Published online Dec 28, 2009. doi: 10.3748/wjg.15.6034
Revised: October 16, 2009
Accepted: October 23, 2009
Published online: December 28, 2009
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 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.