Modulation by opiates of small intestinal prostaglandin E2 and 3',5'cyclic adenosine monophosphate levels and of indomethacin-induced ulceration in the rat.
We studied the effect of parenteral morphine and naloxone administration on intestinal mucosal Prostaglandin E2 (PGE2) and 3',5' cyclic adenosine monophosphate (cAMP) levels and on indomethacin-induced intestinal ulceration in the rat. Compared to the control group, morphine significantly decreased whereas naloxone markedly increased both PGE2 and cAMP mucosal levels, respectively. Morphine or naloxone alone did not cause mucosal injury. However, when given with indomethacin, morphine significantly potentiated the ulcerogenic effect of indomethacin while naloxone exerted a protective effect. These results suggest that opioid peptides may play a role in modulation of intestinal mucosal PGE2 and cAMP levels. In addition, enhancement of indomethacin-induced ulcer formation by morphine and amelioration by naloxone might be in part mediated through their effect on mucosal PGE2 and cAMP levels.
Waisman
Y
Y
Emergency Medical Trauma Center, Children's National Medical Center, Washington D.C. 20010.
Marcus
H
H
Ligumski
M
M
Dinari
G
G
D000818:Animals; D000242:Cyclic AMP / Q000378:metabolism*; D015232:Dinoprostone / Q000378:metabolism*; D007213:Indomethacin; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism; D007421:Intestine, Small / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D009020:Morphine / Q000633:toxicity; D009270:Naloxone / Q000633:toxicity; D009294:Narcotics / Q000633:toxicity*; D051381:Rats; D011919:Rats, Inbred Strains; D014456:Ulcer / Q000139:chemically induced* / Q000188:drug therapy / Q000378:metabolism
D009294:Narcotics; D009270:Naloxone; D009020:Morphine; D000242:Cyclic AMP; D015232:Dinoprostone; D007213:Indomethacin