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Thourani, V.H. et al.

Adenosine A3 pretreatment before cardioplegic arrest attenuates postischemic cardiac dysfunction.

BACKGROUND: The cardioprotective effects of the adenosine A3 receptor in a cardioplegia model have not been described. We tested the hypothesis that infusion of the A3 receptor agonist, Cl-IB-MECA (100 nM), as a pretreatment (PTx) and/or as a cardioplegic (CP) additive reduces postischemic myocardial injury. METHODS: Isolated perfused rat hearts underwent 30 minutes of normothermic ischemia, 60 minutes of intermittent hypothermic cardioplegia (10 degrees C), followed by 2 hours of reperfusion. Hearts were divided into four groups: (1) no pretreatment (PTx) and unsupplemented cardioplegia (CP) (control), (2) Cl-IB-MECA PTx and unsupplemented CP (A3-PTx), (3) no PTx and Cl-IB-MECA CP (A3-CP), or (4) Cl-IB-MECA PTx and Cl-IB-MECA CP (A3-[PTx+CP]). RESULTS: Coronary flow was not increased after A3 pretreatment when compared to baseline values. After 2 hours of reperfusion, left ventricular developed pressure in control and A3-CP groups was depressed to 43% +/- 3% and 47% +/- 2% of baseline; while A3-PTx and A3-[PTx+CP] significantly increased left ventricular developed pressure (65% +/- 3% and 61% +/- 5%) from baseline relative to control and A3-CP. Effluent creatine kinase activity was significantly decreased by A3-PTx (1520 +/- 32 IU/L), A3-[PTx+CP] (1481 +/- 41 IU/L) from control (1734 +/- 54 IU/L) and A3-CP (1750 +/- 43 IU/L). Myocardial edema (% tissue water) was significantly less in A3-PTx (78 +/- 0.6%) and A3-[PTx+CP] (76% +/- 2%) compared with control (85% +/- 0.4%) and A3-CP (83% +/- 2%). CONCLUSIONS: Adenosine A3 receptor stimulation as a pretreatment attenuates postischemic cardiodynamic dysfunction and creatine kinase release but has no cardioprotection as an adjunct to cold cardioplegia.[1]

References

Adenosine A3 pretreatment before cardioplegic arrest attenuates postischemic cardiac dysfunction. Thourani, V.H., Ronson, R.S., Jordan, J.E., Guyton, R.A., Vinten-Johansen, J. Ann. Thorac. Surg. (1999) [Pubmed]

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