BACKGROUND: The role of mechanical distension (stretch and tension) on intestinal contractility is poorly understood. METHODS: We introduce a novel isovolumic myograph to quantify the intestinal contractility in response to mechanical stimulation. To evaluate the role of distension on contractility, an external restraint was used to restrict intestinal distension or stretch induced by inflation pressure. The amplitude of intraluminal pressure at isovolumic condition was defined as an index of intestinal contractility. KEY RESULTS: The in situ maximal contraction (1.42 ± 0.39 mmHg) of duodenum in response to inflation pressure was similar to the in vitro maximal contraction (1.39 ± 0.37 mmHg). As the pressure was increased, the in situ duodenal contraction attenuated faster than the in vitro one. The in situ maximal contraction (4.86 ± 1.32 mmHg) of distal colon in response to inflation pressure was significantly larger than the in vitro maximal contraction (2.31 ± 0.67 mmHg). With increase of pressure, the in situ colonic contractility (1.82 ± 0.87 mmHg) became similar to the in vitro counterpart (1.61 ± 0.98 mmHg). With restraint, the maximal contraction of duodenum and distal colon decreased from 4.86 ± 1.32 and 1.42 ± 0.39 mmHg to 2.91 ± 0.87 and 0.97 ± 0.29 mmHg, respectively. Finally, a significant linear relation was found between strain and amplitude of contraction for both duodenum and colon which became non-significant with restraint. CONCLUSIONS & INFERENCES: Our results suggest that distension is an important stimulus for intestinal contractility and nervous regulation is implicated in the intestinal contractility response to mechanical stimulus.
BACKGROUND: The role of mechanical distension (stretch and tension) on intestinal contractility is poorly understood. METHODS: We introduce a novel isovolumic myograph to quantify the intestinal contractility in response to mechanical stimulation. To evaluate the role of distension on contractility, an external restraint was used to restrict intestinal distension or stretch induced by inflation pressure. The amplitude of intraluminal pressure at isovolumic condition was defined as an index of intestinal contractility. KEY RESULTS: The in situ maximal contraction (1.42 ± 0.39 mmHg) of duodenum in response to inflation pressure was similar to the in vitro maximal contraction (1.39 ± 0.37 mmHg). As the pressure was increased, the in situ duodenal contraction attenuated faster than the in vitro one. The in situ maximal contraction (4.86 ± 1.32 mmHg) of distal colon in response to inflation pressure was significantly larger than the in vitro maximal contraction (2.31 ± 0.67 mmHg). With increase of pressure, the in situ colonic contractility (1.82 ± 0.87 mmHg) became similar to the in vitro counterpart (1.61 ± 0.98 mmHg). With restraint, the maximal contraction of duodenum and distal colon decreased from 4.86 ± 1.32 and 1.42 ± 0.39 mmHg to 2.91 ± 0.87 and 0.97 ± 0.29 mmHg, respectively. Finally, a significant linear relation was found between strain and amplitude of contraction for both duodenum and colon which became non-significant with restraint. CONCLUSIONS & INFERENCES: Our results suggest that distension is an important stimulus for intestinal contractility and nervous regulation is implicated in the intestinal contractility response to mechanical stimulus.