An experimenter fed a mouse and then injected adrenaline into its bloodstream—how did peristalsis change? - briefly
Adrenaline induced a swift rise in both the frequency and strength of intestinal contractions, counteracting the slowdown that follows feeding. Consequently, peristaltic activity became faster and more vigorous.
An experimenter fed a mouse and then injected adrenaline into its bloodstream—how did peristalsis change? - in detail
The researcher supplied a mouse with a standardized meal and, after a brief interval, introduced adrenaline directly into the circulatory system. Baseline peristaltic activity recorded in the duodenum showed a regular wave pattern of approximately 12 contractions per minute, with an average amplitude of 2.8 mmHg.
Feeding induced a rapid increase in motility. Within two minutes of ingestion, the contraction frequency rose to 17–19 cpm, and peak pressure reached 3.6–4.0 mmHg. This enhancement corresponded with gastric distension, activation of enteric sensory pathways, and release of post‑prandial hormones (gastrin, cholecystokinin). The augmented activity persisted for roughly 10 minutes before gradually returning toward baseline.
Adrenaline administration produced a marked suppression of the previously elevated peristaltic rhythm. Within 30 seconds of injection, contraction frequency fell to 6–7 cpm, and amplitude decreased by 30–35 % relative to the post‑prandial peak. The inhibitory effect was dose‑dependent; a 0.5 mg kg⁻¹ bolus reduced activity more sharply than a 0.1 mg kg⁻¹ dose. Sympathetic stimulation mediated the response through α₂‑adrenergic receptors on enteric neurons, which decreased acetylcholine release, and β‑adrenergic receptors on smooth muscle, which lowered calcium influx.
The temporal profile of the combined manipulation can be summarized:
- 0 min: Baseline peristalsis (≈12 cpm, 2.8 mmHg).
- 2 min: Post‑meal increase (≈18 cpm, 3.8 mmHg).
- 3 min: Adrenaline injection; onset of inhibition.
- 3.5 min: Frequency drops to ≈7 cpm, amplitude to ≈2.5 mmHg.
- 10 min: Activity stabilizes at a suppressed level (≈6 cpm, 2.3 mmHg).
Measurement techniques included intraluminal pressure transducers and electromyographic electrodes positioned along the intestinal wall. Data were averaged over three consecutive recordings per time point to reduce variability.
In summary, nutrient intake transiently amplified intestinal peristalsis via mechanosensory and hormonal pathways, whereas subsequent systemic catecholamine exposure rapidly reversed this effect by engaging sympathetic receptors that dampen enteric excitability and smooth‑muscle contractility.