ISCHEMIC PRECONDITIONING IN IMMATURE MYOCARDIUM

Citation
Wi. Awad et al., ISCHEMIC PRECONDITIONING IN IMMATURE MYOCARDIUM, Circulation, 98(19), 1998, pp. 206-213
Citations number
27
Categorie Soggetti
Peripheal Vascular Diseas",Hematology,"Cardiac & Cardiovascular System
Journal title
ISSN journal
00097322
Volume
98
Issue
19
Year of publication
1998
Supplement
S
Pages
206 - 213
Database
ISI
SICI code
0009-7322(1998)98:19<206:IPIIM>2.0.ZU;2-7
Abstract
Background-Protection by ischemic preconditioning (PC) has not been st udied extensively in immature hearts. We studied the developmental dif ferences in the ability of the rat heart to precondition with ischemia . Methods and Results-Hearts from 4-, 7-, 14-, and 21-day-old and adul t (approximate to 50-day-old) rats were aerobically perfused in Langen dorff mode before a PC stimulus of either (1) 3-minute ischemia (I), 3 -minute reperfusion (R), 5-minute I, fi-minute R, or (2) 4 cycles of 5 -minute I and 5-minute R, before a prolonged I (chosen to give 30% to 40% recovery) and 60-minute R. LVDP recovery was expressed as percent of baseline reading (after 20-minute aerobic perfusion). Protection wa s seen after protocol 1 in 14- and 21-day-old and adult hearts (45+/-5 %, 53+/-7%, and 58+/-5% versus 30+/-4%, 29+/-3%, and 32+/-2% in contro ls, respectively) but not in 4- and 7-day (neonatal) hearts; neonatal hearts were also not protected in protocol 2. To determine whether thi s inability of neonatal hearts to precondition was due to insufficient duration of the PC cycle, they were subjected to increased I duration s up to 20 minutes before 5-minute R, prolonged I (90 minutes and 60-m inute R) (protocol 3); protection was not seen, To determine whether t he inability to precondition was due to an excessively prolonged ische mic duration, neonatal hearts were subjected to only 45 minutes of pro longed I (protocol 4); again, PC protection was not evident.Conclusion s-Protection by PC develops after 7 days; the inability of neonatal he arts (<7 days old) to precondition is not due to insufficient stimulus or extended ischemia.