Author + information
- Received March 14, 1994
- Revision received July 29, 1994
- Accepted August 3, 1994
- Published online January 1, 1995.
- Achille Gaspardone, MPhil, MD, FESC∗,a,
- Filippo Crea, MD, FESC, FACC∗,
- Fabrizio Tomai, MD, FESCa,
- Francesco Versaci, MDa,
- Maria Iamele, MDa,
- Gaetano Gioffrè, MDa,
- Luigi Chiariello, MD, FACCa and
- Pier Agostino Gioffrè, MD, FESCa
- ↵∗Address for correspondence: Dr. Achille Gaspardone, Divisione di Cardiochirurgia, Università di Roma Tor Vergata, European Hospital, via Portuense 700, 00149 Rome, Italy.
Objectives. This study attempted to establish whether bamiphylline, a selective antagonist of A1adenosine receptors, prevents the algogenic effects of adenosine in humans.
Background. Experimental findings indicate that the sympathoexcitatory response elicited by adenosine is mediated by A1receptors.
Methods. An intrailiac infusion of increasing doses (from 125 to 2,000 μg/min) of adenosine was given to 20 patients. Adenosine infusion was then repeated after intrailiac infusion of either bamiphylline or saline solution. In 14 other patients with angina, increasing doses of adenosine (from 108 to 1,728 μg/min) were infused into the left coronary artery. Adenosine infusion was then repeated after the intravenous infusion of either bamiphylline or placebo. Coronary blood flow velocity was monitored by a Doppler catheter. Data relative to pain severity are expressed as median and all other data as mean value ± 1 SD.
Results. Bamiphylline prolonged the time to pain onset caused by the intrailiac adenosine infusion from 444 ± 96 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 pain severity were similar to that of baseline (428 ± 112 vs. 430 ± 104 s, p = 0.87 and 44 vs. 43 mm, p = 0.67, respectively). Bamiphylline prolonged the time to pain onset caused by intracoronary adenosine infusion 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). Maximal coronary blood flow velocities before and after bamiphylline administration 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 muscular and cardiac pain but does not affect adenosine-induced coronary vasodilation. These findings indicate that at the dose used in this study, bamiphylline does not detectably block vascular A2-receptor-mediated adenosine effects in humans, which suggests that the muscular and cardiac algogenic effects of adenosine are mediated mainly by A1receptors.
☆ This study was supported in part by Research Grant 40%/1991 from the Ministero dell'Università e della Ricerca Scientifica e Tecnologica, Rome, Italy. (It was previously presented in abstract form in Circulation 1993;88 Suppl 1:1–55.)
- Received March 14, 1994.
- Revision received July 29, 1994.
- Accepted August 3, 1994.