scholarly journals Parkinson's Disease Medication Alters Small Intestinal Motility and Microbiota Composition in Healthy Rats

2021 ◽  
Author(s):  
Sebastiaan van Kessel ◽  
Amber Bullock ◽  
Gertjan vanDijk ◽  
Sahar El Aidy
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Intestinal Motility ◽  
Microbiota Composition ◽  
Small Intestinal Motility ◽  
Small Intestinal

scholarly journals Parkinson' disease medication alters rat small intestinal motility and microbiota composition

2021 ◽  
Author(s):  
Sebastiaan P van Kessel ◽  
Amber Bullock ◽  
Gertjan van Dijk ◽  
Sahar El Aidy
Keyword(s):  
Intestinal Motility ◽  
Bacterial Overgrowth ◽  
Small Intestinal Bacterial Overgrowth ◽  
Gastrointestinal Function ◽  
Microbiota Composition ◽  
Distal Small Intestine ◽  
Intestinal Bacterial Overgrowth ◽  
Small Intestinal Motility ◽  
Per Se ◽  
Small Intestinal

Parkinson's disease (PD) is known to be associated with altered gastrointestinal function and microbiota composition. Altered gastrointestinal function is key in the development of small intestinal bacterial overgrowth, which is a comorbidity often observed in PD patients. Although PD medication could be an important confounder in the reported alterations, its effect per se on the microbiota composition or the gastrointestinal function at the site of drug absorption has not been studied. To this end, healthy (i.e., not PD model) wild-type Groningen rats were employed and treated with dopamine, pramipexole (in combination with levodopa/carbidopa), or ropinirole (in combination with levodopa/carbidopa) for 14 sequential days. Rats treated with dopamine agonists showed a significant reduction in the small intestinal motility and an increase in bacterial overgrowth in the distal small intestine. Importantly, significant alterations in microbial taxa were observed between the treated and vehicle groups, analogous to the changes previously reported in human PD vs HC microbiota studies. These microbial changes included an increase in Lactobacillus and Bifidobacterium, and decrease in Lachnospiraceae and Prevotellaceae. Importantly, certain Lactobacillus species correlated negatively with the plasma levels of levodopa. Overall, the results highlight the significant effect of PD medication per se on the gut microbiota, and the disease-associated comorbidities, including gastrointestinal dysfunction and small intestinal bacterial overgrowth.

scholarly journals Oral Factors That Impact the Oral Microbiota in Parkinson’s Disease

2021 ◽  
Vol 9 (8) ◽  
pp. 1616
Author(s):  
Natalia S. Rozas ◽  
Gena D. Tribble ◽  
Cameron B. Jeter
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Oral Health ◽  
Soft Tissue ◽  
Oral Hygiene ◽  
Beta Diversity ◽  
Oral Microbiota ◽  
Healthy Controls ◽  
Microbiota Composition ◽  
Salivary Ph

Patients with Parkinson’s disease (PD) are at increased risk of aspiration pneumonia, their primary cause of death. Their oral microbiota differs from healthy controls, exacerbating this risk. Our goal was to explore if poor oral health, poor oral hygiene, and dysphagia status affect the oral microbiota composition of these patients. In this cross-sectional case-control study, the oral microbiota from hard and soft tissues of patients with PD (n = 30) and age-, gender-, and education-matched healthy controls (n = 30) was compared using 16S rRNA gene sequencing for bacterial identification. Study participants completed dietary, oral hygiene, drooling, and dysphagia questionnaires, and an oral health screening. Significant differences in soft tissue beta-diversity (p < 0.005) were found, and a higher abundance of opportunistic oral pathogens was detected in patients with PD. Factors that significantly influenced soft tissue beta-diversity and microbiota composition include dysphagia, drooling (both p < 0.05), and salivary pH (p < 0.005). Thus, patients with PD show significant differences in their oral microbiota compared to the controls, which may be due, in part, to dysphagia, drooling, and salivary pH. Understanding factors that alter their oral microbiota could lead to the development of diagnostic and treatment strategies that improve the quality of life and survivability of these patients.

Small intestinal motility in fasted and postprandial states: effect of transient vagosympathetic blockade

1987 ◽  
Vol 252 (3) ◽  
pp. G301-G308 ◽  
Author(s):  
S. A. Chung ◽  
N. E. Diamant
Keyword(s):  
Small Bowel ◽  
Intestinal Motility ◽  
Gastric Fundus ◽  
Phase Iii ◽  
Entire Small Bowel ◽  
Vagal Blockade ◽  
Small Intestinal Motility ◽  
Proximal Small Bowel ◽  
Small Intestinal ◽  
Gastric Contractions

We investigated vagal control of the migrating myoelectric complex (MMC) and postprandial pattern of the canine small intestine. Gastric and small intestinal motility were monitored in six conscious dogs. The vagosympathetic nerves, previously isolated in bilateral skin loops, were blocked by cooling. To feed, a meat-based liquid food was infused by tube into the gastric fundus. MMC phases I, II, III, and IV were observed in the fasted state. On feeding, the fed pattern appeared quickly in the proximal small bowel but was delayed distally. Vagal blockade abolished all gastric contractions and spiking activity as well as the small bowel fed pattern. During vagal blockade, the small bowel exhibited MMC-like migrating bursts of spikes in both the fasted and fed states. The migration and cycling of these bursts were not significantly different from the MMC, but the duodenal and jejunal phase II was absent or shortened. On termination of vagal blockade, normal fasting or fed activity reappeared but with a delay in the fed pattern distally. We conclude: the ileum is the least sensitive to vagal blockade; the fasting vagal influence is exerted primarily on phases I and II of the duodenal and jejunal MMC; the fed pattern throughout the entire small bowel is normally dependent upon vagal integrity; the phase III-like bursts of activity seen during vagal blockade likely represents the intrinsic small bowel MMC, which is vagally independent.

scholarly journals Evaluation of Small Intestinal Motility in a Rat Model of Irritable Bowel Syndrome

2021 ◽  
Author(s):  
Masamichi Sato ◽  
Takahiro Kudo ◽  
Nobuyasu Arai ◽  
Reiko Kyodo ◽  
Kenji Hosoi ◽  
...  
Keyword(s):  
Irritable Bowel Syndrome ◽  
Small Intestine ◽  
Real Time ◽  
Rat Model ◽  
Intestinal Motility ◽  
Restraint Stress ◽  
Rat Models ◽  
Small Intestinal Motility ◽  
Small Intestinal ◽  
Irritable Bowel

Abstract Background: The correlation between small intestinal motility alteration and irritable bowel syndrome (IBS) is not well evaluated. Aims: To assess the small intestinal and colonic transits in an IBS rat model with restraint stress and determine the role of small intestinal motility in the IBS pathophysiology.Methods: Restraint stress was utilized to make adolescent IBS rat models that were evaluated for clinical symptoms, including stool frequency and diarrhea. The small intestinal motility and transit rate were also evaluated. The amounts of mRNA encoding corticotropin-releasing hormone, mast cell, and serotonin (5-Hydroxytryptamine; 5-HT) receptor 3a were quantified using real-time polymerase chain reaction (PCR); the 5-HT expression was evaluated using immunostaining.Results: Restraint stress significantly increased the number of fecal pellet outputs, stool water content, and small intestinal motility in the IBS rat models. There was no difference in real-time PCR results, but immunostaining analysis revealed that 5-HT expression in the small intestine was significantly increased in the IBS rat models.Conclusions: In the adolescent rat model of IBS with restraint stress, we observed an increase in small intestinal and colonic motility. In the small intestine, enhanced 5-HT secretion in the distal portion may be involved in increasing the small intestinal motility.

scholarly journals Evidence that nitric oxide mechanisms regulate small intestinal motility in humans

Gut ◽  
1999 ◽  
Vol 44 (1) ◽  
pp. 72-76 ◽  
Author(s):  
A Russo ◽  
R Fraser ◽  
K Adachi ◽  
M Horowitz ◽  
G Boeckxstaens
Keyword(s):  
Motor Activity ◽  
Intestinal Motility ◽  
Random Order ◽  
Neural Mechanisms ◽  
Phase Iii ◽  
First Episode ◽  
Small Intestinal Motility ◽  
Small Intestinal ◽  
Synthase Inhibitor

BackgroundNon-cholinergic non-adrenergic neural mechanisms involving nerves containing NO have been shown to modulate smooth muscle in the gastrointestinal tract, and it has been suggested that release from tonic NO inhibition may be important in the regulation of cyclical fasting small intestinal motility.AimsTo evaluate the role of NO mechanisms in the regulation of fasting small intestinal motor activity in humans using a specific NO synthase inhibitor,NG-monomethyl-l-arginine ( l-NMMA).MethodsIn seven healthy male volunteers, duodenal and jejunal pressures were measured for four hours with a nine lumen manometric catheter. Volunteers attended on four separate days on which they received an intravenous infusion of either saline or l-NMMA (0.5, 2, or 4 mg/kg/h) in random order. Intravenous infusions began 10 minutes after completion of phase III of the migrating motor complex (MMC).ResultsThe first episode of phase III activity occurred earlier after infusion of 2 and 4 mg/kg/h l-NMMA than after infusion of 0.5 mg/kg/hl-NMMA or saline (mean (95% confidence interval) 52 (36–68) and 57 (18–97) v 116 (69–193) and 145 (64–226) minutes respectively) with a resultant MMC cycle length of 82 (59–105) and 86 (46–126) v 132 (49–198) and 169 (98–240) minutes respectively. The total number of phase III activities during the four hour recording was increased (p<0.05) by l-NMMA at a dose of 4 mg/kg/h (2 (1–3)) but not at 2 mg/kg/h (1.5 (1–2)) or 0.5 mg/kg/h (1.3 (1–2)) compared with saline (1.3 (0.6–2)). l-NMMA had no effect on the duration, velocity, number of contractions per minute, length of migration, or site of origin of phase III of the MMC. The duration of phase I activity was shorter (p<0.05) with 4 mg/kg/hl-NMMA than with saline (12 (1–23)v 31 (19–44) minutes).ConclusionsThese observations suggest that NO mechanisms play a role in the regulation of fasting small intestinal motor activity in humans.

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