1. Academic Validation
  2. Effects of A1 adenosine receptor blockade by bamiphylline on ischaemic preconditioning during coronary angioplasty

Effects of A1 adenosine receptor blockade by bamiphylline on ischaemic preconditioning during coronary angioplasty

  • Eur Heart J. 1996 Jun;17(6):846-53. doi: 10.1093/oxfordjournals.eurheartj.a014965.
F Tomai 1 F Crea A Gaspardone F Versaci R De Paulis P Polisca L Chiariello P A Gioffrè
Affiliations

Affiliation

  • 1 Servizio Speciale di Diagnosi e Cura di Emodinamica, Università di Roma Tor Vergata, European Hospital, Italy.
Abstract

Objective: The role of A1 adenosine receptors in preconditioning in humans is unknown. To establish whether bamiphylline, a selective antagonist of A1 adenosine receptors, abolishes ischaemic preconditioning in man, 36 consecutive patients undergoing single-vessel coronary angioplasty were randomized to receive intravenous infusion of bamiphylline (5 mg.kg-1) or placebo (0.9% NaCl) immediately prior to the procedure.

Design: The mean values (+/- 1 SD) of ST segment shifts on the surface and intracoronary electrocardiograms were measured at the end of the first and second balloon inflations, both 2 min long. The severity of cardiac pain was obtained at the same time using a visual analogue scale.

Results: In bamiphylline-treated patients, the mean ST segment shift and the severity of cardiac pain during the second inflation were similar to those during the first inflation (14 +/- 15 vs 16 +/- 16 mm, ns and 31 +/- 28 vs 31 +/- 29, ns, respectively). Conversely, in placebo-treated patients both the mean ST segment shift and the severity of cardiac pain during the second inflation were significantly less than those during the first inflation (10 +/- 6 vs 17 +/- 7 mm, P < 0.001 and 25 +/- 21 vs 39 +/- 31 mm, P < 0.01, respectively). Thus, bamiphylline abolishes ischaemic preconditioning observed in man during repeated coronary balloon inflations.

Conclusion: These results suggest that, in this setting, ischaemic preconditioning is mediated, at least in part, by A1 adenosine receptors.

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