Neural mechanisms involved in the delay of gastric emptying and gastrointestinal transit of liquid after thoracic spinal cord transection in awake rats
Fda. Gondim et al., Neural mechanisms involved in the delay of gastric emptying and gastrointestinal transit of liquid after thoracic spinal cord transection in awake rats, AUTON NEURO, 87(1), 2001, pp. 52-58
Spinal cord transection (SCT) delays gastric emptying (GE), and intestinal
and gastrointestinal (GI) transit of liquid in awake rats. This study evalu
ates the neural mechanisms involved in this phenomenon. Male Wistar rats (N
= 147) were fasted for 16 h and had the left jugular vein cannulated follo
wed by laminectomy or laminectomy + complete SCT between T-4 and T-5 verteb
rae. The next day, a test meal (1.5 ml of a phenol red solution, 0.5 mg/ml
in 5% glucose) was administered by gavage feeding and 10 min later cervical
dislocation was performed. Dye recovery in the stomach, and proximal, mid
and distal small intestine was determined by spectrophotometry. SCT inhibit
ed GE and GI transit since it increased gastric recovery by 71.3% and decre
ased mid small intestine recovery by 100% (P < 0.05). Subdiaphragmatic vago
tomy, celiac ganglionectomy + section of the splanchnic nerves, i.v. hexame
thonium (20 mg/kg) or yohimbine (3 mg/kg) prevented the development of the
SCT effect on GE and GI transit. Pretreatment with i.v. naloxone (3, mg/kg)
, L-NAME (3 mg/kg) or propranolol (2 mg/kg) was ineffective. Bilateral adre
nalectomy or guanethidine (10 mg/kg) increased the magnitude of the GE inhi
bition, while i.v. prazosin (1 mg/kg) or atropine (0.5 mg/kg) decreased the
magnitude but did not abolish the GE inhibition. In summary, the inhibitio
n of GI motility observed 1 day after thoracic SCT in awake rats seems to i
nvolve vagal and possibly splanchnic pathways. (C) 2001 Elsevier Science B.
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