Terlipressin facilitates gastric and autonomic system dysfunctions in liver cirrhosis.

Background/aims: The aim of this study was to evaluate gastric myoelectric activity and autonomic activity in patients with esophageal varices treated by an analogue of vasopressin.
Methodology: Included in this study are 20 patients divided into two groups: Group A: 10 patients treated with terlipressin (the bleeding from oesophageal varices) and Group B: 10 healthy persons matched with age and gender. The studies were performed before and after intravenous administration of vasopressin (VP) analogue. In both groups the fasting plasma levels of vasopressin, adrenaline and noradrenaline were measured by immunochemistry.
Results: In group A disturbances of gastric myoelectric activity with high timing of dysrhythmic pattern were observed before VP. VP administration further increased the timing of gastric dysrhythmia from 35 ± 16 to 41 ± 13%, and decreased PDF from 1.4 ± 0.6cpm to 1.19 ± 0.6cpm, PDP from 1891 ± 851μV2 to 718 ± 678μV2. VP induced an increase in SDANN, lnLF, nLF (p<0.05) as well as a decrease in SDNN, pNN50, lnHF (p<0.05). Although there was no retching or vomiting, 80% of patients presented with nausea and exhibited a significant increase in plasma levels of VP, adrenaline and noradrenaline after administration of VP analogue.
Conclusions: VPinduced gastroparesis is characterized by suppressed slow wave amplitude and with increase of their frequency. The existing parasympathetic impairment and increased sympathetic drive of the autonomic system is responsible for vasopressin-induced gastric dysrrhythmia and its clinical consequences.