pituitrin and Gastroparesis

pituitrin has been researched along with Gastroparesis* in 3 studies

Reviews

1 review(s) available for pituitrin and Gastroparesis

ArticleYear
[Pathomechanisms of functional gastroparesis].
    Folia medica Cracoviensia, 2006, Volume: 47, Issue:1-4

    Functional diseases of the stomach include visceral hypersensitivity, gastric dysrhythmias, dysfunction of gastric fundus and acommodation, functional diseases of antrum and gastroparesis. A common symptom of this diseases is dyspepsia. A background of dyspepsia state functional and organic abnormalities of upper gastrointestinal tract. The most serious abnormality is gastroparesis. In this review we provide an overview of functional gastroparesis focusing on postoperative and hormonal related gastric dysfunction.

    Topics: Animals; Dopamine; Dyspepsia; Gastric Emptying; Gastroesophageal Reflux; Gastrointestinal Motility; Gastroparesis; Glucagon; Humans; Postoperative Complications; Stomach; Vasopressins

2006

Other Studies

2 other study(ies) available for pituitrin and Gastroparesis

ArticleYear
Gastroparesis is associated with oxytocin deficiency, oesophageal dysmotility with hyperCCKemia, and autonomic neuropathy with hypergastrinemia.
    BMC gastroenterology, 2009, Feb-25, Volume: 9

    Gastrointestinal (GI) dysmotility and autonomic neuropathy are common problems among diabetics with largely unknown aetiology. Many peptides are involved in the autonomic nervous system regulating the GI tract. The aim of this study was to examine if concentrations of oxytocin, cholecystokinin (CCK), gastrin and vasopressin in plasma differ between diabetics with normal function and dysfunction in GI motility.. Nineteen patients with symptoms from the GI tract who had been examined with gastric emptying scintigraphy, oesophageal manometry, and deep-breathing test were included. They further received a fat-rich meal, after which blood samples were collected and plasma frozen until analysed for hormonal concentrations.. There was an increase in postprandial oxytocin plasma concentration in the group with normal gastric emptying (p = 0.015) whereas subjects with delayed gastric emptying had no increased oxytocin secretion (p = 0.114). Both CCK and gastrin levels increased after the meal, with no differences between subjects with normal respective delayed gastric emptying. The concentration of vasopressin did not increase after the meal. In patients with oesophageal dysmotility the basal level of CCK tended to be higher (p = 0.051) and those with autonomic neuropathy had a higher area under the curve (AUC) of gastrin compared to normal subjects (p = 0.007).. Reduced postprandial secretion of oxytocin was found in patients with delayed gastric emptying, CCK secretion was increased in patients with oesophageal dysmotility, and gastrin secretion was increased in patients with autonomic neuropathy. The findings suggest that disturbed peptide secretion may be part of the pathophysiology of digestive complications in diabetics.

    Topics: Autonomic Nervous System Diseases; Case-Control Studies; Cholecystokinin; Diabetic Neuropathies; Esophageal Motility Disorders; Female; Gastric Emptying; Gastrins; Gastroparesis; Humans; Male; Oxytocin; Vasopressins

2009
Gastric stimulation is effective in reversing vasopressin induced gastroparesis.
    Folia medica Cracoviensia, 2004, Volume: 45, Issue:1-2

    The aim of this study was to determine the most effective current parameters reversing vasopressin (VP) induced gastroparesis by gastric electrical stimulation IGES).. Twenty male healthy Wistar rats were included into the study (weight 227 +/- 24 g). Animals were subjected to gastric fistula placement and implantation of two monopolar electrodes for EGG-studies and GES. After 5 days of recovery VP was applied (terlipressin 0.1 mg/kg i.p.) The gastric motility was measured by means of balloon introduced into the stomach through the fistula. The gastric electrical and motor activity were recorded by the PowerLab/8SP system and software. Electrical signals were cleared by 3000 AC/DC differential amplifier A-M System Inc. Gastric electrical stimulation (GES) was generated by Zimmer stimulator SINUS5. The following currents: S01 (monopolar): ampl 2.2 mA, freq 29 Hz, on/off 1 s / 10 s; S02 (bipolar): ampl 2.2 mA, freq 29 Hz, on/off 1s/10s: S03 (monopolar): ampl 2.2 mA, freq 0.5 Hz: S04 (monopolar): ampl 2.2 mA, freq 34 Hz, on/off 5.5 s/15 s were used.. The phasic contractions almost disappeared and amplitude decreased from 12 +/- 5 to 2.9 +/- 1.5 cm H20. The motility index decreased from 276,3 +/- 76.4 to 154.6 +/- 63 cm H2O x s/min. GES S01-S04 increased motility index to: 167.6 +/- 60.8: 155.1 +/- 89.3; 170.3 +/- 92.3: 301.9 +/- 70.5 cm H2O x s/min respectively. The frequency of gastric slow wave increased from 0.04 +/- 0.02 to 0.07 +/- 0.02 Hz after VP administration. GES S01-S04 reversed VP induced increase of slow wave frequency to 0.06 +/- 0.02, 0.055 +/- 0.02, 0.06 +/- 0.01 and 0.04 +/- 0.02 Hz, respectively.. This effectiveness of local GES and the pressure pattern of induced gastroparesis suggest peripheral complex inhibitory-excitatory action of vasopressin on gastric smooth muscles. The mechanism of this action may involve the enteric nervous system, gastric and vasal smooth muscles. The most effective in reversing VP induced functional gastroparesis is high frequency current applied in timing of the natural slow wave.

    Topics: Animals; Electric Stimulation Therapy; Electrophysiology; Gastrointestinal Motility; Gastroparesis; Male; Rats; Rats, Wistar; Vasopressins

2004