Coupling and propagation of normal and dysrhythmic gastric slow waves during acute hyperglycaemia in healthy humans.

Acute hyperglycaemia in healthy humans disrupts slow wave rhythm similar to that observed in diabetic gastropathy, but hyperglycaemic effects on regional dysrhythmias, power, coupling and propagation are unexplored. Using mucosal mapping, we aimed to demonstrate that hyperglycaemia elicits region-specific tachygastria and evokes slow wave uncoupling between adjacent regions. Catheters with bipolar electrodes were affixed 10.5, 6 and 2 cm from the pylorus during endoscopy with midazolam in 10 healthy humans. Recordings were obtained for 1 h under basal conditions and for 1 h with hyperglycaemic clamping to 250 mg dL(-1). In basal recordings, proximal and distal slow wave frequencies were similar [2.91 +/- 0.05 vs 2.81 +/- 0.09 cycles per minute (cpm)]. Tachygastria (>3.6 cpm) was present 1.7 +/- 1.1% of the time proximally and 3.3 +/- 1.8% distally and localized to one lead 67% of the time. Proximal to distal gradients in signal power and power variability were observed. Coupling between adjacent sites was 78 +/- 2% with propagation velocities of 1.3 +/- 0.1 cm s(-1). 2 +/- 1% of segments showed >50% uncoupling. Hyperglycaemic clamping increased mean proximal (3.18 +/- 0.11 cpm) and distal (3.50 +/- 0.12 cpm) frequencies and proximal (15 +/- 6%) and distal (32 +/- 9%) tachygastria (all P < 0.01) that localized to one lead 80% of the time. During periods of normal frequency, coupling decreased proximally (54 +/- 6%) and distally (47 +/- 4%) (P < 0.01). 55 +/- 8% of segments showed >50% uncoupling (P < 0.01). In conclusion, gastric slow waves show stable, highly coupled rhythms under basal conditions. Hyperglycaemia elicits isolated tachygastrias and uncoupling of normal slow waves that are most prominent distally. These findings provide a foundation for studying slow wave conduction defects in diabetic gastropathy.

Directed endoscopic mucosal mapping of normal and dysrhythmic gastric slow waves in healthy humans.

Frequency and amplitude characteristics of normal and dysrhythmic slow waves in different gastric regions are poorly characterized. Using endoscopic mucosal mapping, we quantified slow wave frequency and power at predetermined sites under control conditions and with glucagon. Twelve healthy volunteers underwent gastroscopy with midazolam. Bipolar recording electrodes were directed to 12, 7, and 2 cm proximal to the pylorus along the greater and lesser curvatures. Dominant frequencies at all sites were 2.96 +/- 0.07 cycles min(-1) (cpm). Powers of the dominant frequency were 59 +/- 7% lower 12 cm vs 2 cm from the pylorus (P < 0.01), but were similar along the greater and lesser curvatures. Glucagon (0.3 mg IV) decreased dominant frequencies (1.40 +/- 0.10 cpm, P < 0.01) and elicited power reductions which varied by region (36 +/- 37% at 12 cm vs 79 +/- 20% at 2 cm, P < 0.01). Comparing dominant frequencies from mucosal recordings and electrogastrography revealed minimal slow wave uncoupling. In conclusion, endoscopic mucosal mapping demonstrates slow wave power gradients from the proximal to distal stomach under normal conditions. Glucagon evokes bradygastria with minimal uncoupling and elicits inhibitory effects on slow wave power which are more potent in the distal antrum. This method provides insight into the mechanisms of action of gastric slow wave dysrhythmic stimuli.

Inhibitory actions of a high fibre diet on intestinal gas transit in healthy volunteers.

BACKGROUND: Fibre treatment often produces gaseous symptoms which have been attributed to fermentation by colonic bacteria with increased gas production. Effects of fibre ingestion on intestinal gas flow are unexplored. AIMS: We aimed to test the hypothesis that consumption of a high fibre diet retards gas transit. SUBJECTS: Ten healthy volunteers participated. METHODS: To investigate the effects of fibre on gas dynamics, physiological gas mixtures were jejunally perfused at 12 ml/min x 2 hours after a standard diet for seven days with and without psyllium 30 g/day in a crossover fashion. Gas was collected from an intrarectal catheter to bypass the anus and evacuation was quantified in real time using a barostat. RESULTS: On initiating gas perfusion under control conditions, an initial lag phase with no gas expulsion was observed (1129 (274) seconds). Thereafter, gas evacuation from the rectum proceeded with cumulative volumes of 1429 (108) ml by the end of the second hour. Evacuation was pulsatile with passage of 20.9 (2.5) boluses, with mean volumes of 68.2 (5.0) ml. Fibre prolonged the lag time (2265 (304) seconds; p<0.05) and reduced cumulative gas evacuation volumes (1022 (80) ml; p<0.05). Decreased gas evacuation resulted from reductions in the numbers of bolus passages (14.2 (1.1); p<0.05) but not bolus volumes (70.7 (3.4) ml; p = 0.66). CONCLUSIONS: Consumption of a high fibre diet retards intestinal gas transit by decreasing bolus propulsion to the rectum. Thus, in addition to increasing gas production by colonic flora, fibre ingestion may elicit gaseous symptoms by promoting gas retention.