Gastric myoelectric activity in patients with end-stage liver disease.

BACKGROUND: Abnormalities of gastrointestinal motility and transit time have been reported in association with end-stage liver disease. Motility abnormalities could be routinely studied if a simple noninvasive test were available. The electrogastrogram is a cutaneous measure of gastric myoelectric activity and correlates well with serosal recordings of gastric myoelectric activity. The aim of this study was to evaluate gastric myoelectric activity in patients with end-stage liver disease. METHODS: Fourteen patients with end-stage liver disease had gastric myoelectric activity measured with the electrogastrogram. An electrogastrogram was considered abnormal when normal gastric slow waves were seen less than 70% of the time or there was no increase in the electrogastrogram amplitude after a meal. RESULTS: Abnormal electrogastrograms were present in 8 of 14 (57%) end-stage liver disease patients. CONCLUSIONS: Abnormal gastric myoelectric activity is common in end-stage liver disease.

The effect of intravenous vasopressin on gastric myoelectrical activity in human subjects.

UNLABELLED: Vasopressin's role in the sensation of nausea is incompletely understood. In this study, our goals were to investigate whether high intravenous vasopressin levels in normal subjects would induce nausea and vomiting and to determine the electrogastrographic (EGG) pattern which would develop at these concentrations. METHODS: EGG recordings were made on five fasting healthy subjects (three females, mean age: 27 years). Vasopressin was infused (0.15 or 0.3 U kg-1 h-1) for 1 h after a 30-min baseline recording. Serum vasopressin levels were measured every 15 min. Symptoms of nausea, cramping, retching, vomiting and bloating were graded from 0 to 5 (0 = none, 5 = most severe). Normal saline at the same rate was then infused for 1 h, with recording of symptoms and measuring blood levels of vasopressin as done previously. RESULTS: EGG data showed a 43% reduction in the percentage of normal slow waves (96-53%) at a vasopressin rate of 0.3 U kg-1 h-1. A 29% reduction (88-59%) occurred at 0.15 U kg-1 h-1. The EGG dominant frequency decreased by 0.8 cpm (3.07-2.25) for the high dose, while only 0.2 cpm reduction (2.9-2.7) occurred at the lower dose. Bradygastria (< 2.4 cpm) rather than tachygastria (> 3.7 cpm) was the predominant abnormality with the high dose. Symptoms of nausea correlated with the infusion of vasopressin and significantly increased with the higher dose. CONCLUSIONS: (i) At supraphysiological vasopressin levels, nausea was present in 80% of subjects but there was no retching or vomiting, (ii) bradygastria was the predominant dysrhythmia at these high vasopressin concentrations, (iii) increasing vasopressin levels correlated symptomatically with increases in nausea.