TY - JOUR
T1 - Gastric mucosal protection from enteral nutrients
T2 - Role of motility
AU - Ephgrave, Kimberly S.
AU - Brasel, Karen J.
AU - Cullen, Joseph J.
AU - Broadhurst, Kimberly A.
N1 - Funding Information:
Supported by a Merit Review Grant to K. Ephgrave from the Department of Veterans Affairs.
PY - 1998
Y1 - 1998
N2 - Background: Cold restraint stress increases the force of gastric contractions and produces gastric mucosal injury in rats. The aim of our study was to determine whether enteral glucose or hyperglycemia alone would alter the stress-induced gastric motility pattern and ameliorate the associated gastric mucosal injury. Methods: Adult male rats underwent surgical placement of gastric catheters, jugular venous catheters, and gastric strain gauge transducers 5 days before cold restraint. Three groups of rats received different substances during the same cold restraint stress protocol. Group 1 received 0.9% NaCl, 2 mL/h infused both intravenously (IV) and intragastrically (IG); group 2 received 0.9% NaCl, 2 mL/h IG plus 25% glucose, 2 mL/h IV; and group 3 received 0.9% NaCl, 2 mL/h IV plus 25% glucose IG. Following baseline gastric motility measurements, all rats were restrained for 2 hours at 20°C followed by 2 hours at 4°C. Results: Restraint even at room temperature increased the force of gastric contractions; the cold environment gradually prolonged gastric contractions. Enteral glucose blunted the effects of stress on gastric motility, increased gastric residual volume, decreased gastric acidity, and prevented gastric mucosal injury. Parenteral glucose had little effect on any gastric parameters. Conclusions: Enteral glucose prevents the abnormal gastric motility pattern that is necessary to produce the gastric mucosal injury associated with cold restraint stress, but hyperglycemia alone has little effect on the pathophysiology of cold restraint.
AB - Background: Cold restraint stress increases the force of gastric contractions and produces gastric mucosal injury in rats. The aim of our study was to determine whether enteral glucose or hyperglycemia alone would alter the stress-induced gastric motility pattern and ameliorate the associated gastric mucosal injury. Methods: Adult male rats underwent surgical placement of gastric catheters, jugular venous catheters, and gastric strain gauge transducers 5 days before cold restraint. Three groups of rats received different substances during the same cold restraint stress protocol. Group 1 received 0.9% NaCl, 2 mL/h infused both intravenously (IV) and intragastrically (IG); group 2 received 0.9% NaCl, 2 mL/h IG plus 25% glucose, 2 mL/h IV; and group 3 received 0.9% NaCl, 2 mL/h IV plus 25% glucose IG. Following baseline gastric motility measurements, all rats were restrained for 2 hours at 20°C followed by 2 hours at 4°C. Results: Restraint even at room temperature increased the force of gastric contractions; the cold environment gradually prolonged gastric contractions. Enteral glucose blunted the effects of stress on gastric motility, increased gastric residual volume, decreased gastric acidity, and prevented gastric mucosal injury. Parenteral glucose had little effect on any gastric parameters. Conclusions: Enteral glucose prevents the abnormal gastric motility pattern that is necessary to produce the gastric mucosal injury associated with cold restraint stress, but hyperglycemia alone has little effect on the pathophysiology of cold restraint.
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U2 - 10.1016/S1072-7515(98)00048-9
DO - 10.1016/S1072-7515(98)00048-9
M3 - Article
C2 - 9544958
AN - SCOPUS:0031940889
SN - 1072-7515
VL - 186
SP - 434
EP - 440
JO - Journal of the American College of Surgeons
JF - Journal of the American College of Surgeons
IS - 4
ER -