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Title: Afferent and efferent activity of vagal nerve in vasopressin induced gastroparesis : the role of prostaglandin and nitic oxide
Abstract:
Gastroparesis is the severe neuromuscular dysfunction and is defined as delayed gastric emptying of solids in the absence of mechanical obstruction. Patients with this disorder may present dyspepsia symptoms as early satiety, upper abdominal discomfort, bloating, or nausea with or without vomiting. It can frequently result from longstanding diabetes mellitus and vagal nerve injury or can be idiopathic in it’s nature. Gastroparesis may be due to processes that affect the gastric enteric neurons, smooth muscle, or interstitial cells of Cajal. Frequently, gastric dysrhythmias occur in patients with gastroparesis and seems to be an underlying mechanism of decreased gastric emptying. Commonly, the causes of these gastric neuromuscular disorders are unknown. Among substances known to induce significant inhibition of the gastric motility are hormones: glucagon and vasopressin. Recent investigations proved the crucial role of vasopressin in motion sickness seizures. High vasopressin serum level correlates with during motion sickness and vasopressin has been reported as a mediator of tachygastria. The aim of this study was to evaluate mechanism of vasopressin induced gastroparesis. Gastric motility was measured by mean of balloon introduced to stomach via previously implanted stainless-steel fistula groups of rats: control group, pre-treated with L-NNA, indometacine, sympathectomized an ; d vagotomized rats. Pharmacologic sympathectomy was performed with 6-hydroxydopamine and subdiaphragmatic vagotomy was performed during gastric fistula implantation. In control group after vasopressin induced gastroparesis, carbachol was administered and recording continued. All surgical procedures were performed in surgical anaesthesia. Gastric slow wave frequency was recorded via previously implanted on gastric antrum silver electrodes and tunnelled on the neck of the rat. Cuff electrode was placed on isolated afferent and efferent cut end of the cervical left vagus nerve and vagal afferent and efferent recordings were performed in anaesthetised fasted control, pretreated with L-NNA and indometacine and after vasopressin analogue (AVP) administration in every group of rats. Results: AVP administration caused transient increase of basal tonic contraction of the stomach and suppressed occurrence of phasic contractions. Sympathectomy, vagotomy, indometacin and nifedipine did not prevented occurrence of transient AVP-induced gastroparesis. Administration of cholinomimetic- carbachol reversed AVP-induced gastroparesis. Vagal afferent and efferent activity did not changed significantly under influence of AVP among group of rats pretreated with L-NNA and indometacine. In summary mechanism of vasopressin induced gastroparesis is not dependent on nitric oxide and prostaglandins and is ; peripheral. Also this mechanism seems not to be related to the ischemic effect of given AVP. Reversing it with carbachol indicate cholinergic mechanism located in enteric nervous system of the stomach.
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Last modified:
Jul 7, 2022
In our library since:
Nov 21, 2012
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http://dl.cm-uj.krakow.pl:8080/publication/1373
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| Edition name | Date |
|---|---|
| ZB-99722 | Jul 7, 2022 |
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