Post-ischemic accumulation of autacoids during postconditioning (PostC) triggered cardioprotection. Intermittent targeting of specific cellular sites (i.e. bradykinin B2 receptors) during early reperfusion triggered PostC-like protection via redox signalling. Here we tested if PostC triggering includes adenosine receptors activation. Isolated rat hearts underwent 30 min ischemia and 120 min reperfusion. Left ventricular pressure was monitored and infarct size was evaluated using nitro-blue-tetrazolium staining. In Control hearts infarct size was 64 ± 4% of risk area. Postconditioning (5 cycles of 10 s reperfusion/ischemia) reduced infarct size to 28 ± 3% (p < 0.01). Postconditioning protection was abolished by 3 min of the infusion of the non-selective adenosine receptor-antagonists (8-SPT) during PostC maneuvers. Since 3 min of adenosine-infusion (1 mM or 30 mM) did not trigger PostC protection, protocol with intermittent-adenosine infusion (5 cycles of 10 s buffer-no-adenosine/buffer plus adenosine) was used to mimic PostC. Also intermittent-adenosine din not attenuate infarct size (75 ± 2%; p NS vs adenosine and Control; p < 0.01 vs PostC). Despite disparities on infarct size, post-ischemic systolic function were similar among groups. Data suggest an adenosine-dependent anti-infarct effect, but no an anti-stunning effect by PostC. Thus, neither intermittent-adenosine nor 3 min continuous adenosine can trigger protection against infarct size extension. Yet, 3 min adenosine-antagonist can prevent PostC protection. It is, thus, likely that endogenous-adenosine binding with receptors during early reperfusion is necessary to induce protection against infarct size extension, but it is not sufficient.
INTERMITTENT ADENOSINE AT THE BEGINNING OF REPERFUSION DOES NOT TRIGGER CARDIOPROTECTION
MANCARDI, Daniele;TULLIO, FRANCESCA;PERRELLI, MARIA-GIULIA;PAGLIARO, Pasquale;PENNA, Claudia
2008-01-01
Abstract
Post-ischemic accumulation of autacoids during postconditioning (PostC) triggered cardioprotection. Intermittent targeting of specific cellular sites (i.e. bradykinin B2 receptors) during early reperfusion triggered PostC-like protection via redox signalling. Here we tested if PostC triggering includes adenosine receptors activation. Isolated rat hearts underwent 30 min ischemia and 120 min reperfusion. Left ventricular pressure was monitored and infarct size was evaluated using nitro-blue-tetrazolium staining. In Control hearts infarct size was 64 ± 4% of risk area. Postconditioning (5 cycles of 10 s reperfusion/ischemia) reduced infarct size to 28 ± 3% (p < 0.01). Postconditioning protection was abolished by 3 min of the infusion of the non-selective adenosine receptor-antagonists (8-SPT) during PostC maneuvers. Since 3 min of adenosine-infusion (1 mM or 30 mM) did not trigger PostC protection, protocol with intermittent-adenosine infusion (5 cycles of 10 s buffer-no-adenosine/buffer plus adenosine) was used to mimic PostC. Also intermittent-adenosine din not attenuate infarct size (75 ± 2%; p NS vs adenosine and Control; p < 0.01 vs PostC). Despite disparities on infarct size, post-ischemic systolic function were similar among groups. Data suggest an adenosine-dependent anti-infarct effect, but no an anti-stunning effect by PostC. Thus, neither intermittent-adenosine nor 3 min continuous adenosine can trigger protection against infarct size extension. Yet, 3 min adenosine-antagonist can prevent PostC protection. It is, thus, likely that endogenous-adenosine binding with receptors during early reperfusion is necessary to induce protection against infarct size extension, but it is not sufficient.
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