MUSCULAR AND CARDIAC ADENOSINE-INDUCED PAIN IS MEDIATED BY A(1) RECEPTORS

Objectives. This study attempted to establish whether bamiphylline, a selective antagonist of A, adenosine receptors, pre vents the algogeni c effects of adenosine in humans. Background. Experimental findings in dicate that the sympathoexcitatory response elicited by adenosine is m ediated by A(1) receptors. Methods. An intrailiac infusion of increasi ng doses (from 125 to 2,000 mu g/min) of adenosine was given to 20 pat ients. Adenosine infusion was then repeated after intrailiac infusion of either bamiphylline or saline solution. In 14 other patients with a ngina, increasing doses of adenosine (from 108 to 1,728 mu g/min) were infused into the left coronary artery. Adenosine infusion was then re peated after the intravenous infusion of either bamiphylline or placeb o. Coronary blood flow velocity was monitored by a Doppler catheter. D ata relative to pain severity are expressed as median and all other da ta as mean value +/- 1 SD. Results. Bamiphylline prolonged the time to pain onset caused by the intrailiac adenosine infusion from 444 +/- 9 6 to 749 +/- 120 s (p < 0.001) and reduced pain severity from 45 to 24 mm (p < 0.01). After placebo infusion, the time to pain onset and pai n severity were similar to that of baseline (428 +/- 112 vs. 430 +/- 1 04 s, p = 0.87 and 44 vs. 43 mm, p = 0.67, respectively). Bamiphylline prolonged the time to pain onset caused by intracoronary adeno sine i nfusion from 519 +/- 128 to 603 +/- 146 s (p < 0.01) and reduced pain severity from 58 to 28 mm (p < 0.02). After placebo infusion, the time to pain onset and pain severity were similar to that at baseline (542 +/- 87 vs. 551 +/- 79 s, p = 0.14 and 55 vs. 50 mm, p = 0.61). Maxima l coronary blood flow velocities before and after bamiphylline adminis tration were similar (47 +/- 22 vs. 49 +/- 24 cm/s, p = 0.36) as well as before and after placebo administration (40 +/- 20 vs. 41 +/- 20 cm /s, p = 0.07). Conclusions. Bamiphylline reduces adenosine-induced mus cular and cardiac pain but does not affect adenosine-induced coronary vasodilation. These findings indicate that at the dose used in this st udy, bamiphylline does not detectably block vascular A(2)-receptor-med iated adenosine effects in humans, which suggests that the muscular an d cardiac algogenic effects of adenosine are mediated mainly by A(1) r eceptors.