Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Horimoto, H. et al.

Nitric oxide-generating beta-adrenergic blocker nipradilol preserves postischemic cardiac function.

BACKGROUND: Preconditioning protects the heart from ischemic injury, but some of its effects are reversed by beta-adrenergic blockade. We hypothesize that because nitric oxide is known to precondition the heart, the nitric oxide-generating beta-blocker nipradilol may simultaneously precondition and provide clinically relevant beta-blockade. METHODS: Isolated, crystalloid-perfused rabbit hearts underwent 1 hour of left anterior descending coronary artery ischemia followed by 1 hour of reperfusion. Before ischemia, six hearts received nipradilol, six received the nitric oxide donor L-arginine, four hearts received the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester before L-arginine, nine underwent ischemic preconditioning, and six received beta-blockade by esmolol before ischemic preconditioning. Seven hearts received no pretreatment (control). Action potential duration and ventricular pressure were measured. Infarct size was determined at the end of reperfusion. RESULTS: Both L-arginine and ischemic preconditioning prolonged action potential duration significantly at 60 minutes of reperfusion. Compared with control, infarct size was reduced by ischemic preconditioning (26%+/-4% versus 49%+/-3%, IPC versus control; p<0.01), L-arginine (24%+/-2%; p<0.01 versus control), and nipradilol (24%+/-2%; p<0.01 versus control). Only nipradilol preserved peak developed pressure during reperfusion. CONCLUSIONS: Despite its properties as a beta-adrenergic blocking agent, nipradilol was able to precondition the heart, probably as a result of its ability to produce nitric oxide.[1]

References

Nitric oxide-generating beta-adrenergic blocker nipradilol preserves postischemic cardiac function. Horimoto, H., Saltman, A.E., Gaudette, G.R., Krukenkamp, I.B. Ann. Thorac. Surg. (1999) [Pubmed]

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