,14,17-eicosatrienoic acid had no effect on calcium uptake velocity and ATPase activity at both pH 7.0 and pH 5.5. These results suggest that damage to the masseter muscle is caused by a free radical superoxide anion generated as a result of increased prostaglandins synthesis, and by the production of more lethal hydroxyl radical switched from the production of superoxide anion at low pH.
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