TY - JOUR
T1 - Mechanisms of Canine Gastric Dysrhythmia
AU - Kim, Chung H.
AU - Zinsmeister, Alan R.
AU - Malagelada, Juan R.
N1 - Funding Information:
Received April 4, 1986. Accepted October 2, 1986. Address requests for reprints to: Juan-R. Malagelada, M.D., Gastroenterology Unit, Mayo Clinic, 200 First Street, S.W., Rochester, Minnesota 55905. This work was supported in part by grants AM 26428, AM 07198, and AM 34988 from the National Institutes of Health. The authors thank Dr. F. Azpiroz for surgical assistance and Velda Woyczik for typing and preparing the manuscript. © 1987 by the American Gastroenterological Association
PY - 1987
Y1 - 1987
N2 - We postulated that local synthesis and release of prostaglandins might be the paracrine pathway that triggers gastric dysrhythmia when exogenously activated. The study was divided into three parts. In part 1, a dose-response study was performed in 7 dogs to estimate the 95% effective dose for four pharmacologic agents known to cause gastric dysrhythmia. In part 2, we determined the relative efficacy of three putative blockers in preventing pharmacologic induction of gastric dysrhythmia. In part 3, several ancillary experiments were performed. The results show that an intraarterial bolus of epinephrine, met-enkephalin, prostaglandin E2, and glucagon each induced episodes of gastric dysrhythmia, whereas- saline injections did not. The 95% effective dose of these dysrhythmic drugs were 10.5, 77.0, 35.0, and 407.0 μg/kg, respectively. The dysrhythmic action of epinephrine was blocked by phentolamine and indomethacin but not by naloxone. The dysrhythmic action of met-enkephalin was blocked by naloxone and indomethacin but not by phentolamine. The dysrhythmic action of glucagon was not blocked by phentolamine, naloxone, or indomethacin. The- inhibitory effect of indomethacin on epinephrine-induced gastric dysrhythmia was shared by meclof enamate. Thus, we conclude that local prostaglandins mediate the production of gastric dysrhythmias by epinephrine and met-enkephalin; however, glucagon causes gastric dysrhythmias by a non-prostaglandin-mediated mechanism.
AB - We postulated that local synthesis and release of prostaglandins might be the paracrine pathway that triggers gastric dysrhythmia when exogenously activated. The study was divided into three parts. In part 1, a dose-response study was performed in 7 dogs to estimate the 95% effective dose for four pharmacologic agents known to cause gastric dysrhythmia. In part 2, we determined the relative efficacy of three putative blockers in preventing pharmacologic induction of gastric dysrhythmia. In part 3, several ancillary experiments were performed. The results show that an intraarterial bolus of epinephrine, met-enkephalin, prostaglandin E2, and glucagon each induced episodes of gastric dysrhythmia, whereas- saline injections did not. The 95% effective dose of these dysrhythmic drugs were 10.5, 77.0, 35.0, and 407.0 μg/kg, respectively. The dysrhythmic action of epinephrine was blocked by phentolamine and indomethacin but not by naloxone. The dysrhythmic action of met-enkephalin was blocked by naloxone and indomethacin but not by phentolamine. The dysrhythmic action of glucagon was not blocked by phentolamine, naloxone, or indomethacin. The- inhibitory effect of indomethacin on epinephrine-induced gastric dysrhythmia was shared by meclof enamate. Thus, we conclude that local prostaglandins mediate the production of gastric dysrhythmias by epinephrine and met-enkephalin; however, glucagon causes gastric dysrhythmias by a non-prostaglandin-mediated mechanism.
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U2 - 10.1016/0016-5085(87)90975-9
DO - 10.1016/0016-5085(87)90975-9
M3 - Article
C2 - 3557006
AN - SCOPUS:0023158609
SN - 0016-5085
VL - 92
SP - 993
EP - 999
JO - Gastroenterology
JF - Gastroenterology
IS - 4
ER -