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Articles in PresS, published online ahead of print February 7, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00929.2001
Submitted on October 25, 2001
Accepted on January 31, 2002
1 Diaprtimento di Medicina Clinica, Scienze Cardiovascolari ed Immunologiche, Universita di Napoli, Naples, Italy
2 Dipartimento delle Malattie del Metabolismo e dell'Invecchiamento, Seconda Universita di Napoli, Naples, Italy; Centro medico di Telese, Fondazione, Benevento, Italy
3 UO Riabilitazione ASL4 Basso Molise, Fondazione, Larino, Italy
4 Centro medico di Telese, Fondazione, Benevento, Italy
5 Diaprtimento di Medicina Clinica, Scienze Cardiovascolari ed Immunologiche, Universita di Napoli, Naples, Italy; Department of Medicine, University of California, San Diego, USA
6 Diaprtimento di Medicina Clinica, Scienze Cardiovascolari ed Immunologiche, Universita di Napoli, Naples, Italy; Centro medico di Telese, Fondazione, Benevento, Italy
* To whom correspondence should be addressed. E-mail: p.abete{at}unina.it.
Ischemic preconditioning (PC) has been proposed as an endogenous form of protection against-ischemia reperfusion injury. We have shown that PC does not prevent post-ischemic dysfunction in the aging heart. This phenomenon could be due to the reduction of cardiac norepinephrine release and it has also been previously demonstrated that age-related decrease of norepinephrine release from cardiac adrenergic nerves may be restored by caloric restriction. Here, we investigated the effects on mechanical parameters of PC against 20 min of global ischemia followed by 40 min of reperfusion in isolated hearts from adult (6 months) and "ad libitum" fed and food-restricted senescent (24 months) rats. Norepinephrine release in coronary effluent was determined by high performance liquid cromatography. Final recovery of percent-developed pressure was significantly improved after preconditioning in adult hearts vs unconditioned controls (85.2±19.0% vs 51.5±10%, p<0.01). The effect of PC on developed pressure recovery was absent in "ad libitum" fed but it was restored in food-restricted senescent hearts (66.6±13 vs 38.3±11%, p<.05). Accordingly, norepinephrine release significantly increased after PC in both adult and in food-restricted senescent hearts and depletion of myocardial norepinephrine stores by reserpine abolished PC effect in both adult and in food-restricted senescent hearts. We conclude that PC reduces post-ischemic dysfunction in adult and food-restricted but not in "ad libitum" fed senescent hearts. Despite the possibility of multiple age-related mechanisms, the protection afforded by PC was correlated with increased norepinephrine release and it was blocked by reserpine in both adult and food-restricted senescent hearts. Thus, caloric restriction may restore PC in the aging heart probably via increased norepinephrine release.
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