mark wrote:
Quote:
14. The following increase peristalsis of the small intestine
a. vagal blockade
b. mechanical distension of the intestine
c. stimulation of the splanchnic nerves
d. acetylcholinesterase
e. blockade of the ventral roots of the spinal cord in the subarachnoid portion of their course below ~T4
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a F b T c F d F e F
The small intestine has specialised contractile properties that promote digestion of food, absorption of nutrients and propulsion of material along its lumen. Slow waves occur spontaneously at 12-18 cycles per minute; these do not produce contraction but bring the membrane potential towards threshold. When sufficiently depolarised, spike potentials are triggered and it is these that result in muscle contraction. The activity of the smooth muscle of the intestine is influenced by both humoral and neural factors. Gastrin, cholesystokinin and motolin increase slow wave amplitude, spike potential frequency and muscle contraction; whereas secretin, somastotatin and glucagon reduce slow wave amplitude and hence intestinal motility. In terms of neural influences the most improtant is that of the intrinsic myenteric (Auerbachs) plexus that lies between longitudinal and circular smooth muscle. The peristaltic reflex wherby stretching of a segment of the bowel leads to proximal contraction (Ach) and distal relaxation (NANC), and forward propulsion of luminal contents, relies on the integrity of this plexus. Vagal innervation is not reqired for intestinal peristalsis.
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