D. Schulman et al., Effect of aging on the ability of preconditioning to protect rat hearts from ischemia-reperfusion injury, AM J P-HEAR, 281(4), 2001, pp. H1630-H1636
Citations number
43
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Ischemic preconditioning (IP) reduces infarct size in young animals; howeve
r, its impact on aging is underinvestigated. The effect of variations in IP
stimuli was studied in young, middle-aged, and aged rat hearts. Isolated h
earts underwent 35 min of regional ischemia and 120 min of reperfusion. Hea
rts with IP were subjected to either one ischemia-reperfusion cycle (5 min
of ischemia and 5 min of reperfusion per cycle) or three successive cycles
before 35 min of regional ischemia. Additional studies investigated the eff
ects of pharmacological preconditioning in aged hearts using the adenosine
A, receptor agonist 2-chloro-N-6-cyclopentyladenosine, the protein kinase C
analog 1,2-dioctanoyl-sn-glycerol, and the mitochondrial ATP-sensitive pot
assium (K-ATP)-channel opener diazoxide. Infarct sizes indicated that the a
ged rat heart could not be preconditioned via ischemic or pharmacological m
eans. The middle-aged rat heart had a blunted IP response compared with the
young adult (only an increased IP stimulus caused a significant reduction
in infarct size). These results suggest that there are defects within the I
P signaling cascade of the aged heart. Clinical relevance is important if w
e are to use any IP-like mimetics to the benefit of an aging population.