There are a variety of causes but the major ones are medication, especially tricyclic antidepressants and sympathomimetic drugs, head and neck irradiation, and auto-immune inflammatory diseases such as Sjogren’s syndrome, which targets exocrine glands in general[13]

There are a variety of causes but the major ones are medication, especially tricyclic antidepressants and sympathomimetic drugs, head and neck irradiation, and auto-immune inflammatory diseases such as Sjogren’s syndrome, which targets exocrine glands in general[13]. Hyposalivation is not usually possible to distinguish from xerostomia because the etiology of hyposalivation is not very different from that of xerostomia. The saliva weight at 0-30 min was significantly (p 0.01) increased after administration of pilocarpine, compared to control rats. An additional administration of mosapride and rebamipide increased the saliva weight at 0-30 min. The total volume of saliva for 150 min after administration of pilocarpine was the highest after preadministration of rebamipide, followed by mosapride, and risperidone. Conclusions: Increase in salivation produced by i.p. pilocarpine was enhanced by preadministration of rebamipide and mosapride. strong class=”kwd-title” Keywords: pilocalpine- induced salivation, mosapride, rebamipide Introduction Since exposure of the distal esophagus to acid is usually implicated in elicitation of both symptoms and mucosal damage, the importance of esophageal clearance is generally recognized[1,2]. During esophageal acid clearance, salivation plays an important role in defending the esophageal mucosa[3,4]. It is considered that systemically administered pilocarpine induces the salivary secretion. Additionally, it has been reported that intracerebroventricular injection of pilocarpine also induces salivary secretion in anesthetized rats[5,6]. Takakura et al[7] also exhibited that this pretreatment with intracerebroventricular injection of atropine inhibited the salivation induced by intraperitoneally administrated pilocarpine, suggesting that this salivary secretion elicited by systemically administered pilocarpine is usually mediated through the central nervous system as well as through the salivary glands. Many studies suggest that proton pump inhibitors (PPIs) are the most effective medical therapy to control gastro-esophageal reflux disease (GERD) symptoms and heal esophagitis[8,9]. PPIs are the major acid-suppressing drugs used Itga2b for the treatment of GERD and have better characteristics for the long-term treatment of GERD, because they have a long-lasting, strong effect of raising intragastric pH and have no tachyphylaxis/tolerance phenomena on repeated dosing. However, PPI failure has become more prevalent with the increasing use of PPI as the first-line agent in the treatment of GERD[10]. On the other hand, laryngopharyngeal reflux (LPR) is ENOblock (AP-III-a4) usually a major cause of laryngeal inflammation and presents with a constellation of symptoms different from classic gastroesophageal reflux disease. Although LPR is frequently treated with empiric PPIs, most patients require more aggressive and prolonged treatment to achieve regression of symptoms[11]. Mosapride, which has been known to have both a 5-HT4 receptor agonistic and a 5-HT3 antagonist action and to be an agent used in chronic, long-term therapy of GERD was regarded as mediating its efficacy through prokinetic properties. Rebamipide is also widely used as an anti-gastritis and anti-ulcer agent in GERD patients with chronic gastritis. However, these other effects of the study drugs would make these brokers even more attractive in the ENOblock (AP-III-a4) treatment of patients ENOblock (AP-III-a4) with GERD. Therefore, in the present study, we investigated the effects of rebamipide, mosapride, and risperidone around the salivation induced by pilocarpine. Material & Methods The experiments were conducted on 4-week male SD rats (120-150g). They were maintained under standard animal-housing conditions and had access to water and laboratory pellets except during the experimental ENOblock (AP-III-a4) period. After a 24-h fast, under urethane anesthesia, a tracheal catheter was inserted after incising the trachea to secure the airway. Laboratory diet pellets were removed one hour before the measurement of salivary secretion. The salivation was induced by intraperitoneally administrated pilocarpine (0.5 mg/kg of body weight), and saliva was collected using preweighted small cotton balls inserted into the animal’s mouth every 30 min for 180 min. On the day of the experiments, rats were sedated with urethane (1mg/g) intrapertoneally, and kept in lateral decubitus. The cotton ball, 0.5 cm in diameter, was prepared and weighed in an analytic electronic scale. The first cotton ball was inserted under the rat’s tongue. The salivary excretion is determined through the difference in weight of the cotton ball before and after collection. The procedure of saliva collection with the cotton ball was done at 30-min intervals after pilocarpine was administered intraperitoneally. Thirteen minutes before intraperitoneal administration of pilocarpine, rebamipide (10mg/kg),.