Ischemic post conditioning reduces infarct size through the alfa-1 adrenergic receptor pathway

BUCHHOLZ BX; D ANNUNZIO V; GIANI JF; SIACHOQUE N; DOMINICI FP; TURYN D; PEREZ V; DONATO M; GELPI RJ

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY

LIPPINCOTT WILLIAMS & WILKINS

Lugar: Philadelphia; Año: 2014 vol. 63 p. 504 - 511

0160-2446

The α1-adrenergic receptors (α1-ARs) are involved in preconditioning. Given that certain intracellular pathways appear to be shared by preconditioning and postconditioning, it is possible that postconditioning could be also mediated by α1-ARs. The objective was to evaluate, by analyzing infarct size, if α1-ARs activation could trigger postconditioning; and also determine Akt and glycogen synthase kinase-3β (GSK-3β) phosphorylation. Langendorff-perfused rat hearts were subjected to 30 minutes of ischemia and 120 minutes of reperfusion (I/R; n=8). After 30 min of global ischemia, we performed 6 cycles of reperfusion/ischemia of 10 sec each, followed by 120 min of reperfusion (postcon; n=9). In another postcon group, we administered prazosin during postcon protocol (postcon + prazosin; n=7). Finally, we repeated the I/R group but prazosin (prazosin; n=7), phenylephrine (PE; n=5) and clonidine (CL; n=6), were administered during the first 2 minutes of reperfusion. Infarct size was measured using the triphenyltetrazolium chloride technique. Total and phosphorylated Akt and mitochondrial GSK-3β expression were measured by Western blot. Infarct size was 58.1±5.1% in I/R. Postcon and PE reduced infarct size to 40.1±2.9% and 35.3±5.5% respectively (p