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Introduction Diseases in the central nervous system such as cerebral infarction and Parkinsonism are often associated with disorders of the micturition reflex. Recently, much attention has been given to controlling [...], We investigated the effects of the centrally acting antitussives dextromethorphan and cloperastine on urinary bladder dysfunction 24 h after cerebral infarction in rats using the cystometry technique. First, cystometrography was performed in conscious male Sprague-Dawley rats. Cerebral infarction was then induced by occlusion of the left middle cerebral artery. Twenty-four hours after cerebral infarction, the effect of each drug on micturition disorder was estimated for 5 parameters: bladder capacity, maximum voiding pressure, micturition latency, flow rate, and urethral resistance. Cerebral infarction markedly reduced bladder capacity, micturition latency, and flow rate and increased urethral resistance. After cerebral infarction, intravenous dosing of saline had no effect on these parameters. Dextromethorphan (20 mg/kg) and cloperastine (2.5 and 5.0 mg/kg) at antitussive effective doses significantly increased bladder capacity and micturition latency. Unlike dextromethorphan, cloperastine ameliorated decreases in flow rate and increases in urethral resistance caused by cerebral infarction. These results suggest that cloperastine may have therapeutic value for the treatment of disorders of the micturition reflex associated with cerebral infarction, and that the drug may become a base compound from which to develop more active drugs for such disorders. Key words: disorders of micturition reflex, cerebral infarction, cystometry, cloperastine, dextromethorphan, conscious, rat. Nous avons examine; par la technique de cystomeetrie les effets des antitussifs d'action centrale, dextromethorphane et cloperastine, sur la dysfonction du canal urinaire 24 h apres un infarctus cerebral chez des rats. Nous avons d'abord effectuee une cystometrographie chez des rats Sprague-Dawley males conscients, puis nous avons induit un infarctus cerebral par l'occlusion de l'artere cerebrale moyenne gauche. Vingt-quatre heures apres l'induction de l'infarctus, nous avons e value l'effet de chaque medicament sur le trouble mictionnel, en considerant les 5 parametres suivants : capacite vesicale, pression de miction, latence mictionnelle, debit et resistance uretrale. L'infarctus cerebral a significativement reduit la capacite vesicale, la latence mictionnelle et le debit, et augmente la resistance uretrale. Apres l'infarctus cerebral, l'administration d'une solution saline par voie intraveineuse n'a pas eu d'effet sur ces parametres. Le dextromethorphane (20 mg/kg) et la cloperastine (2,5 et 5,0 mg/kg), aux doses antitussives efficaces, ont augmente considerablement la capacite vesicale et la latence mictionnelle. Contrairement au dextromethorphane, la cloperastine a attenue les diminutions du debit et les augmentations de la resistance uretrale causees par l'infarctus. Ces resultats donnent a penser que la cloperastine pourrait avoir une valeur theerapeutique en ce qui concerne le traitement des troubles du reflexe mictionnel associesa l'infarctus cerebral et qu'elle pourrait devenir un compose; de base pour la mise au point de medicaments de plus grande efficacite;. Mots-cles: troubles du reflexe mictionnel, infarctus cerebral, cystometrie, clopeerastine, dextromethorphane, conscient, rat. [Traduit par la Redaction]

Asthma is a pulmonary inflammation characterized by the excessive production of airway mucus. So far, the treatment of asthma has been limited to glucocorticoids. Herein, human pulmonary mucoepidermoid carcinoma cells were examined after dexamethasone treatment. The cells showed an increase in mRNA levels of two human mucin genes, MUC-2 and MUC-5AC. They also produced low levels of high-molecular-weight glycoconjugates. These results indicate that dexamethasone may be an effective approach for managing inflammation in asthma.

Protein kinase C plays a role in the release of high-molecular weight glycoconjugates (HMWG) in hamster tracheal epithelial cells in culture. 1-oleoyl-2-acetyl-sn-glycerol and 4 beta-phorbol 12-alpha myristate 13-acetate (PMA), two protein kinase C stimulators activate HMWG secretion. PMA incites protein kinase C transport to membrane from cytosol.