UNLABELLED: Reports from other investigators have shown the ability of pretreatment with either parenteral (glucose) or enteral (bolus Vivonex HN) nutrition to protect against stress ulcer formation, suggesting that the mechanism of protection may be substrate availability. However, these prior animal studies have used inordinately high amounts of Vivonex HN (equal to 1050 ml/hr in a human). This study compared cytoprotection afforded by pretreatment with a continuous infusion of Vivonex HN at a more clinically applicable level to that of both parenteral (ip) and enteral (po) glucose to test the above hypothesis. One hundred eight rats were infused (0.1 ml/min) for 30 min with: po water, ip water, po 25% glucose, ip 25% glucose, or po Vivonex HN. This was followed by 2 hr of cold-restraint stress. Serum glucose was determined. Poststress, animals were sacrificed, stomachs inspected, and mean ulcer index was calculated. Only oral 25% glucose offered significant gastric cytoprotection. Serum glucose was highest in both glucose groups. CONCLUSIONS: (1) Vivonex HN pretreatment failed to cytoprotect in this model, (2) gastric cytoprotection by oral but not by parenteral glucose in the presence of similar serum glucose levels suggests that luminal factors, in addition to substrate availability, are necessary for this protection to occur.
UNLABELLED: Reports from other investigators have shown the ability of pretreatment with either parenteral (glucose) or enteral (bolus Vivonex HN) nutrition to protect against stress ulcer formation, suggesting that the mechanism of protection may be substrate availability. However, these prior animal studies have used inordinately high amounts of Vivonex HN (equal to 1050 ml/hr in a human). This study compared cytoprotection afforded by pretreatment with a continuous infusion of Vivonex HN at a more clinically applicable level to that of both parenteral (ip) and enteral (po) glucose to test the above hypothesis. One hundred eight rats were infused (0.1 ml/min) for 30 min with: po water, ip water, po 25% glucose, ip 25% glucose, or po Vivonex HN. This was followed by 2 hr of cold-restraint stress. Serum glucose was determined. Poststress, animals were sacrificed, stomachs inspected, and mean ulcer index was calculated. Only oral 25% glucose offered significant gastric cytoprotection. Serum glucose was highest in both glucose groups. CONCLUSIONS: (1) Vivonex HN pretreatment failed to cytoprotect in this model, (2) gastric cytoprotection by oral but not by parenteral glucose in the presence of similar serum glucose levels suggests that luminal factors, in addition to substrate availability, are necessary for this protection to occur.