[Action of adenosine on intestinal motility after experimental mesenteric ischemia in dogs]

The purpose of the present work was to demonstrate beneficial action of adenosine on intestinal motility in the dog after experimental ischemia and to establish the role of A1- and A2-purinergic receptors. Adenosine was compared to an A1-agonist (N6-cyclohexyl-adenosine or CHA), an A2-agonist (5'-(N-ethyl) carboxamido-adenosine or NECA) and an inhibitor of adenosine cellular uptake (dipyridamole). Motility was analyzed by recording the electromyogram with intraparietal electrodes. Experimental ischemia was obtained by clamping the superior mesenteric artery during two hours. Under physiologic conditions, adenosine (1 mg.kg-1.i.v.) increased myoelectric complexes frequency by 49 p. 100 and the jejunal motility index by 46 p. 100. CHA (1 microgram.kg-1.i.v.) and dipyridamole (0.5 mg.kg-1.i.v.) increased myoelectric complexes frequency by 42 p. 100 and 67 p. 100 while NECA (1 microgram.kg-1.i.v.), increased the motility index by 30 p. 100. Adenosine and NECA increased mesenteric arterial blood flow by 35 p. 100 and 57 p. 100 respectively. After a two hours ischemia the return to normal electromyogram was 10.1 +/- 5.7 h. Adenosine (administered 10 min after the end of ischemia) reduced this recovery period to 3.3 +/- 0.8 h, NECA to 1.3 +/- 0.8 h and dipyridamole to 5.0 +/- 2.6 h. We conclude that, under physiological conditions, adenosine modifies jejunal motility directly via A1-receptors of smooth muscle and indirectly via A2-receptors of mesenteric vessels. On the other hand, after experimental ischemia, adenosine improves the post-ischemic restoration via vessels A2-receptors only.