Search

Objective: The ATP sensitive potassium (K ATP ) channel plays an important role in the regulation of resting membrane potential and membrane excitability. The role of the K ATP channel in modulating gastric motility is unclear. The aim of this study was to investigate the role and mechanism of the K ATP channel in modulating gastric tone and accommodation in dogs., Materials and Methods: Gastric volume under a constant pressure reflecting gastric tone was measured using a barostat device in dogs equipped with a gastric cannula. Gastric accommodation was evaluated by the difference in gastric volume before and after a liquid meal. The roles of cholinergic and nitrergic pathways in the inhibitory effect of pinacidil (a K ATP opener) were assessed., Results: 1) Pinacidil dose-dependently decreased gastric tone at a dosage of 30 (p = 0.628), 100 (p = 0.013) and 300 μg kg -1 (p < 0.001). 2) Glibenclamide, a K ATP blocker, completely blocked the inhibitory effect of pinacidil on gastric tone. 3) Atropine did not block the inhibitory effect of pinacidil on gastric tone but N ω -Nitro-L-arginine methyl ester markedly attenuated the inhibitory effect of pinacidil (p = 0.004). 4) Glibenclamide significantly reduced gastric accommodation (p < 0.001) while pinacidil had no effects on gastric accommodation. 5) Glibenclamide significantly reduced nitric oxide donor sodium nitroprusside-induced gastric relaxation., Conclusions: These findings indicate that the K ATP channel plays an important role in modulating gastric tone and accommodation in dogs. The inhibitory effect of pinacidil on gastric tone was through the nitrergic pathway as well as acting directly on smooth muscle cells.

Introduction: The goals of this experiment were to study therapeutic potential of intestinal electrical stimulation (IES) for obesity, its mechanisms involving gastrointestinal motility and hormones, and role of pulse width in diet-induced obese rats., Methods: In a 4-week study, rats equipped with one pair of electrodes at the duodenum were assigned to receive either a sham or IES of varied pulse widths in a sequential way. Food intake was measured daily and body weight measured weekly. Blood samples were collected for the measurement of glucagon-like peptide-1 (GLP-1). Solid gastric emptying (GE) and small bowel transit (SIT) tests were performed at the end of the experiment., Results: The results of the study were as follows: (1) Daily food intake, not affected by IES of 0.3 ms, was pulse width-dependently reduced by 1.9 g with 1 ms and by 5.7 g with 3 ms. Accordingly, body weight was pulse width-dependently reduced by 2.4 g with 1 ms and by 12.8 g with 3 ms compared to a gain of 5.6 g in sham. (2) GLP-1 level was elevated by both 0.3 and 3 ms at 15 min, but was elevated only with 3 ms at 60 min. (3) GE was delayed to 52.3 % by IES of 3 ms but not 0.3 ms, compared to that at 64.4 % with sham IES. (4) Compared to the geometric center of 7.0 with sham IES, SIT was accelerated by 3 ms to 7.8 but not by 0.3 ms., Conclusion: IES pulse width-dependently reduces food intake and body weight, attributed to the delay of gastric emptying and the acceleration of small bowel transit, as well as the enhancement of GLP-1 secretion.

Introduction: Postoperative ileus (POI) is a heavy burden for healthcare industries and reduces the postoperative quality of life. The aim of this study was to investigate the effects and mechanisms of the intraoperative vagus nerve stimulation (iVNS) on gastrointestinal motility in a rodent model of POI.Methods: For control group (control, n = 8), electrodes were placed on the chest wall for recording the electrocardiogram and on the stomach and small intestine for measuring gastric slow waves (GSWs) and small intestinal slow waves (SSWs). For sham group (sham, n = 8) and iVNS group (VNS, n = 8), after the same surgery as the control, intestinal manipulation (IM) was performed to induce POI. iVNS was performed during the surgery for the iVNS group. Small intestinal transit (SIT), gastric emptying (GE), postoperative pain, and plasma TNF-α were evaluated after operation.Results: IM delayed GE that was normalized by iVNS (P < 0.05). iVNS reduced plasma TNF-α increased by IM (P = 0.04). iVNS prevents the injury of ileum mucosa induced by IM (P < 0.05). iVNS reduced the postoperative pain (P < 0.05). iVNS prevented the IM-induced decrease in vagal activity (sham 0-30 min vs. 150-180 min, P = 0.03, VNS 0-30 min vs. 150-180 min, P = 0.58) and increase in sympathovagal balance (sham 0-30 min vs. 150-180 min, P = 0.04, VNS 0-30 min vs. 150-180 min, P = 0.72).Conclusions: iVNS accelerates postoperative recovery by improving GE, reducing postoperative pain, and preventing the injury of ileum mucosa mediated via the autonomic mechanisms. [ABSTRACT FROM AUTHOR]

Introduction: The goals of this experiment were to study therapeutic potential of intestinal electrical stimulation (IES) for obesity, its mechanisms involving gastrointestinal motility and hormones, and role of pulse width in diet-induced obese rats. Methods: In a 4-week study, rats equipped with one pair of electrodes at the duodenum were assigned to receive either a sham or IES of varied pulse widths in a sequential way. Food intake was measured daily and body weight measured weekly. Blood samples were collected for the measurement of glucagon-like peptide-1 (GLP-1). Solid gastric emptying (GE) and small bowel transit (SIT) tests were performed at the end of the experiment. Results: The results of the study were as follows: (1) Daily food intake, not affected by IES of 0.3 ms, was pulse width-dependently reduced by 1.9 g with 1 ms and by 5.7 g with 3 ms. Accordingly, body weight was pulse width-dependently reduced by 2.4 g with 1 ms and by 12.8 g with 3 ms compared to a gain of 5.6 g in sham. (2) GLP-1 level was elevated by both 0.3 and 3 ms at 15 min, but was elevated only with 3 ms at 60 min. (3) GE was delayed to 52.3 % by IES of 3 ms but not 0.3 ms, compared to that at 64.4 % with sham IES. (4) Compared to the geometric center of 7.0 with sham IES, SIT was accelerated by 3 ms to 7.8 but not by 0.3 ms. Conclusion: IES pulse width-dependently reduces food intake and body weight, attributed to the delay of gastric emptying and the acceleration of small bowel transit, as well as the enhancement of GLP-1 secretion. [ABSTRACT FROM AUTHOR]

Background: Gastric electrical stimulation (GES) has been applied to treat gastric motility disorders for decades. This study was designed to investigate the effects and mechanisms of GES for visceral hypersensitivity in a rodent model of functional dyspepsia (FD). Methods: Male Sprague‐Dawley rat pups at 10‐days old received 0.1% iodoacetamide (IA) daily for 6 days. The experiments were performed when the rats reached 8‐11 weeks of age, and visceral hypersensitivity was established. Then, GES parameters were optimized and the chronic effects of GES on gastric hypersensitivity were assessed by electromyogram (EMG). Naloxone (3 mg/kg), D‐Phe‐Cys‐Tyr‐D‐Trp‐Orn‐Thr‐Pen‐Thr‐NH2 (CTOP, 1 mg/kg), and anti‐NGF (16 μg/kg) were individually intraperitoneally injected to investigate opioid and nerve growth factor (NGF) mechanisms. Tissues were analyzed for NGF expression. Key Results: In the IA‐treated rats, the visceromotor response to gastric distension was significantly increased, and both acute GES with optimized stimulation parameters (0.25 seconds on, 0.25 seconds off, 100 Hz, 0.25 ms, 6 mA) and chronic GES (7 days, 2 hours/day) normalized gastric hypersensitivity. The inhibitory effect of GES on gastric hypersensitivity was blocked by naloxone and CTOP. Anti‐NGF normalized EMG responses in IA‐treated rats. The expressions of NGF in the tissues of IA‐treated rats were dramatically increased, and these increases were suppressed with GES. Conclusions and Inferences: GES with optimized parameters improves gastric hypersensitivity induced by neonatal treatment of IA mediated peripherally by suppressing NGF and via the opioid mechanism involving the µ receptor. GES as a potential therapy for treating visceral pain may be explored in clinical studies. [ABSTRACT FROM AUTHOR]

Background: Chemotherapy‐associated dyspepsia syndrome (CADS) is among the most intensive side effects and critical concerns for patients with cancer. To investigate the effects and mechanisms of chronic electroacupuncture (EA) at ST36 on chemotherapy‐associated dyspeptic symptoms (CADS) in rats. Methods: Cisplatin (8 mg/kg, ip) was given once to establish CADS model. EA or sham‐EA treatment was then performed one hour daily for 21 days. Key Results: (a) EA treatment decreased kaolin intake within 24 hours (1.67 ± 0.23 g vs 2.36 ± 0.37 g in sham‐EA, P < 0.05); EA increased food intake (9.43 ± 2.28 vs 4.32 ± 1.26 in sham‐EA, P < 0.05) and cisplatin‐induced reduction of body weight (426.38 ± 13.25 vs 407.92 ± 13.26 in sham‐EA, P = 0.05). (b) The incidence of normal behavioral satiety sequence (53%) in EA group was greater than that in sham‐EA (32%) group (X2 = 17.68, P < 0.01). (c) EA increased the percentage of normal gastric slow waves (82.6 ± 5.98 vs 22.8 ± 1.90 in sham‐EA, P < 0.05). (d) EA normalized cisplatin delayed gastric emptying (71.3% ± 6.8% vs 44.6% ± 11.2% in control, P < 0.05). (e) EA decreased ratio of heart rate variability (0.30 ± 0.03 vs 0.56 ± 0.05 in sham‐EA, P < 0.05). (f) EA decreased fasting ghrelin, glucagon‐like peptide‐1 and peptide YY (P < 0.01 vs sham‐EA for all). Conclusions and Inferences: Chronic EA ameliorates dyspepsia symptom and improves gastric dysmotility induced by Cisplatin, mediated via the vagal and gastrointestinal hormonal mechanisms. Chronic EA improves acute CINV and dyspeptic symptoms, and gastric motility by enhancing vagal efferent activity and suppressing anorexigenic hormones of PYY and GLP‐1. Chronic electroacupuncture at ST36 is a promising method for treating CADS. [ABSTRACT FROM AUTHOR]