Adenosine preferentially increases blood flow to the esophageal mucosa, antral mucosa, and small intestine in rabbits, an effect mediated by A2-subtype P1-purinergic receptors.
Adenosine A2 agonism augments GI mucosal perfusion in rabbits; leaves open translation to human ischemia or shock.
The potential of adenosine to regulate organ blood flow (ml/min/100 g tissue) in the intact rabbit upper alimentary tract was evaluated using the radioactive microsphere technique. Adenosine (1.0 mumole/kg/min) produced significant, greater than threefold increases in esophageal mucosal blood flow (37 +/- 2 to 127 +/- 47) and threefold increases in antral mucosal (39 +/- 3 to 144 +/- 24) and transmural small intestinal blood flow (duodenum, 60 +/- 13 to 187 +/- 22; jejunum, 42 +/- 3 to 138 +/- 16; ileum, 27 +/- 2 to 80 +/- 22). Inosine did not reproduce these effects. P1-purinergic receptor antagonism with theophylline blocked the effects of adenosine. 5'-(N-Ethylcarboxamido)adenosine, an agonist of A2-subtype, P1-purinergic receptors, increased gastrointestinal organ blood flow similarly to adenosine with nmole/kg/min doses. Similar doses of the A1-subtype agonist, N5-cyclohexyladenosine, were ineffective, but mumole/kg/min doses produced small effects on esophageal mucosa and ileum. Our results indicate that in rabbit alimentary organs, adenosine preferentially increases blood flow to esophageal mucosa, antral mucosa, and small intestine. Its effects are mediated by the A2-subtype of P1-purinergic receptors.
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Pennanen et al. (1994) studied this question.
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