scholarly journals Electroacupuncture at ST36 Relieves Visceral Hypersensitivity via the NGF/TrkA/TRPV1 Peripheral Afferent Pathway in a Rodent Model of Post-Inflammation Rectal Hypersensitivity [Erratum]

2021 ◽  
Vol Volume 14 ◽  
pp. 393-394
Author(s):  
Yan Chen ◽  
Jiafei Cheng ◽  
Yiling Zhang ◽  
Jiande DZ Chen ◽  
Florin M Selaru
Keyword(s):  
Rodent Model ◽  
Visceral Hypersensitivity ◽  
Afferent Pathway ◽  
Rectal Hypersensitivity

Desvenlafaxine succinate ameliorates visceral hypersensitivity but delays solid gastric emptying in rats

2013 ◽  
Vol 305 (4) ◽  
pp. G333-G339 ◽  
Author(s):  
Fei Dai ◽  
Yong Lei ◽  
Shiying Li ◽  
Gengqing Song ◽  
Jiande D. Z. Chen
Keyword(s):  
Acetic Acid ◽  
Gastric Emptying ◽  
Rodent Model ◽  
Visceral Hypersensitivity ◽  
Enzyme Linked Immunosorbent Assay ◽  
Visceral Sensitivity ◽  
Gastric Distention ◽  
Way 100635 ◽  
Norepinephrine Reuptake Inhibitor ◽  
Norepinephrine Reuptake

Desvenlafaxine succinate (DVS) is a novel serotonin and norepinephrine reuptake inhibitor. The aim of this study was to investigate the effects of DVS on visceral hypersensitivity and solid gastric emptying in a rodent model of gastric hyperalgesia. Twenty-eight gastric hyperalgesia rats and 20 control rats were used. Visceral sensitivity during gastric distention (GD) was assessed by recording of electromyogram (EMG) at pressures of 20, 40, 60, and 80 mmHg. DVS with doses of 1, 10, and 30 mg/kg were administrated by gavage, 5-HT1A antagonist (WAY-100635, 0.3 mg/kg) was given subcutaneously, and 5-HT2A antagonist (ketanserin, 1 mg/kg) was given intraperitoneally. The level of norepinephrine in plasma was measured by enzyme-linked immunosorbent assay. We found that 1) visceral hypersensitivity induced by acetic acid was validated. 2) DVS dose-dependently reduced visceral hypersensitivity in the gastric hypersensitivity rats. The EMG (% of baseline value without GD) during GD at 60 and 80 mmHg with DVS at a dose of 30 mg/kg were 119.4 ± 2.3% (vs. saline 150.9 ± 2.7%, P < 0.001) and 128.2 ± 3.2% (vs. saline 171.1 ± 2.4%, P < 0.001). Similar findings were observed at a dose of 10 mg/kg. DVS at a dose of 1 mg/kg reduced visceral hypersensitivity only during GD at 60 mmHg. 3) Neither WAY-100635 nor ketanserin blocked the effect of DVS on visceral sensitivity. 4) DVS at 30 mg/kg significantly increased plasma NE level ( P = 0.012 vs. saline). 5) DVS at 30 mg/kg significantly delayed solid gastric emptying ( P < 0.05 vs. saline). We conclude that DVS reduces visceral sensitivity in a rodent model of visceral hypersensitivity and delays solid gastric emptying. Caution should be made when DVS is used for treating patients.

scholarly journals Central neural mechanisms mediating human visceral hypersensitivity

2001 ◽  
Vol 281 (5) ◽  
pp. G1196-G1202 ◽  
Author(s):  
Sanchoy Sarkar ◽  
Anthony R. Hobson ◽  
Paul L. Furlong ◽  
Clifford J. Woolf ◽  
David G. Thompson ◽  
...  
Keyword(s):  
Central Sensitization ◽  
Pain Threshold ◽  
Visceral Pain ◽  
Functional Gastrointestinal Disorders ◽  
Neural Mechanisms ◽  
Visceral Hypersensitivity ◽  
Afferent Pathway ◽  
Healthy Human ◽  
Pain Pathway ◽  
Stimulation Of

Although visceral hypersensitivity is thought to be important in generating symptoms in functional gastrointestinal disorders, the neural mechanisms involved are poorly understood. We recently showed that central sensitization (hyperexcitability of spinal cord sensory neurones) may play an important role. In this study, we demonstrate that after a 30-min infusion of 0.15 M HCl acid into the healthy human distal esophagus, we see a reduction in the pain threshold to electrical stimulation of the non-acid-exposed proximal esophagus (9.6 ± 2.4 mA) and a concurrent reduction in the latency of the N1 and P2 components of the esophageal evoked potentials (EEP) from this region (10.4 ± 2.3 and 15.8 ± 5.3 ms, respectively). This reduced EEP latency indicates a central increase in afferent pathway velocity and therefore suggests that hyperexcitability within the central visceral pain pathway contributes to the hypersensitivity within the proximal, non-acid-exposed esophagus (secondary hyperalgesia/allodynia). These findings provide the first electrophysiological evidence that central sensitization contributes to human visceral hypersensitivity.

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