BACKGROUND: Gastrointestinal disorders are frequently reported in patients with Parkinson's disease whose disorders reduce the absorption of nutrients and drugs, worsening the clinical condition of patients. However, the mechanisms involved in modifying gastrointestinal pathophysiology have not yet been fully explained. AIM: To evaluate its effects on gastrointestinal motility and the involvement of the vagal and splanchnic pathways. METHODS: Male Wistar rats (250-300 g, n = 84) were used and divided into two groups. Group I (6-OHDA) received an intrastriatal injection of 6-hydroxydopamine (21 µg/animal). Group II (control) received a saline solution (NaCl, 0.9%) under the same conditions. The study of gastric emptying, intestinal transit, gastric compliance and operations (vagotomy and splanchnotomy) were performed 14 days after inducing neurodegeneration. Test meal (phenol red 5% glucose) was used to assess the rate of gastric emptying and intestinal transit. RESULTS: Parkinson's disease delayed gastric emptying and intestinal transit at all time periods studied; however, changes in gastric compliance were not observed. The delay in gastric emptying was reversed by pretreatment with vagotomy and splanchnotomy+celiac gangliectomy, thus suggesting the involvement of such pathways in the observed motor disorders. CONCLUSION: Parkinson's disease compromises gastric emptying, as well as intestinal transit, but does not alter gastric compliance. The delay in gastric emptying was reversed by truncal vagotomy, splanchnotomy and celiac ganglionectomy, suggesting the involvement of such pathways in delaying gastric emptying.
BACKGROUND:Gastrointestinal disorders are frequently reported in patients with Parkinson's disease whose disorders reduce the absorption of nutrients and drugs, worsening the clinical condition of patients. However, the mechanisms involved in modifying gastrointestinal pathophysiology have not yet been fully explained. AIM: To evaluate its effects on gastrointestinal motility and the involvement of the vagal and splanchnic pathways. METHODS: Male Wistar rats (250-300 g, n = 84) were used and divided into two groups. Group I (6-OHDA) received an intrastriatal injection of 6-hydroxydopamine (21 µg/animal). Group II (control) received a saline solution (NaCl, 0.9%) under the same conditions. The study of gastric emptying, intestinal transit, gastric compliance and operations (vagotomy and splanchnotomy) were performed 14 days after inducing neurodegeneration. Test meal (phenol red 5% glucose) was used to assess the rate of gastric emptying and intestinal transit. RESULTS:Parkinson's disease delayed gastric emptying and intestinal transit at all time periods studied; however, changes in gastric compliance were not observed. The delay in gastric emptying was reversed by pretreatment with vagotomy and splanchnotomy+celiac gangliectomy, thus suggesting the involvement of such pathways in the observed motor disorders. CONCLUSION:Parkinson's disease compromises gastric emptying, as well as intestinal transit, but does not alter gastric compliance. The delay in gastric emptying was reversed by truncal vagotomy, splanchnotomy and celiac ganglionectomy, suggesting the involvement of such pathways in delaying gastric emptying.
Authors: F Blandini; B Balestra; G Levandis; M Cervio; R Greco; C Tassorelli; M Colucci; M Faniglione; E Bazzini; G Nappi; P Clavenzani; S Vigneri; R De Giorgio; M Tonini Journal: Neurosci Lett Date: 2009-10-14 Impact factor: 3.046
Authors: F A Gondim; C L Rodrigues; J R da Graça; F D Camurça; H M de Alencar; A A dos Santos; F H Rola Journal: Auton Neurosci Date: 2001-02-20 Impact factor: 3.145
Authors: Dayane Pessoa de Araújo; Caren Nádia Soares De Sousa; Paulo Victor Pontes Araújo; Carlos Eduardo de Souza Menezes; Francisca Taciana Sousa Rodrigues; Sarah Souza Escudeiro; Nicole Brito Cortez Lima; Manoel Claúdio Azevedo Patrocínio; Lissiana Magna Vasconcelos Aguiar; Glauce Socorro de Barros Viana; Silvânia Maria Mendes Vasconcelos Journal: Evid Based Complement Alternat Med Date: 2013-08-19 Impact factor: 2.629