Reduced normogastric electrical activity associated with emesis: a telemetric study in ferrets.

AIM

To characterize the gastric myoelectric activity (GMA) and intra-abdominal pressure changes induced by emetic stimuli (apomorphine and cisplatin) in the ferret.

METHODS

GMA and intra-abdominal pressure were recorded in conscious, unrestrained ferrets surgically implanted with radiotelemetry transmitters. Animals were challenged with apomorphine (0.25 mg/kg sc) and cisplatin (10 mg/kg ip), and the emetic response was quantified via direct observation and intra-abdominal pressure recording for 1 h and 4 h, respectively. The GMA was analyzed by spectral analysis; the parameters used to characterize the GMA were the dominant frequency (DF) and the repartition of spectral power in the bradygastric, normogastric and tachygastric frequency ranges.

RESULTS

Retches were identified on the intra-abdominal pressure trace as peaks 0.30 +/- 1.01 s in duration and 59.57 +/- 2.74 mmHg in amplitude, vomit peaks were longer (0.82 +/- 0.06 s, P < 0.01) and reached a higher pressure (87.73 +/- 8.12 mmHg, P < 0.001). The number of retches and vomits quantified via direct observation [apomorphine: 65.5 +/- 11.8 retches + vomits (R+V), cisplatin: 202.6 +/- 64.1 R+V] and intra-abdominal pressure (apomorphine: 68.3 +/- 13.7 R+V, n = 8; cisplatin: 219.0 +/- 69.2 R+V, n = 8) were correlated (r = 0.97, P < 0.0001) and the timing of emesis was consistent between the 2 methods. Apomorphine induced a decrease in normogastria from 45.48% +/- 4.35% to 36.70 +/- 4.34% (n = 8, P < 0.05) but the DF of the slow waves was not changed [8.95 +/- 0.25 counts/min (cpm) vs 8.68 +/- 0.35 cpm, n = 8, P > 0.05]. Cisplatin induced a decrease in normogastria from 55.83% +/- 4.30% to 29.22% +/- 5.16% and an increase in bradygastria from 14.28% +/- 2.32% to 31.19% +/- 8.33% (n = 8, P < 0.001) but the DF (9.14 +/- 0.13 cpm) remained unchanged (P > 0.05). The GMA changes induced by cisplatin preceded the emetic response as normogastria was reduced for 1 h before the onset of emesis (57.61% +/- 5.66% to 39.91% +/- 5.74%, n = 6, P < 0.05). Peri-emesis analysis revealed that the GMA was significantly disturbed during and immediately after, but not immediately before, the emetic episodes.

CONCLUSION

The induction of emesis is reliably associated with a disrupted GMA, but changes may also occur prior to and following the emetic response.