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Articles in PresS, published online ahead of print February 21, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01031.2001
Submitted on November 27, 2001
Accepted on February 14, 2002
1 Experimental Cardiology, Thoraxcenter, Cardiovascular Research Institute COEUR, Erasmus University Rotterdam, Rotterdam, Netherlands
* To whom correspondence should be addressed. E-mail: liem{at}tch.fgg.eur.nl.
The mechanism underlying interorgan preconditioning of the heart remains elusive, although a role for adenosine and activation of a neurogenic pathway have been postulated. We tested in rats the hypothesis that adenosine released by the remote ischemic organ stimulates local afferent nerves, which leads to activation of myocardial adenosine receptors. Preconditioning with a 15-min mesenteric artery occlusion (MAO15) reduced infarct size produced by a 60-min coronary artery occlusion (60-min CAO) from 68±2% to 48±4% (P<0.05). Pretreatment with ganglion blocker hexamethonium or 8-(p-sulfophenyl)theophylline (8-SPT) abolished the protection by MAO15. Intramesenteric artery (but not intraportal vein) infusion of adenosine 10 µg/min was as cardioprotective as MAO15, which was also abolished by hexamethonium. Whereas administration of hexamethonium at 5 min reperfusion following MAO15 had no effect, 8-SPT at 5 min reperfusion abolished the protection. Permanent reocclusion of the mesenteric artery before the 60-min CAO enhanced the cardioprotection by MAO15 (30±5%) but all protection was abolished when 8-SPT was administered after reocclusion of the mesenteric artery. Together these findings demonstrate the involvement of myocardial adenosine receptors. In conclusion, locally released adenosine during small intestinal ischemia, stimulates afferent nerves in the mesenteric bed during early reperfusion, initiating a neurogenic pathway that leads to activation of myocardial adenosine receptors.
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