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   <subfield code="a">E. coli lipopolysaccharide attenuates adenosine A1 receptor-mediated increase in plasma exudation from the hamster cheek pouch</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Xiao-pei Gao, Israel Rubinstein]</subfield>
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   <subfield code="a">Objective and design: To determine whether exposure to E. coli lipopolysaccharide (LPS) modulates adenosine A1 receptor-induced increase in plasma exudation from the intact hamster cheek pouch microcirculation. Methods and results: Using intravital microscopy, we found that suffusion of R(−)-N 6-(2-phenylisopropyl)-adenosine (R(−)-PIA) (1.0 and 10.0nM), a selective adenosine A1 receptor agonist, onto the intact cheek pouch elicited significant, concentration-dependent leaky site formation and increase in clearance of fluorescein thioisocyanate-dextran (mol mass, 70kDa) from post-capillary venules (p&lt;0.05). These responses were significantly attenuated by pre-treatment of hamsters with LPS (p&lt;0.05). By contrast, LPS had no significant effects on CGS-21680-, a selective adenosine A2A receptor agonist, bradykinin- and substance P-induced increases in plasma exudation from the cheek pouch. Conclusion: These data indicate that LPS attenuates adenosine A1 receptor-induced increase in plasma exudation in vivo in a specific fashion. We suggest that this phenomenon represents an endogenous anti-inflammatory cue to avoid excessive inflammation during Gram-negative bacterial infections.</subfield>
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